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Gene Information
Gene symbol: HTR2B
Gene name: 5-hydroxytryptamine (serotonin) receptor 2B, G protein-coupled
HGNC ID: 5294
Synonyms: 5-HT(2B), 5-HT2B
Related Genes
Related Sentences
| # | PMID | Sentence |
| 1 | 39973 | Tyrosine (Tyr), tyrosine hydroxylase (TH), tryptophan (Trp), serotonin (5-HT), and 5-hydroxyindole acetic acid (5-HIAA) were assayed spectrofluorometrically and radioenzymatically in various regions of post-mortem brains of human patients with hepatic, uremic, and diabetic coma, liver cirrhosis without coma, and hepatic coma treated with parenteral administration of L-valine, a branched-chain amino acid. |
| 2 | 1279445 | In addition, an alternative method was used to assess 5-HT activity in thyroidectomized (TX) rats, i.e. measurement of 5-HT disappearance after inhibition of tryptophan hydroxylase with p-chlorophenylalanine (PCPA). |
| 3 | 1506131 | Control animals showed a large 5-HT concentration-dependent increase in leakage of albumin in V3 venules, but this response was inhibited in the Diabetic-Tone animals. |
| 4 | 1671378 | Amphetamine-induced stereotypy and turnover of dopamine (DA) and serotonin (5-HT) in the CNS were assessed in streptozocin-induced diabetic rats 48 h after withdrawal from insulin treatment and compared with nondiabetic controls, diabetic rats receiving continued insulin treatment, and chronically hyperglycemic diabetic rats. |
| 5 | 1671378 | DA turnover was significantly reduced in striatum and hypothalamus in all diabetic groups. 5-HT turnover was reduced in chronically hyperglycemic diabetic rats in all four brain regions but normalized in insulin-treated diabetic rats. |
| 6 | 1671378 | Insulin-withdrawn diabetic rats had significantly reduced 5-HT turnover in frontal cortex. |
| 7 | 1671378 | Taken together, the findings indicate that insulin replacement does not normalize diabetes-induced reduction in DA turnover and that short-term insulin withdrawal, e.g., occurring clinically with noncompliance, affects both 5-HT turnover in some brain regions and behavior. |
| 8 | 1671378 | Amphetamine-induced stereotypy and turnover of dopamine (DA) and serotonin (5-HT) in the CNS were assessed in streptozocin-induced diabetic rats 48 h after withdrawal from insulin treatment and compared with nondiabetic controls, diabetic rats receiving continued insulin treatment, and chronically hyperglycemic diabetic rats. |
| 9 | 1671378 | DA turnover was significantly reduced in striatum and hypothalamus in all diabetic groups. 5-HT turnover was reduced in chronically hyperglycemic diabetic rats in all four brain regions but normalized in insulin-treated diabetic rats. |
| 10 | 1671378 | Insulin-withdrawn diabetic rats had significantly reduced 5-HT turnover in frontal cortex. |
| 11 | 1671378 | Taken together, the findings indicate that insulin replacement does not normalize diabetes-induced reduction in DA turnover and that short-term insulin withdrawal, e.g., occurring clinically with noncompliance, affects both 5-HT turnover in some brain regions and behavior. |
| 12 | 1671378 | Amphetamine-induced stereotypy and turnover of dopamine (DA) and serotonin (5-HT) in the CNS were assessed in streptozocin-induced diabetic rats 48 h after withdrawal from insulin treatment and compared with nondiabetic controls, diabetic rats receiving continued insulin treatment, and chronically hyperglycemic diabetic rats. |
| 13 | 1671378 | DA turnover was significantly reduced in striatum and hypothalamus in all diabetic groups. 5-HT turnover was reduced in chronically hyperglycemic diabetic rats in all four brain regions but normalized in insulin-treated diabetic rats. |
| 14 | 1671378 | Insulin-withdrawn diabetic rats had significantly reduced 5-HT turnover in frontal cortex. |
| 15 | 1671378 | Taken together, the findings indicate that insulin replacement does not normalize diabetes-induced reduction in DA turnover and that short-term insulin withdrawal, e.g., occurring clinically with noncompliance, affects both 5-HT turnover in some brain regions and behavior. |
| 16 | 1671378 | Amphetamine-induced stereotypy and turnover of dopamine (DA) and serotonin (5-HT) in the CNS were assessed in streptozocin-induced diabetic rats 48 h after withdrawal from insulin treatment and compared with nondiabetic controls, diabetic rats receiving continued insulin treatment, and chronically hyperglycemic diabetic rats. |
| 17 | 1671378 | DA turnover was significantly reduced in striatum and hypothalamus in all diabetic groups. 5-HT turnover was reduced in chronically hyperglycemic diabetic rats in all four brain regions but normalized in insulin-treated diabetic rats. |
| 18 | 1671378 | Insulin-withdrawn diabetic rats had significantly reduced 5-HT turnover in frontal cortex. |
| 19 | 1671378 | Taken together, the findings indicate that insulin replacement does not normalize diabetes-induced reduction in DA turnover and that short-term insulin withdrawal, e.g., occurring clinically with noncompliance, affects both 5-HT turnover in some brain regions and behavior. |
| 20 | 1675174 | Using quantification by image analysis and double-labeling immunohistochemistry on mesenteric veins, significant reductions in the density of nerve plexuses staining for 5-hydroxytryptamine (5-HT) and tyrosine hydroxylase (TH) were shown in vessels from diabetic rats compared to controls. |
| 21 | 1675174 | No reductions were observed in the density of nerve plexuses stained for the neuronal marker, PGP 9.5, or for substance P (SP), a marker for afferent nerve fibers. |
| 22 | 2420666 | Furthermore, the effect of chronic tolbutamide contrasted with that of chronic insulin administration where hypothalamic NE neuronal activity was increased, while hypothalamic 5-HT neuronal activity was unchanged. |
| 23 | 2935473 | The effect of 5-hydroxytryptamine (5-HT) alteration on brain dopamine (DA), norepinephrine (NE), beta-endorphin (beta E) and immunoreactive insulin (IRI) was studied in Sprague-Dawley diabetic and control rats. |
| 24 | 2935473 | PCPA treatment significantly decreased brain content of 5-HT and 5-hydroxyindole acetic acid (5-HIAA) while it caused significant increase and decrease in brain beta E and insulin levels, respectively, in both normal and diabetic rat. |
| 25 | 2935473 | Meanwhile, the administration of fluoxetine resulted in significant increase in brain content of 5-HT, DA, NE and insulin but significant decline of beta E in diabetic and saline control rats. |
| 26 | 2935473 | The results of this experiment indicate that 5-HT may be regulating both beta E and insulin regardless of the availability of pancreatic insulin. |
| 27 | 2935473 | The effect of 5-hydroxytryptamine (5-HT) alteration on brain dopamine (DA), norepinephrine (NE), beta-endorphin (beta E) and immunoreactive insulin (IRI) was studied in Sprague-Dawley diabetic and control rats. |
| 28 | 2935473 | PCPA treatment significantly decreased brain content of 5-HT and 5-hydroxyindole acetic acid (5-HIAA) while it caused significant increase and decrease in brain beta E and insulin levels, respectively, in both normal and diabetic rat. |
| 29 | 2935473 | Meanwhile, the administration of fluoxetine resulted in significant increase in brain content of 5-HT, DA, NE and insulin but significant decline of beta E in diabetic and saline control rats. |
| 30 | 2935473 | The results of this experiment indicate that 5-HT may be regulating both beta E and insulin regardless of the availability of pancreatic insulin. |
| 31 | 2935473 | The effect of 5-hydroxytryptamine (5-HT) alteration on brain dopamine (DA), norepinephrine (NE), beta-endorphin (beta E) and immunoreactive insulin (IRI) was studied in Sprague-Dawley diabetic and control rats. |
| 32 | 2935473 | PCPA treatment significantly decreased brain content of 5-HT and 5-hydroxyindole acetic acid (5-HIAA) while it caused significant increase and decrease in brain beta E and insulin levels, respectively, in both normal and diabetic rat. |
| 33 | 2935473 | Meanwhile, the administration of fluoxetine resulted in significant increase in brain content of 5-HT, DA, NE and insulin but significant decline of beta E in diabetic and saline control rats. |
| 34 | 2935473 | The results of this experiment indicate that 5-HT may be regulating both beta E and insulin regardless of the availability of pancreatic insulin. |
| 35 | 2935473 | The effect of 5-hydroxytryptamine (5-HT) alteration on brain dopamine (DA), norepinephrine (NE), beta-endorphin (beta E) and immunoreactive insulin (IRI) was studied in Sprague-Dawley diabetic and control rats. |
| 36 | 2935473 | PCPA treatment significantly decreased brain content of 5-HT and 5-hydroxyindole acetic acid (5-HIAA) while it caused significant increase and decrease in brain beta E and insulin levels, respectively, in both normal and diabetic rat. |
| 37 | 2935473 | Meanwhile, the administration of fluoxetine resulted in significant increase in brain content of 5-HT, DA, NE and insulin but significant decline of beta E in diabetic and saline control rats. |
| 38 | 2935473 | The results of this experiment indicate that 5-HT may be regulating both beta E and insulin regardless of the availability of pancreatic insulin. |
| 39 | 2970524 | Blockade of wet-dog shakes by 5-HT receptor antagonists strengthens the proposal that this behavior is a good index of central 5-HT activity. |
| 40 | 3063593 | Insulin incubation in bathing medium for 4-5 hr enhances the decreased gastro-intestinal responses to sal, but not to 5-HT. 4. |
| 41 | 3139426 | Intraplatelet serotonin (5-HT) content was determined in 23 patients with type I (insulin-dependent) diabetes mellitus (IDDM), 23 patients with type II (non-insulin-dependent) diabetes mellitus (NIDDM), 29 patients with peripheral vascular disease (PVD) and 34 age-matched normal subjects. |
| 42 | 3139426 | The median intraplatelet 5-HT content was significantly lower (P less than 0.002) in IDDM patients: 3.0 (range 1.3-6.3), NIDDM patients: 2.5 (range 1.7-5.8), PVD patients: 2.42 (range 0.94-4.98) nmol 10(-9) platelets than that in all young + elderly healthy subjects. |
| 43 | 3139426 | Insulin-dependent diabetes mellitus patients had greater plasma 5-HT concentrations but this did not achieve statistical significance despite a 66% increment in its value. |
| 44 | 3139426 | Intraplatelet serotonin (5-HT) content was determined in 23 patients with type I (insulin-dependent) diabetes mellitus (IDDM), 23 patients with type II (non-insulin-dependent) diabetes mellitus (NIDDM), 29 patients with peripheral vascular disease (PVD) and 34 age-matched normal subjects. |
| 45 | 3139426 | The median intraplatelet 5-HT content was significantly lower (P less than 0.002) in IDDM patients: 3.0 (range 1.3-6.3), NIDDM patients: 2.5 (range 1.7-5.8), PVD patients: 2.42 (range 0.94-4.98) nmol 10(-9) platelets than that in all young + elderly healthy subjects. |
| 46 | 3139426 | Insulin-dependent diabetes mellitus patients had greater plasma 5-HT concentrations but this did not achieve statistical significance despite a 66% increment in its value. |
| 47 | 3139426 | Intraplatelet serotonin (5-HT) content was determined in 23 patients with type I (insulin-dependent) diabetes mellitus (IDDM), 23 patients with type II (non-insulin-dependent) diabetes mellitus (NIDDM), 29 patients with peripheral vascular disease (PVD) and 34 age-matched normal subjects. |
| 48 | 3139426 | The median intraplatelet 5-HT content was significantly lower (P less than 0.002) in IDDM patients: 3.0 (range 1.3-6.3), NIDDM patients: 2.5 (range 1.7-5.8), PVD patients: 2.42 (range 0.94-4.98) nmol 10(-9) platelets than that in all young + elderly healthy subjects. |
| 49 | 3139426 | Insulin-dependent diabetes mellitus patients had greater plasma 5-HT concentrations but this did not achieve statistical significance despite a 66% increment in its value. |
| 50 | 3297210 | Histochemical and immunohistochemical techniques were used to determine the pattern and density of perivascular nerves containing catecholamine, 5-hydroxytryptamine (5-HT), vasoactive intestinal polypeptide (VIP) and neuropeptide Y (NPY). |
| 51 | 3427882 | Umbilical arteries from the severe proteinuric PIH group were significantly more responsive to 5-HT as assessed by affinity constants (P less than 0.05). |
| 52 | 3607357 | The decrease in maximal contraction to NA, 5-HT and KCl seen in diabetic animals was prevented by insulin replacement. |
| 53 | 6115040 | Subsensitivity to 5-hydroxytryptamine agonists occurs in streptozocin-diabetic rats with no change in [3H]-5-HT receptor binding. |
| 54 | 6172788 | Moreover, significantly higher increase in 5-HT blood level and enhanced 5-HIAA excretion with the urine were seen in patients with juvenile diabetes mellitus comparatively to those with insulin-depending type of the disease. |
| 55 | 7504133 | These results suggest that for aortas from 2- and 6-week diabetic rats, the diminished responses to 5-HT and DOI may be a result of reductions in 5-HT2-receptor-mediated responses of smooth muscle. |
| 56 | 7508209 | Both high and low doses of protamine zinc insulin normalized diabetes-induced reductions in 5-hydroxyindole-3-acetic acid [5-HIAA; the principal metabolite of 5-hydroxytryptamine (5-HT)] and 5-HT turnover (5-HIAA/5-HT), despite the failure of the low-dose regimen to normalize plasma glucose. |
| 57 | 7562555 | Tiapride dose-dependently attenuated the biphasic nociceptive responses induced by s.c. injection of formalin to the hindpaw of mice, and its activity on the first (ED50 = 110 mg/kg p.o.) and the second (ED50 = 32.0 mg/kg p.o.) phases paralleled that on the nociceptive response to intrathecal injection of substance P (ED50 = 190 mg/kg p.o.) and somatostatin (ED50 = 56.0 mg/kg p.o.), respectively. |
| 58 | 7562555 | The effects of tiapride (100 mg/kg p.o.) on both phases of the formalin test in normal mice were abolished by pretreatment with p-chlorophenylalanine (800 x 2 mg/kg p.o.), a 5-hydroxytryptamine (5-HT) depletor, or pindolol (1 mg/kg i.p.), a 5-HT1 antagonist, but were scarcely affected by 3-tropanyl-indole-3-carboxylate, a 5-HT3 antagonist. |
| 59 | 7620714 | Interaction between 5-HT (0.1 microM-0.1 mM) and threshold concentrations of endothelin-1 (ET-1) or the thromboxane (Tx)A2-mimetic, U46619, were examined in endothelium-intact and -denuded aortae from control and 2-week streptozotocin-diabetic rats. 5. |
| 60 | 7620714 | Maximum responses to 5-HT in the presence of a threshold concentration of ET-1 (3 nM), in endothelium-intact aortae from diabetic rats, were not significantly different from those of control rats. 6. |
| 61 | 7620714 | Maximum responses to 5-HT in the combined presence of ET-1 (3 nM) and GR32191B (1 microM), in endothelium-intact aortae from diabetic rats, were significantly reduced compared to those obtained in aortae from controls. 7. |
| 62 | 7620714 | Maximum responses to 5-HT in the presence of ET-1 (3 nM) in endothelium-denuded aortae from diabetic rats were significantly reduced compared to those from controls. 8. |
| 63 | 7620714 | Endothelial-derived TxA2 also appears to play a role in the potentiation of 5-HT responses by ET-1 in aortae from diabetic rats. |
| 64 | 7620714 | Interaction between 5-HT (0.1 microM-0.1 mM) and threshold concentrations of endothelin-1 (ET-1) or the thromboxane (Tx)A2-mimetic, U46619, were examined in endothelium-intact and -denuded aortae from control and 2-week streptozotocin-diabetic rats. 5. |
| 65 | 7620714 | Maximum responses to 5-HT in the presence of a threshold concentration of ET-1 (3 nM), in endothelium-intact aortae from diabetic rats, were not significantly different from those of control rats. 6. |
| 66 | 7620714 | Maximum responses to 5-HT in the combined presence of ET-1 (3 nM) and GR32191B (1 microM), in endothelium-intact aortae from diabetic rats, were significantly reduced compared to those obtained in aortae from controls. 7. |
| 67 | 7620714 | Maximum responses to 5-HT in the presence of ET-1 (3 nM) in endothelium-denuded aortae from diabetic rats were significantly reduced compared to those from controls. 8. |
| 68 | 7620714 | Endothelial-derived TxA2 also appears to play a role in the potentiation of 5-HT responses by ET-1 in aortae from diabetic rats. |
| 69 | 7620714 | Interaction between 5-HT (0.1 microM-0.1 mM) and threshold concentrations of endothelin-1 (ET-1) or the thromboxane (Tx)A2-mimetic, U46619, were examined in endothelium-intact and -denuded aortae from control and 2-week streptozotocin-diabetic rats. 5. |
| 70 | 7620714 | Maximum responses to 5-HT in the presence of a threshold concentration of ET-1 (3 nM), in endothelium-intact aortae from diabetic rats, were not significantly different from those of control rats. 6. |
| 71 | 7620714 | Maximum responses to 5-HT in the combined presence of ET-1 (3 nM) and GR32191B (1 microM), in endothelium-intact aortae from diabetic rats, were significantly reduced compared to those obtained in aortae from controls. 7. |
| 72 | 7620714 | Maximum responses to 5-HT in the presence of ET-1 (3 nM) in endothelium-denuded aortae from diabetic rats were significantly reduced compared to those from controls. 8. |
| 73 | 7620714 | Endothelial-derived TxA2 also appears to play a role in the potentiation of 5-HT responses by ET-1 in aortae from diabetic rats. |
| 74 | 7620714 | Interaction between 5-HT (0.1 microM-0.1 mM) and threshold concentrations of endothelin-1 (ET-1) or the thromboxane (Tx)A2-mimetic, U46619, were examined in endothelium-intact and -denuded aortae from control and 2-week streptozotocin-diabetic rats. 5. |
| 75 | 7620714 | Maximum responses to 5-HT in the presence of a threshold concentration of ET-1 (3 nM), in endothelium-intact aortae from diabetic rats, were not significantly different from those of control rats. 6. |
| 76 | 7620714 | Maximum responses to 5-HT in the combined presence of ET-1 (3 nM) and GR32191B (1 microM), in endothelium-intact aortae from diabetic rats, were significantly reduced compared to those obtained in aortae from controls. 7. |
| 77 | 7620714 | Maximum responses to 5-HT in the presence of ET-1 (3 nM) in endothelium-denuded aortae from diabetic rats were significantly reduced compared to those from controls. 8. |
| 78 | 7620714 | Endothelial-derived TxA2 also appears to play a role in the potentiation of 5-HT responses by ET-1 in aortae from diabetic rats. |
| 79 | 7620714 | Interaction between 5-HT (0.1 microM-0.1 mM) and threshold concentrations of endothelin-1 (ET-1) or the thromboxane (Tx)A2-mimetic, U46619, were examined in endothelium-intact and -denuded aortae from control and 2-week streptozotocin-diabetic rats. 5. |
| 80 | 7620714 | Maximum responses to 5-HT in the presence of a threshold concentration of ET-1 (3 nM), in endothelium-intact aortae from diabetic rats, were not significantly different from those of control rats. 6. |
| 81 | 7620714 | Maximum responses to 5-HT in the combined presence of ET-1 (3 nM) and GR32191B (1 microM), in endothelium-intact aortae from diabetic rats, were significantly reduced compared to those obtained in aortae from controls. 7. |
| 82 | 7620714 | Maximum responses to 5-HT in the presence of ET-1 (3 nM) in endothelium-denuded aortae from diabetic rats were significantly reduced compared to those from controls. 8. |
| 83 | 7620714 | Endothelial-derived TxA2 also appears to play a role in the potentiation of 5-HT responses by ET-1 in aortae from diabetic rats. |
| 84 | 7687210 | The effects of insulin and/or tryptophan (Try) administration on Try, serotonin (5-HT), 5-hydroxyindolacetic acid (5-HIAA) in raphe nuclei and hypothalamus and serum levels of large neutral amino acids [Try, valine, isoleucine, leucine, tyrosine and phenylalanine, (LNAA)] was investigated in diabetic rats. 2. |
| 85 | 7687210 | The administration of Try in combination with insulin to diabetic rats altered the levels of brain Try, 5-HT, 5-HIAA and serum concentrations of valine, leucine and isoleucine towards the values in the control (nondiabetic) group. 5. |
| 86 | 7687210 | Our results suggest that simultaneous use of Try and insulin has positive effect on the alterations in Try and 5-HT metabolism, that occurred in long-term alloxan diabetic rats despite insulin application. |
| 87 | 7687210 | The effects of insulin and/or tryptophan (Try) administration on Try, serotonin (5-HT), 5-hydroxyindolacetic acid (5-HIAA) in raphe nuclei and hypothalamus and serum levels of large neutral amino acids [Try, valine, isoleucine, leucine, tyrosine and phenylalanine, (LNAA)] was investigated in diabetic rats. 2. |
| 88 | 7687210 | The administration of Try in combination with insulin to diabetic rats altered the levels of brain Try, 5-HT, 5-HIAA and serum concentrations of valine, leucine and isoleucine towards the values in the control (nondiabetic) group. 5. |
| 89 | 7687210 | Our results suggest that simultaneous use of Try and insulin has positive effect on the alterations in Try and 5-HT metabolism, that occurred in long-term alloxan diabetic rats despite insulin application. |
| 90 | 7687210 | The effects of insulin and/or tryptophan (Try) administration on Try, serotonin (5-HT), 5-hydroxyindolacetic acid (5-HIAA) in raphe nuclei and hypothalamus and serum levels of large neutral amino acids [Try, valine, isoleucine, leucine, tyrosine and phenylalanine, (LNAA)] was investigated in diabetic rats. 2. |
| 91 | 7687210 | The administration of Try in combination with insulin to diabetic rats altered the levels of brain Try, 5-HT, 5-HIAA and serum concentrations of valine, leucine and isoleucine towards the values in the control (nondiabetic) group. 5. |
| 92 | 7687210 | Our results suggest that simultaneous use of Try and insulin has positive effect on the alterations in Try and 5-HT metabolism, that occurred in long-term alloxan diabetic rats despite insulin application. |
| 93 | 7762635 | The diabetogenic effects of streptozotocin (STZ) were studied on blood glucose, plasma insulin, feeding and drinking, body weight, islet morphology, and hypothalamic serotonin (5-HT) release in vehicle-pretreated rats and in rats pretreated with either intracerebroventricular injection of 5,7-dihydroxytryptamine (5,7-DHT; a 5-HT nerve fiber depletor), intraperitoneal injection of p-chlorophenylalanine (PCPA; a tryptophan hydroxylase inhibitor), or intraperitoneal injection of p-chloroamphetamine (PCA; a neurotoxin for 5-HT nerve fiber). |
| 94 | 7762635 | At four days after STZ administration, vehicle-treated rats displayed hyperglycemia, polydipsia, polyphagia, decreased plasma insulin level, derangement of islet morphology (few insulin cells, accumulation of glucagon cells), and elevated 5-HT release in the hypothalamus. |
| 95 | 7762635 | The diabetogenic effects of streptozotocin (STZ) were studied on blood glucose, plasma insulin, feeding and drinking, body weight, islet morphology, and hypothalamic serotonin (5-HT) release in vehicle-pretreated rats and in rats pretreated with either intracerebroventricular injection of 5,7-dihydroxytryptamine (5,7-DHT; a 5-HT nerve fiber depletor), intraperitoneal injection of p-chlorophenylalanine (PCPA; a tryptophan hydroxylase inhibitor), or intraperitoneal injection of p-chloroamphetamine (PCA; a neurotoxin for 5-HT nerve fiber). |
| 96 | 7762635 | At four days after STZ administration, vehicle-treated rats displayed hyperglycemia, polydipsia, polyphagia, decreased plasma insulin level, derangement of islet morphology (few insulin cells, accumulation of glucagon cells), and elevated 5-HT release in the hypothalamus. |
| 97 | 7826819 | Venoconstriction was observed after local administration of alpha-adrenoceptor and 5-HT-receptor agonists, ergot derivatives, angiotensinogen, angiotensin I and II, and several prostaglandins. 6. |
| 98 | 7992257 | Platelet aggregation in the whole blood induced by collagen (2 micrograms/ml), ADP (10 microM), arachidonic acid (0.5 mM) and epinephrine (10 microM), and in PRP induced by collagen (2 micrograms/ml), ADP (5 microM), arachidonic acid (250 microM), epinephrine (10 microM) and serotonin-5-HT (1 microM) was measured at 7:30, 11:30, 17:00, 23:00, 4:00 and 7:00. |
| 99 | 8012721 | Cumulative concentration-response curves to 5-HT, and the 5-HT receptor agonists, alpha-methyl 5-HT (alpha-Me-5-HT, 5-HT2/1C agonist), (+/-)-1-(2,5-dimethoxy-4-iodophenyl)-2- aminopropane (DOI, 5-HT2/1C agonist) and 5-carboxamidotryptamine (5-CT, 5-HT1A/1B/1D agonist), were examined in endothelium-intact and -denuded aortae from 2-week streptozotocin (STZ)-diabetic and control rats. 3. |
| 100 | 8012721 | The attenuated responses to 5-HT of aortae from diabetic rats were normalized by chronic insulin treatment of the rats (5 units day-1, s.c.), but not by altering the glucose concentration of the bathing fluid. 5. |
| 101 | 8012721 | The nitric oxide synthase inhibitor N-nitro-L-arginine (NOLA, 0.1 mM) significantly potentiated responses to both 5-HT and alpha-Me-5-HT in endothelium-intact aortae. |
| 102 | 8012721 | The attenuated contractile responses observed to 5-HT in aortae from 2-week diabetic rats do not appear to be mediated by changes in either endothelial cell function or an alteration in 5-HT receptor affinity or density. |
| 103 | 8012721 | Cumulative concentration-response curves to 5-HT, and the 5-HT receptor agonists, alpha-methyl 5-HT (alpha-Me-5-HT, 5-HT2/1C agonist), (+/-)-1-(2,5-dimethoxy-4-iodophenyl)-2- aminopropane (DOI, 5-HT2/1C agonist) and 5-carboxamidotryptamine (5-CT, 5-HT1A/1B/1D agonist), were examined in endothelium-intact and -denuded aortae from 2-week streptozotocin (STZ)-diabetic and control rats. 3. |
| 104 | 8012721 | The attenuated responses to 5-HT of aortae from diabetic rats were normalized by chronic insulin treatment of the rats (5 units day-1, s.c.), but not by altering the glucose concentration of the bathing fluid. 5. |
| 105 | 8012721 | The nitric oxide synthase inhibitor N-nitro-L-arginine (NOLA, 0.1 mM) significantly potentiated responses to both 5-HT and alpha-Me-5-HT in endothelium-intact aortae. |
| 106 | 8012721 | The attenuated contractile responses observed to 5-HT in aortae from 2-week diabetic rats do not appear to be mediated by changes in either endothelial cell function or an alteration in 5-HT receptor affinity or density. |
| 107 | 8012721 | Cumulative concentration-response curves to 5-HT, and the 5-HT receptor agonists, alpha-methyl 5-HT (alpha-Me-5-HT, 5-HT2/1C agonist), (+/-)-1-(2,5-dimethoxy-4-iodophenyl)-2- aminopropane (DOI, 5-HT2/1C agonist) and 5-carboxamidotryptamine (5-CT, 5-HT1A/1B/1D agonist), were examined in endothelium-intact and -denuded aortae from 2-week streptozotocin (STZ)-diabetic and control rats. 3. |
| 108 | 8012721 | The attenuated responses to 5-HT of aortae from diabetic rats were normalized by chronic insulin treatment of the rats (5 units day-1, s.c.), but not by altering the glucose concentration of the bathing fluid. 5. |
| 109 | 8012721 | The nitric oxide synthase inhibitor N-nitro-L-arginine (NOLA, 0.1 mM) significantly potentiated responses to both 5-HT and alpha-Me-5-HT in endothelium-intact aortae. |
| 110 | 8012721 | The attenuated contractile responses observed to 5-HT in aortae from 2-week diabetic rats do not appear to be mediated by changes in either endothelial cell function or an alteration in 5-HT receptor affinity or density. |
| 111 | 8012721 | Cumulative concentration-response curves to 5-HT, and the 5-HT receptor agonists, alpha-methyl 5-HT (alpha-Me-5-HT, 5-HT2/1C agonist), (+/-)-1-(2,5-dimethoxy-4-iodophenyl)-2- aminopropane (DOI, 5-HT2/1C agonist) and 5-carboxamidotryptamine (5-CT, 5-HT1A/1B/1D agonist), were examined in endothelium-intact and -denuded aortae from 2-week streptozotocin (STZ)-diabetic and control rats. 3. |
| 112 | 8012721 | The attenuated responses to 5-HT of aortae from diabetic rats were normalized by chronic insulin treatment of the rats (5 units day-1, s.c.), but not by altering the glucose concentration of the bathing fluid. 5. |
| 113 | 8012721 | The nitric oxide synthase inhibitor N-nitro-L-arginine (NOLA, 0.1 mM) significantly potentiated responses to both 5-HT and alpha-Me-5-HT in endothelium-intact aortae. |
| 114 | 8012721 | The attenuated contractile responses observed to 5-HT in aortae from 2-week diabetic rats do not appear to be mediated by changes in either endothelial cell function or an alteration in 5-HT receptor affinity or density. |
| 115 | 8072377 | Kinetic studies were conducted on the contractile response elicited by phenylephrine (PE) and 5-hydroxytryptamine (5-HT) activation of the alpha 1-adrenergic- and 5-HT2 receptor subtypes, respectively, in aortic rings isolated from streptozotocin (STZ)-diabetic and age-matched control rats. |
| 116 | 8077800 | Treadmill-test; ADP-, PAF-, 5-HT-induced platelet aggregation; D-dimer; PAI-1 activity; blood viscosity at high and low shear rate; hematocrit were performed. |
| 117 | 8412520 | Thus in the present study the effect of 5-HT on insulin-mediated glucose uptake was assessed. |
| 118 | 8412520 | Rat hindlimbs were perfused at constant flow with medium containing 8.3 mM glucose and a tracer amount of 2-deoxy-D-[1-3]glucose (2DG) with and without 10 microM 5-HT, 15 nM insulin and a combination of the two. 5-HT inhibited insulin-mediated stimulation of glucose uptake by 30.4% when added after insulin and 34.4% when added before insulin. |
| 119 | 8412520 | In addition, 5-HT inhibited insulin-mediated 2DG uptake by perfused muscles with inhibition ranging from 32% (soleus) to 80% (extensor digitorum longus). |
| 120 | 8412520 | The effects of 5-HT on insulin-mediated glucose uptake were partially reversed by vasodilation with carbachol. |
| 121 | 8412520 | In contrast to the results for the hindlimb, 10 microM 5-HT had no significant effect on either basal glucose uptake or the stimulation of glucose uptake mediated by 15 nM insulin by isolated incubated soleus or extensor digitorum longus muscles. |
| 122 | 8412520 | It is concluded that 5-HT impairs insulin-mediated glucose uptake in the perfused rat hindlimb that may derive from vascular shunting not apparent when muscles are incubated with 5-HT in vitro. |
| 123 | 8412520 | Thus in the present study the effect of 5-HT on insulin-mediated glucose uptake was assessed. |
| 124 | 8412520 | Rat hindlimbs were perfused at constant flow with medium containing 8.3 mM glucose and a tracer amount of 2-deoxy-D-[1-3]glucose (2DG) with and without 10 microM 5-HT, 15 nM insulin and a combination of the two. 5-HT inhibited insulin-mediated stimulation of glucose uptake by 30.4% when added after insulin and 34.4% when added before insulin. |
| 125 | 8412520 | In addition, 5-HT inhibited insulin-mediated 2DG uptake by perfused muscles with inhibition ranging from 32% (soleus) to 80% (extensor digitorum longus). |
| 126 | 8412520 | The effects of 5-HT on insulin-mediated glucose uptake were partially reversed by vasodilation with carbachol. |
| 127 | 8412520 | In contrast to the results for the hindlimb, 10 microM 5-HT had no significant effect on either basal glucose uptake or the stimulation of glucose uptake mediated by 15 nM insulin by isolated incubated soleus or extensor digitorum longus muscles. |
| 128 | 8412520 | It is concluded that 5-HT impairs insulin-mediated glucose uptake in the perfused rat hindlimb that may derive from vascular shunting not apparent when muscles are incubated with 5-HT in vitro. |
| 129 | 8412520 | Thus in the present study the effect of 5-HT on insulin-mediated glucose uptake was assessed. |
| 130 | 8412520 | Rat hindlimbs were perfused at constant flow with medium containing 8.3 mM glucose and a tracer amount of 2-deoxy-D-[1-3]glucose (2DG) with and without 10 microM 5-HT, 15 nM insulin and a combination of the two. 5-HT inhibited insulin-mediated stimulation of glucose uptake by 30.4% when added after insulin and 34.4% when added before insulin. |
| 131 | 8412520 | In addition, 5-HT inhibited insulin-mediated 2DG uptake by perfused muscles with inhibition ranging from 32% (soleus) to 80% (extensor digitorum longus). |
| 132 | 8412520 | The effects of 5-HT on insulin-mediated glucose uptake were partially reversed by vasodilation with carbachol. |
| 133 | 8412520 | In contrast to the results for the hindlimb, 10 microM 5-HT had no significant effect on either basal glucose uptake or the stimulation of glucose uptake mediated by 15 nM insulin by isolated incubated soleus or extensor digitorum longus muscles. |
| 134 | 8412520 | It is concluded that 5-HT impairs insulin-mediated glucose uptake in the perfused rat hindlimb that may derive from vascular shunting not apparent when muscles are incubated with 5-HT in vitro. |
| 135 | 8412520 | Thus in the present study the effect of 5-HT on insulin-mediated glucose uptake was assessed. |
| 136 | 8412520 | Rat hindlimbs were perfused at constant flow with medium containing 8.3 mM glucose and a tracer amount of 2-deoxy-D-[1-3]glucose (2DG) with and without 10 microM 5-HT, 15 nM insulin and a combination of the two. 5-HT inhibited insulin-mediated stimulation of glucose uptake by 30.4% when added after insulin and 34.4% when added before insulin. |
| 137 | 8412520 | In addition, 5-HT inhibited insulin-mediated 2DG uptake by perfused muscles with inhibition ranging from 32% (soleus) to 80% (extensor digitorum longus). |
| 138 | 8412520 | The effects of 5-HT on insulin-mediated glucose uptake were partially reversed by vasodilation with carbachol. |
| 139 | 8412520 | In contrast to the results for the hindlimb, 10 microM 5-HT had no significant effect on either basal glucose uptake or the stimulation of glucose uptake mediated by 15 nM insulin by isolated incubated soleus or extensor digitorum longus muscles. |
| 140 | 8412520 | It is concluded that 5-HT impairs insulin-mediated glucose uptake in the perfused rat hindlimb that may derive from vascular shunting not apparent when muscles are incubated with 5-HT in vitro. |
| 141 | 8412520 | Thus in the present study the effect of 5-HT on insulin-mediated glucose uptake was assessed. |
| 142 | 8412520 | Rat hindlimbs were perfused at constant flow with medium containing 8.3 mM glucose and a tracer amount of 2-deoxy-D-[1-3]glucose (2DG) with and without 10 microM 5-HT, 15 nM insulin and a combination of the two. 5-HT inhibited insulin-mediated stimulation of glucose uptake by 30.4% when added after insulin and 34.4% when added before insulin. |
| 143 | 8412520 | In addition, 5-HT inhibited insulin-mediated 2DG uptake by perfused muscles with inhibition ranging from 32% (soleus) to 80% (extensor digitorum longus). |
| 144 | 8412520 | The effects of 5-HT on insulin-mediated glucose uptake were partially reversed by vasodilation with carbachol. |
| 145 | 8412520 | In contrast to the results for the hindlimb, 10 microM 5-HT had no significant effect on either basal glucose uptake or the stimulation of glucose uptake mediated by 15 nM insulin by isolated incubated soleus or extensor digitorum longus muscles. |
| 146 | 8412520 | It is concluded that 5-HT impairs insulin-mediated glucose uptake in the perfused rat hindlimb that may derive from vascular shunting not apparent when muscles are incubated with 5-HT in vitro. |
| 147 | 8412520 | Thus in the present study the effect of 5-HT on insulin-mediated glucose uptake was assessed. |
| 148 | 8412520 | Rat hindlimbs were perfused at constant flow with medium containing 8.3 mM glucose and a tracer amount of 2-deoxy-D-[1-3]glucose (2DG) with and without 10 microM 5-HT, 15 nM insulin and a combination of the two. 5-HT inhibited insulin-mediated stimulation of glucose uptake by 30.4% when added after insulin and 34.4% when added before insulin. |
| 149 | 8412520 | In addition, 5-HT inhibited insulin-mediated 2DG uptake by perfused muscles with inhibition ranging from 32% (soleus) to 80% (extensor digitorum longus). |
| 150 | 8412520 | The effects of 5-HT on insulin-mediated glucose uptake were partially reversed by vasodilation with carbachol. |
| 151 | 8412520 | In contrast to the results for the hindlimb, 10 microM 5-HT had no significant effect on either basal glucose uptake or the stimulation of glucose uptake mediated by 15 nM insulin by isolated incubated soleus or extensor digitorum longus muscles. |
| 152 | 8412520 | It is concluded that 5-HT impairs insulin-mediated glucose uptake in the perfused rat hindlimb that may derive from vascular shunting not apparent when muscles are incubated with 5-HT in vitro. |
| 153 | 8524696 | Platelet aggregation (in PRP according to Born) induced by collagen (2 micrograms/ml), ADP (5 microM), epinephrine (10 microM) arachidonic acid (0.25 mM) and 5-HT (1 microM) was found to be significantly enhanced in diabetic relative to controls. |
| 154 | 8674892 | The responses to serotonin (5-HT) in the INS group were similar to those in the control group. |
| 155 | 8719787 | This study was designed to investigate the effect of meta-chlorophenylpiperazine (m-CPP; a 5-hydroxytryptamine (5-HT) receptor agonist) on the formalin-induced nociceptive responses in normal, insulin-dependent streptozotocin (STZ) diabetic and non-insulin dependent genetically diabetic (db/db) mice. 2. |
| 156 | 8719787 | The antinociceptive activities of m-CPP (1 mg kg-1, p.o.) were significantly inhibited by pretreatment with pindolol (a 5-HT1-receptor antagonist, 1 mg kg-1, i.p.) or ketanserin (a 5-HT2 receptor antagonist, 1 mg kg-1, i.p.) but were hardly affected by ICS205-930 (a 5-HT3 receptor antagonist, 1 mg kg-1, i.p.). 5. |
| 157 | 8788422 | Vasoconstrictor responses to 5-hydroxytryptamine (5-HT), alpha-methyl-5-HT, endothelin-1, arachidonic acid and the thromboxane A2-mimetic U46619 ((15S)-hydroxy-11 alpha, 9 alpha-(epoxymethano)prosta-5Z,13E-dienoic acid) were obtained in blood-perfused hindquarters of 6-week streptozotocin-diabetic rats. |
| 158 | 8846842 | The effect of 4 weeks streptozotocin-induced diabetes on ocular vascular resistance responses to noradrenalin (NA), adrenalin (A), phenylephrine (PHE), isoproterenol (ISOP), prostaglandin F2 alpha (PGF2 alpha). 5-hydroxytryptamine (5-HT) and angiotensin II (ANG II), was determined using a newly-developed, isolated, arterially-perfused rat eye preparation, by comparing responses from control and diabetic eyes. |
| 159 | 8910254 | Results suggest that the contractile response to 5-HT in DM is related to the altered Ca2+ signal transduction system via disturbed protein kinase C (PKC) activity, and that there are alterations of receptor characteristics and of the density in 5-HT receptor subtypes, especially 5-HT1A, during DM development. |
| 160 | 8931100 | The pressor effects of 5-HT in normal and diabetic pulmonary arterial rings were totally abolished by either the 5-HT receptor antagonist, ketanserin (200 nmol/l) or the calcium channel blocker, verapamil (5.5 nmol/l). |
| 161 | 8931100 | NG-nitro-L-arginine methyl ester (100 nmol/l), an inhibitor of nitric oxide synthase, significantly potentiated the contractile response of 5-HT in normal as well as diabetic pulmonary arterial rings. |
| 162 | 8931100 | Furthermore, 5-HT alone or in combination with indomethacin, NDGA and a nitric oxide synthase inhibitor may be used to induce experimental pulmonary hypertension and possibly pulmonary edema. |
| 163 | 8931100 | The pressor effects of 5-HT in normal and diabetic pulmonary arterial rings were totally abolished by either the 5-HT receptor antagonist, ketanserin (200 nmol/l) or the calcium channel blocker, verapamil (5.5 nmol/l). |
| 164 | 8931100 | NG-nitro-L-arginine methyl ester (100 nmol/l), an inhibitor of nitric oxide synthase, significantly potentiated the contractile response of 5-HT in normal as well as diabetic pulmonary arterial rings. |
| 165 | 8931100 | Furthermore, 5-HT alone or in combination with indomethacin, NDGA and a nitric oxide synthase inhibitor may be used to induce experimental pulmonary hypertension and possibly pulmonary edema. |
| 166 | 8931100 | The pressor effects of 5-HT in normal and diabetic pulmonary arterial rings were totally abolished by either the 5-HT receptor antagonist, ketanserin (200 nmol/l) or the calcium channel blocker, verapamil (5.5 nmol/l). |
| 167 | 8931100 | NG-nitro-L-arginine methyl ester (100 nmol/l), an inhibitor of nitric oxide synthase, significantly potentiated the contractile response of 5-HT in normal as well as diabetic pulmonary arterial rings. |
| 168 | 8931100 | Furthermore, 5-HT alone or in combination with indomethacin, NDGA and a nitric oxide synthase inhibitor may be used to induce experimental pulmonary hypertension and possibly pulmonary edema. |
| 169 | 8966194 | Superfusion with 5 mU/ml insulin did not alter S2/S1 ratios in normal [3H]5-HT loaded slices, but did increase the diabetic NTS slice S2/S1 ratio to 1.40 +/- 0.06 (p < 0.01). |
| 170 | 8966194 | Insulin superfusion augmented [3H]5-HT release in the diabetic NTS slices, possibly through increased transmitter synthesis or improved synaptic release. |
| 171 | 8966194 | Superfusion with 5 mU/ml insulin did not alter S2/S1 ratios in normal [3H]5-HT loaded slices, but did increase the diabetic NTS slice S2/S1 ratio to 1.40 +/- 0.06 (p < 0.01). |
| 172 | 8966194 | Insulin superfusion augmented [3H]5-HT release in the diabetic NTS slices, possibly through increased transmitter synthesis or improved synaptic release. |
| 173 | 9088870 | We investigated protein kinase C participation in the contractile response to 5-hydroxytryptamine (5-HT), and in the interaction between 5-HT and endothelin-1, in aortas from control and diabetic rats. |
| 174 | 9088870 | The protein kinase C inhibitor calphostin C (1 microM) significantly reduced responses to 5-HT only in aortas from control rats. |
| 175 | 9088870 | In diabetic rats, maximum responses to 5-HT, in the presence of endothelin-1 (3 nM), were not significantly different to controls. |
| 176 | 9088870 | We investigated protein kinase C participation in the contractile response to 5-hydroxytryptamine (5-HT), and in the interaction between 5-HT and endothelin-1, in aortas from control and diabetic rats. |
| 177 | 9088870 | The protein kinase C inhibitor calphostin C (1 microM) significantly reduced responses to 5-HT only in aortas from control rats. |
| 178 | 9088870 | In diabetic rats, maximum responses to 5-HT, in the presence of endothelin-1 (3 nM), were not significantly different to controls. |
| 179 | 9088870 | We investigated protein kinase C participation in the contractile response to 5-hydroxytryptamine (5-HT), and in the interaction between 5-HT and endothelin-1, in aortas from control and diabetic rats. |
| 180 | 9088870 | The protein kinase C inhibitor calphostin C (1 microM) significantly reduced responses to 5-HT only in aortas from control rats. |
| 181 | 9088870 | In diabetic rats, maximum responses to 5-HT, in the presence of endothelin-1 (3 nM), were not significantly different to controls. |
| 182 | 9138434 | The effect of streptozotocin (STZ)-induced diabetes and a combination of chronic treatment with haloperidol (HPD) on dopamine (DA)D2, serotonin (5-HT) 5-HT1A and 5-HT2A receptors was investigated in rat brain. |
| 183 | 9138434 | Sixteen days after the last injection of HPD or vehicle, rats were sacrificed, and the density of binding sites was determined using [3H]spiperone as ligand in the striatum (D2),[3H]8-hydroxy-2-(di-n-propyl)-aminotetraline in the hippocampus (5-HT1A), and [3H]ketanserin in the frontal cortex (5-HT2A). |
| 184 | 9138434 | The affinity constants for D2, 5-HT1A, and 5-HT2A receptors were not affected by any treatment. |
| 185 | 9166737 | By means of in situ hybridization, we have investigated the expression of dopamine, noradrenaline, and serotonin transporter (DA-T, NA-T, and 5-HT-T, respectively) mRNAs in the brains of alloxan- and streptozotocin-diabetic rats. |
| 186 | 9211811 | Blockade of nitric oxide decreases the renal vasodilatory effect of neuropeptide Y in the insulin-treated diabetic rat. |
| 187 | 9211811 | Strong and similar contractions were induced by potassium (60 mM), 5-hydroxytryptamine (5-HT) and endothelin-1 (ET-1) in renal and intrarenal arteries in diabetic and control rats. |
| 188 | 9211811 | The vasodilatory reactivity, after precontraction with 5-HT, of neuropeptide Y (NPY) was similar to that of acetylcholine (ACh), calcitonin gene-related peptide (CGRP) and vasoactive intestinal polypeptide (VIP) and was similar in diabetic and control rats. |
| 189 | 9211811 | The relaxing effect of NPY was decreased (40%) only in the diabetic group by blockade of nitric oxide synthase with NG-nitro-L-arginine methyl ester (10(-4) M) and by blockade (50%) of NPY with alpha-trinositol (10(-6) M). |
| 190 | 9211811 | Blockade of nitric oxide decreases the renal vasodilatory effect of neuropeptide Y in the insulin-treated diabetic rat. |
| 191 | 9211811 | Strong and similar contractions were induced by potassium (60 mM), 5-hydroxytryptamine (5-HT) and endothelin-1 (ET-1) in renal and intrarenal arteries in diabetic and control rats. |
| 192 | 9211811 | The vasodilatory reactivity, after precontraction with 5-HT, of neuropeptide Y (NPY) was similar to that of acetylcholine (ACh), calcitonin gene-related peptide (CGRP) and vasoactive intestinal polypeptide (VIP) and was similar in diabetic and control rats. |
| 193 | 9211811 | The relaxing effect of NPY was decreased (40%) only in the diabetic group by blockade of nitric oxide synthase with NG-nitro-L-arginine methyl ester (10(-4) M) and by blockade (50%) of NPY with alpha-trinositol (10(-6) M). |
| 194 | 9228515 | In order to clarify the effect of exogenous corticotropin-releasing factor (CRF) on catecholaminergic and serotoninergic system activity in the mediobasal hypothalamus-median eminence (MBH-ME) of ewes the changes in extracellular levels of noradrenaline (NA) and serotonin (5HT), and main metabolites of monoamines, 4-hydroxy-3-methoxyphenylglycol (MHPG), 3,4-dihydroxy-phenylacetic acid (DOPAC), homovanilic acid (HVA), and 5-hydroxy-indolo-3-acetic acid (5-HIAA) were quantified in the perfusates collected from MBH-ME. |
| 195 | 9228515 | CRF induced a rise in extracellular concentration of NA and 5-HT only in the estrous ewes prior to a preovulatory LH surge. |
| 196 | 9228515 | CRF treatment caused a heterogenous effect on extra-cellular concentrations of 5-HT in ewes during the preovulatory LH surge. |
| 197 | 9228515 | It is suggested that: 1) the responses of monoaminergic systems activity in the MBH-ME to CRF in large degree is dependent upon physiological state of ewes and 2) in some endocrinological phases CRF may affect LHRH and other hypothalamic hormone secretion indirectly by altering monoaminergic system activity in the MBH-ME. |
| 198 | 9228515 | In order to clarify the effect of exogenous corticotropin-releasing factor (CRF) on catecholaminergic and serotoninergic system activity in the mediobasal hypothalamus-median eminence (MBH-ME) of ewes the changes in extracellular levels of noradrenaline (NA) and serotonin (5HT), and main metabolites of monoamines, 4-hydroxy-3-methoxyphenylglycol (MHPG), 3,4-dihydroxy-phenylacetic acid (DOPAC), homovanilic acid (HVA), and 5-hydroxy-indolo-3-acetic acid (5-HIAA) were quantified in the perfusates collected from MBH-ME. |
| 199 | 9228515 | CRF induced a rise in extracellular concentration of NA and 5-HT only in the estrous ewes prior to a preovulatory LH surge. |
| 200 | 9228515 | CRF treatment caused a heterogenous effect on extra-cellular concentrations of 5-HT in ewes during the preovulatory LH surge. |
| 201 | 9228515 | It is suggested that: 1) the responses of monoaminergic systems activity in the MBH-ME to CRF in large degree is dependent upon physiological state of ewes and 2) in some endocrinological phases CRF may affect LHRH and other hypothalamic hormone secretion indirectly by altering monoaminergic system activity in the MBH-ME. |
| 202 | 9230640 | Results indicated (1) significant improvement in mean HAM-D (22.6 +/- 3.4 to 4.9 +/- 5.9, p < .001) and in mean Beck Depression Inventory (BDI) scores (21.9 +/- 10.5 to 12.7 +/- 8.3, p < .001); (2) fall in platelet serotonin (5-HT) content (79.7 +/- 22.5 to 13.6 +/- 12.7 ng/10(8) platelets, p < .001); (3) correlation of baseline platelet 5-HT content with response to sertraline by BDI scores (r = 0.51, p < .05); (4) improved dietary compliance for those with baseline value below 70 percent (59.7% to 69.1%, p < .005); and (5) 13 of 17 patients with baseline glycosylated hemoglobin A (HbA1c) levels greater than 8.0, showed a reduction (p = .018). |
| 203 | 9246837 | The role of neuropeptide Y (NPY), leptin and 5-HT and other neurotransmitters implicated in the regulation of energy balance are only now being fully investigated. |
| 204 | 9246837 | Hence perturbation of a single system, such as hypothalamic NPY or leptin, is unlikely to be directly responsible for the development of most obesity. |
| 205 | 9246837 | At present, however, it is unclear whether NPY, leptin, or other apparently strong candidates will be the winner in the lucrative race for the ideal anti-obesity drug. |
| 206 | 9326291 | The equal increases in dialysate 5-HT and 5-HIAA and the better restoration of the 5-HIAA/5-HT ratio after insulin therapy indicate that serotonergic activity may depend on the levels of circulating insulin more than on noradrenergic activity. |
| 207 | 10564740 | 5-Hydroxytryptamine (5-HT, serotonin), synthesized in midbrain raphe nuclei and released in various hypothalamic sites, decreases food intake but the specific 5-HT receptor subtypes involved are controversial. |
| 208 | 10564740 | Here, we have studied changes in the regional density of binding to 5-HT receptors and transporters and the levels of tryptophan hydroxylase, in rats with obesity induced by feeding a palatable high-energy diet for 7 weeks. |
| 209 | 10564740 | We mapped binding at 5-HT receptor subtypes and transporters using quantitative autoradiography and determined tryptophan hydroxylase protein levels by Western blotting. |
| 210 | 10564740 | In conclusion, we have demonstrated regionally specific changes in binding to certain 5-HT receptor subtypes in obesity induced by voluntary overeating of a palatable diet. |
| 211 | 10564740 | 5-Hydroxytryptamine (5-HT, serotonin), synthesized in midbrain raphe nuclei and released in various hypothalamic sites, decreases food intake but the specific 5-HT receptor subtypes involved are controversial. |
| 212 | 10564740 | Here, we have studied changes in the regional density of binding to 5-HT receptors and transporters and the levels of tryptophan hydroxylase, in rats with obesity induced by feeding a palatable high-energy diet for 7 weeks. |
| 213 | 10564740 | We mapped binding at 5-HT receptor subtypes and transporters using quantitative autoradiography and determined tryptophan hydroxylase protein levels by Western blotting. |
| 214 | 10564740 | In conclusion, we have demonstrated regionally specific changes in binding to certain 5-HT receptor subtypes in obesity induced by voluntary overeating of a palatable diet. |
| 215 | 10564740 | 5-Hydroxytryptamine (5-HT, serotonin), synthesized in midbrain raphe nuclei and released in various hypothalamic sites, decreases food intake but the specific 5-HT receptor subtypes involved are controversial. |
| 216 | 10564740 | Here, we have studied changes in the regional density of binding to 5-HT receptors and transporters and the levels of tryptophan hydroxylase, in rats with obesity induced by feeding a palatable high-energy diet for 7 weeks. |
| 217 | 10564740 | We mapped binding at 5-HT receptor subtypes and transporters using quantitative autoradiography and determined tryptophan hydroxylase protein levels by Western blotting. |
| 218 | 10564740 | In conclusion, we have demonstrated regionally specific changes in binding to certain 5-HT receptor subtypes in obesity induced by voluntary overeating of a palatable diet. |
| 219 | 10564740 | 5-Hydroxytryptamine (5-HT, serotonin), synthesized in midbrain raphe nuclei and released in various hypothalamic sites, decreases food intake but the specific 5-HT receptor subtypes involved are controversial. |
| 220 | 10564740 | Here, we have studied changes in the regional density of binding to 5-HT receptors and transporters and the levels of tryptophan hydroxylase, in rats with obesity induced by feeding a palatable high-energy diet for 7 weeks. |
| 221 | 10564740 | We mapped binding at 5-HT receptor subtypes and transporters using quantitative autoradiography and determined tryptophan hydroxylase protein levels by Western blotting. |
| 222 | 10564740 | In conclusion, we have demonstrated regionally specific changes in binding to certain 5-HT receptor subtypes in obesity induced by voluntary overeating of a palatable diet. |
| 223 | 10884525 | The tachykinin NK(1) receptor antagonist (S)-1-[2-[3-(3, 4-dichlorophenyl)-1 (3-isopropoxyphenylacetyl)piperidin-3-yl] ethyl]-4-phenyl-1 azoniabicyclo [2.2.2]octane cloride (SR140333; 120 nmol/kg, s.c.+120 nmol/kg, i.v.) significantly inhibited plasma exudation and paw oedema evoked by staphylococcal enterotoxin B. |
| 224 | 10884525 | The tachykinin NK(2) receptor antagonist (S)-N-methyl-N[4-(4-acetylamino-4-phenyl piperidino)-2-(3, 4-dichlorophenyl)butyl]-benzamide (SR48968) had no effect on the staphylococcal enterotoxin B-induced responses. |
| 225 | 10884525 | The 5-HT receptor antagonist methysergide (10 mg/kg, i.v.) and the histamine H(1) receptor antagonist mepyramine (10 mg/kg, i.v.) produced a significant reduction in paw oedema whereas plasma exudation was reduced only by methysergide. |
| 226 | 11281972 | Knockout Corner: Neurobehavioural consequences of a serotonin 5-HT(2C) receptor gene mutation. |
| 227 | 11281972 | Studies employing nonselective serotonin 5-HT(2C) receptor agonists and antagonists have implicated this receptor subtype in many of the actions of serotonin. |
| 228 | 11281972 | Knockout Corner: Neurobehavioural consequences of a serotonin 5-HT(2C) receptor gene mutation. |
| 229 | 11281972 | Studies employing nonselective serotonin 5-HT(2C) receptor agonists and antagonists have implicated this receptor subtype in many of the actions of serotonin. |
| 230 | 11453030 | Serotonin (5-HT), GABA and catecholamines (CA) have qualitative differences in the effects on GnRH and LH secretion in early prepubertal than in late prepubertal and adult female rats. |
| 231 | 11453030 | The administration of 5-hydroxytryptophan a precursor of serotonin (5-HT) which increases 5-HT hypothalamic levels induces GnRH and LH release in early prepubertal female rats, these effects dissapear in late prepubertal stage having an inhibitory action in adult female rats. |
| 232 | 11453030 | Serotonin (5-HT), GABA and catecholamines (CA) have qualitative differences in the effects on GnRH and LH secretion in early prepubertal than in late prepubertal and adult female rats. |
| 233 | 11453030 | The administration of 5-hydroxytryptophan a precursor of serotonin (5-HT) which increases 5-HT hypothalamic levels induces GnRH and LH release in early prepubertal female rats, these effects dissapear in late prepubertal stage having an inhibitory action in adult female rats. |
| 234 | 11460094 | OBJECTIVES: The distribution of serotonin (5-HT) and its effect on insulin and glucagon secretion were investigated to examine whether there are changes in the pattern of distribution and effect of 5-HT after the onset of experimental diabetes. |
| 235 | 11460094 | METHODS: The pattern of 5-HT and its effect of insulin and glucagon secretion was examined using immunohistochemical and radioimmunoassay techniques, respectively. |
| 236 | 11460094 | The perivascular, periductal, periacinar and periinsular regions of diabetic pancreas all contained 5-HT positive nerves. 5-HT elicited marked increases in insulin secretion from normal pancreas but had an inhibitory effect on insulin secretion from diabetic pancreatic tissues. |
| 237 | 11460094 | In contrast, 5HT inhibited glucagon secretion from normal pancreatic tissue fragments but stimulated glucagon release from diabetic pancreatic tissue fragments. conclusion: 5-HT is well distributed in normal and diabetic pancreatic tissues and has stimulatory effects on insulin secretion from normal pancreas and glucagon secretion from diabetic pancreas. |
| 238 | 11460094 | This result indicates that although 5-HT may help in the maintenance of the blood sugar level in normal pancreas by increasing insulin secretion and decreasing glucagon secretion, it may also aggravate the hyperglycemia observed in diabetes mellitus and hence exacerbate the symptoms of hyperglycemia in poorly controlled diabetes mellitus. |
| 239 | 11460094 | OBJECTIVES: The distribution of serotonin (5-HT) and its effect on insulin and glucagon secretion were investigated to examine whether there are changes in the pattern of distribution and effect of 5-HT after the onset of experimental diabetes. |
| 240 | 11460094 | METHODS: The pattern of 5-HT and its effect of insulin and glucagon secretion was examined using immunohistochemical and radioimmunoassay techniques, respectively. |
| 241 | 11460094 | The perivascular, periductal, periacinar and periinsular regions of diabetic pancreas all contained 5-HT positive nerves. 5-HT elicited marked increases in insulin secretion from normal pancreas but had an inhibitory effect on insulin secretion from diabetic pancreatic tissues. |
| 242 | 11460094 | In contrast, 5HT inhibited glucagon secretion from normal pancreatic tissue fragments but stimulated glucagon release from diabetic pancreatic tissue fragments. conclusion: 5-HT is well distributed in normal and diabetic pancreatic tissues and has stimulatory effects on insulin secretion from normal pancreas and glucagon secretion from diabetic pancreas. |
| 243 | 11460094 | This result indicates that although 5-HT may help in the maintenance of the blood sugar level in normal pancreas by increasing insulin secretion and decreasing glucagon secretion, it may also aggravate the hyperglycemia observed in diabetes mellitus and hence exacerbate the symptoms of hyperglycemia in poorly controlled diabetes mellitus. |
| 244 | 11460094 | OBJECTIVES: The distribution of serotonin (5-HT) and its effect on insulin and glucagon secretion were investigated to examine whether there are changes in the pattern of distribution and effect of 5-HT after the onset of experimental diabetes. |
| 245 | 11460094 | METHODS: The pattern of 5-HT and its effect of insulin and glucagon secretion was examined using immunohistochemical and radioimmunoassay techniques, respectively. |
| 246 | 11460094 | The perivascular, periductal, periacinar and periinsular regions of diabetic pancreas all contained 5-HT positive nerves. 5-HT elicited marked increases in insulin secretion from normal pancreas but had an inhibitory effect on insulin secretion from diabetic pancreatic tissues. |
| 247 | 11460094 | In contrast, 5HT inhibited glucagon secretion from normal pancreatic tissue fragments but stimulated glucagon release from diabetic pancreatic tissue fragments. conclusion: 5-HT is well distributed in normal and diabetic pancreatic tissues and has stimulatory effects on insulin secretion from normal pancreas and glucagon secretion from diabetic pancreas. |
| 248 | 11460094 | This result indicates that although 5-HT may help in the maintenance of the blood sugar level in normal pancreas by increasing insulin secretion and decreasing glucagon secretion, it may also aggravate the hyperglycemia observed in diabetes mellitus and hence exacerbate the symptoms of hyperglycemia in poorly controlled diabetes mellitus. |
| 249 | 11460094 | OBJECTIVES: The distribution of serotonin (5-HT) and its effect on insulin and glucagon secretion were investigated to examine whether there are changes in the pattern of distribution and effect of 5-HT after the onset of experimental diabetes. |
| 250 | 11460094 | METHODS: The pattern of 5-HT and its effect of insulin and glucagon secretion was examined using immunohistochemical and radioimmunoassay techniques, respectively. |
| 251 | 11460094 | The perivascular, periductal, periacinar and periinsular regions of diabetic pancreas all contained 5-HT positive nerves. 5-HT elicited marked increases in insulin secretion from normal pancreas but had an inhibitory effect on insulin secretion from diabetic pancreatic tissues. |
| 252 | 11460094 | In contrast, 5HT inhibited glucagon secretion from normal pancreatic tissue fragments but stimulated glucagon release from diabetic pancreatic tissue fragments. conclusion: 5-HT is well distributed in normal and diabetic pancreatic tissues and has stimulatory effects on insulin secretion from normal pancreas and glucagon secretion from diabetic pancreas. |
| 253 | 11460094 | This result indicates that although 5-HT may help in the maintenance of the blood sugar level in normal pancreas by increasing insulin secretion and decreasing glucagon secretion, it may also aggravate the hyperglycemia observed in diabetes mellitus and hence exacerbate the symptoms of hyperglycemia in poorly controlled diabetes mellitus. |
| 254 | 11460094 | OBJECTIVES: The distribution of serotonin (5-HT) and its effect on insulin and glucagon secretion were investigated to examine whether there are changes in the pattern of distribution and effect of 5-HT after the onset of experimental diabetes. |
| 255 | 11460094 | METHODS: The pattern of 5-HT and its effect of insulin and glucagon secretion was examined using immunohistochemical and radioimmunoassay techniques, respectively. |
| 256 | 11460094 | The perivascular, periductal, periacinar and periinsular regions of diabetic pancreas all contained 5-HT positive nerves. 5-HT elicited marked increases in insulin secretion from normal pancreas but had an inhibitory effect on insulin secretion from diabetic pancreatic tissues. |
| 257 | 11460094 | In contrast, 5HT inhibited glucagon secretion from normal pancreatic tissue fragments but stimulated glucagon release from diabetic pancreatic tissue fragments. conclusion: 5-HT is well distributed in normal and diabetic pancreatic tissues and has stimulatory effects on insulin secretion from normal pancreas and glucagon secretion from diabetic pancreas. |
| 258 | 11460094 | This result indicates that although 5-HT may help in the maintenance of the blood sugar level in normal pancreas by increasing insulin secretion and decreasing glucagon secretion, it may also aggravate the hyperglycemia observed in diabetes mellitus and hence exacerbate the symptoms of hyperglycemia in poorly controlled diabetes mellitus. |
| 259 | 11518692 | Changes in serotonin levels and 5-HT receptor activity in duodenum of streptozotocin-diabetic rats. |
| 260 | 11518692 | The 5-hydroxytryptamine (5-HT) receptor subtype 4 (5-HT(4)) antagonist SB-204070 dose dependently reduced motor activity in both control and diabetic rats, whereas the 5-HT(3) receptor antagonist azasetron, even at a higher concentration, failed to affect motor activity in diabetic rat duodenum but dose dependently reduced motor activity in control rat duodenum. |
| 261 | 11518692 | These results suggest that 5-HT(3) receptor activity was impaired but 5-HT(4) receptor activity was intact in STZ-diabetic rat duodenum. |
| 262 | 12213354 | We have recently demonstrated that serotonin (5-HT) increases the production of type 4 collagen by cultured human mesangial cells. |
| 263 | 12213354 | We then investigated the effects of 24-month treatment with sarpogrelate hydrochloride, a 5-HT(A2) receptor antagonist, on urinary albumin level in 10 type 2 diabetics with microalbuminuria, compared with not treated control group. |
| 264 | 12213354 | We have recently demonstrated that serotonin (5-HT) increases the production of type 4 collagen by cultured human mesangial cells. |
| 265 | 12213354 | We then investigated the effects of 24-month treatment with sarpogrelate hydrochloride, a 5-HT(A2) receptor antagonist, on urinary albumin level in 10 type 2 diabetics with microalbuminuria, compared with not treated control group. |
| 266 | 12540602 | Hyperactivity and reduced energy cost of physical activity in serotonin 5-HT(2C) receptor mutant mice. |
| 267 | 12540602 | We have observed late-onset obesity in mutant mice lacking the serotonin 5-HT(2C) receptor. |
| 268 | 12540602 | These results indicate that a mutation of the 5-HT(2C) receptor gene (htr2c) increases LA, which contributes to the maintenance of normal body composition in young adult mutants despite their hyperphagia. |
| 269 | 12540602 | Hyperactivity and reduced energy cost of physical activity in serotonin 5-HT(2C) receptor mutant mice. |
| 270 | 12540602 | We have observed late-onset obesity in mutant mice lacking the serotonin 5-HT(2C) receptor. |
| 271 | 12540602 | These results indicate that a mutation of the 5-HT(2C) receptor gene (htr2c) increases LA, which contributes to the maintenance of normal body composition in young adult mutants despite their hyperphagia. |
| 272 | 12540602 | Hyperactivity and reduced energy cost of physical activity in serotonin 5-HT(2C) receptor mutant mice. |
| 273 | 12540602 | We have observed late-onset obesity in mutant mice lacking the serotonin 5-HT(2C) receptor. |
| 274 | 12540602 | These results indicate that a mutation of the 5-HT(2C) receptor gene (htr2c) increases LA, which contributes to the maintenance of normal body composition in young adult mutants despite their hyperphagia. |
| 275 | 12720492 | For instance, selective 5-HT subtype 3 receptor (5-HT(3)) antagonists may have potential in the treatment of the pain associated with myocardial infarction. |
| 276 | 12720492 | In hypertension, agonists at the 5-HT(7) and antagonists at the 5-HT(2B) may reduce blood pressure, and in diabetes, sarpogrelate may protect against nephropathy. |
| 277 | 12720492 | For instance, selective 5-HT subtype 3 receptor (5-HT(3)) antagonists may have potential in the treatment of the pain associated with myocardial infarction. |
| 278 | 12720492 | In hypertension, agonists at the 5-HT(7) and antagonists at the 5-HT(2B) may reduce blood pressure, and in diabetes, sarpogrelate may protect against nephropathy. |
| 279 | 12911638 | A second gene encoding a functional tryptophan hydroxylase activity has recently been described (TPH2), which is expressed abundantly in brainstem, the primary site of serotonergic neurons in the CNS. |
| 280 | 12911638 | As serotonin (5-HT) has an important role as a precursor of the nocturnal synthesis of the pineal gland hormone, melatonin, it was of interest to determine the relative expression of TPH1 and 2 mRNA in the rat pineal during the light:dark (L:D) cycle using sensitive real-time RT-PCR assays which were developed for each TPH isoform. |
| 281 | 12911638 | TPH1 mRNA expression was 105-fold more abundant in rat pineal than TPH2, and showed a significant approximately 4-fold nocturnal increase in expression which may contribute to the previously described nocturnal increase in pineal tryptophan hydroxylase activity. |
| 282 | 12941435 | Mechanisms for hyperleptinemia elicited by a serotonin (5-hydroxytryptamine, 5-HT) precursor, 5-hydroxytryptophan (5-HTP), were investigated. 5-HTP elicited apparent increases in serum leptin levels of mice. |
| 283 | 12941435 | Furthermore, neither 5-HTP nor 5-HT increased leptin secretion from isolated fat pads of mice. |
| 284 | 12941435 | Since insulin is known to enhance leptin release, involvement of insulin in 5-HTP-induced hyperleptinemia was examined. 5-HTP significantly elevated serum insulin levels. |
| 285 | 12941435 | In mice treated with streptozotocin, which depletes insulin, 5-HTP did not increase serum leptin levels. |
| 286 | 12941435 | Mechanisms for hyperleptinemia elicited by a serotonin (5-hydroxytryptamine, 5-HT) precursor, 5-hydroxytryptophan (5-HTP), were investigated. 5-HTP elicited apparent increases in serum leptin levels of mice. |
| 287 | 12941435 | Furthermore, neither 5-HTP nor 5-HT increased leptin secretion from isolated fat pads of mice. |
| 288 | 12941435 | Since insulin is known to enhance leptin release, involvement of insulin in 5-HTP-induced hyperleptinemia was examined. 5-HTP significantly elevated serum insulin levels. |
| 289 | 12941435 | In mice treated with streptozotocin, which depletes insulin, 5-HTP did not increase serum leptin levels. |
| 290 | 12971908 | The effects of the changed level of blood glucose due to insulin administration on the levels of NO, 5-HT, and DA were assessed. |
| 291 | 12971908 | The results in the present study showed that: (1) the plasma levels of NOx in both diabetic rats were low compared to those in control rats, (2) the hippocampal NOx levels in both diabetic rats were almost the same as those in control rats, while the levels of 5-HT and DA were low in the diabetics, and (3) a sudden decrease in the plasma glucose level due to insulin administration reduced the NOx level as well as enhanced the 5-HT level in the diabetic hippocampus, a finding consistent with the results of 7 days administration of insulin. |
| 292 | 12971908 | The effects of the changed level of blood glucose due to insulin administration on the levels of NO, 5-HT, and DA were assessed. |
| 293 | 12971908 | The results in the present study showed that: (1) the plasma levels of NOx in both diabetic rats were low compared to those in control rats, (2) the hippocampal NOx levels in both diabetic rats were almost the same as those in control rats, while the levels of 5-HT and DA were low in the diabetics, and (3) a sudden decrease in the plasma glucose level due to insulin administration reduced the NOx level as well as enhanced the 5-HT level in the diabetic hippocampus, a finding consistent with the results of 7 days administration of insulin. |
| 294 | 14571351 | From other studies in our laboratory we have shown that Cr3+ treatment can modify brain 5-HT function, perhaps by altering the sensitivity of central 5-HT2A receptors. |
| 295 | 14693692 | During the experimental period, somatostatin, fourfold basal intraportal insulin, basal intraportal glucagon, and peripheral glucose (to double the hepatic glucose load) were infused. |
| 296 | 14693692 | Intraportal 5-HT enhances NHGU but blunts nonhepatic glucose uptake, raising the possibility that hepatic-targeted 5-HT or 5-HT receptor agonists might reduce postprandial hyperglycemia. |
| 297 | 14983974 | Increasing, albeit as yet limited, evidence has implicated alterations in 5-hydroxytryptamine (5-HT) release, and the subsequent interaction of 5-HT with specific 5-HT receptor subtypes, in the altered gut function of patients with irritable bowel syndrome (IBS) and other functional bowel diseases. |
| 298 | 15107299 | The effects of tetrodotoxin, atropine, and 5-HT receptor antagonists were studied. |
| 299 | 15125025 | The immunohistochemical data showed that, among the established islet hormones, insulin was present in more than 50% of cells, whereas glucagon and somatostatin occurred only sporadically. |
| 300 | 15125025 | Though cells positive for pancreatic polypeptide (PP) were not found, PP-related peptides (NPY and PYY) however could be detected in a minority of cells. |
| 301 | 15125025 | The great majority of RINm5F cells were immunoreactive for chromogranin B (CgB), followed by insulin, chromogranin A (CgA), and serotonin (5-HT). |
| 302 | 15212624 | Sarpogrelate inhibits responses to 5-HT mediated by 5-HT2A receptors such as platelet aggregation, vasoconstriction and vascular smooth muscle proliferation. |
| 303 | 15342107 | In this study, we investigated the concentrations of 5-hydroxytryptamine (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA) in discrete areas of brain viz. striatum (ST), hippocampus (HC), hypothalamus (HT), midbrain (MB), pons medulla (PM), cerebellum (CB) and cerebral cortex (CCX) of control, untreated diabetic and insulin treated diabetic rats after 30 days. |
| 304 | 15342107 | The expressions of PKC-alpha studied by immunoblotting also showed significant changes in ST, HC, MB, PM, CB and CCX that is identical to the changes of both 5-HT and 5-HIAA under similar condition, suggesting that the PKC-alpha may regulate the synthesis and release of indoleamines in diabetic animals. |
| 305 | 15342107 | In this study, we investigated the concentrations of 5-hydroxytryptamine (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA) in discrete areas of brain viz. striatum (ST), hippocampus (HC), hypothalamus (HT), midbrain (MB), pons medulla (PM), cerebellum (CB) and cerebral cortex (CCX) of control, untreated diabetic and insulin treated diabetic rats after 30 days. |
| 306 | 15342107 | The expressions of PKC-alpha studied by immunoblotting also showed significant changes in ST, HC, MB, PM, CB and CCX that is identical to the changes of both 5-HT and 5-HIAA under similar condition, suggesting that the PKC-alpha may regulate the synthesis and release of indoleamines in diabetic animals. |
| 307 | 15601754 | Previous studies have shown the presence of 5-HT2A, 5-HT2B, and 5-HT1B receptors in vascular smooth muscle cells (VSMCs). |
| 308 | 15601754 | There are currently no data regarding 5-HT2B and 5-HT1B receptor activation of the JAK/STAT pathway in VSMCs and resultant potential alterations in 5-HT signaling in diabetes. |
| 309 | 15601754 | Therefore, we tested the hypothesis that 5-HT differentially activates the JAK/STAT pathway in VSMCs under conditions of normal (5 mM) and high (25 mM) glucose. |
| 310 | 15601754 | Treatment of rat VSMCs with 5-HT (10(-6) M) resulted in time-dependent activation ( approximately 2-fold) of JAK2, JAK1, and STAT1, but not STAT3 (maximal at 5 min, returned to baseline by 30 min). |
| 311 | 15601754 | The 5-HT2B receptor agonist BW723C86 and the 5-HT1B receptor agonist CGS12066A (10(-9)-10(-5) M, 5-min stimulation) did not activate the JAK/STAT pathway. |
| 312 | 15601754 | Treatment with the 5-HT2A receptor antagonist ketanserin (10 nM) inhibited JAK2 activation by 5-HT. |
| 313 | 15601754 | Treatment of streptozotocin-induced diabetic rats with ketanserin (5 mg.kg-1.day-1) reduced activation of JAK2 and STAT1 but not STAT3 in endothelium-denuded thoracic aorta in vivo. 5-HT (10(-6) M) treatment resulted in increased cell proliferation and increased DNA synthesis, which were inhibited by the JAK2 inhibitor AG490. |
| 314 | 15601754 | Further studies with apocynin, diphenyleneiodonium chloride, catalase, and virally transfected superoxide dismutase had no effect at either glucose concentration on activation of the JAK/STAT pathway by 5-HT. |
| 315 | 15601754 | Therefore, we conclude that 5-HT activates JAK2, JAK1, and STAT1 via the 5-HT2A receptors in a reactive oxygen species-independent manner under both normal and high glucose conditions. |
| 316 | 15601754 | Previous studies have shown the presence of 5-HT2A, 5-HT2B, and 5-HT1B receptors in vascular smooth muscle cells (VSMCs). |
| 317 | 15601754 | There are currently no data regarding 5-HT2B and 5-HT1B receptor activation of the JAK/STAT pathway in VSMCs and resultant potential alterations in 5-HT signaling in diabetes. |
| 318 | 15601754 | Therefore, we tested the hypothesis that 5-HT differentially activates the JAK/STAT pathway in VSMCs under conditions of normal (5 mM) and high (25 mM) glucose. |
| 319 | 15601754 | Treatment of rat VSMCs with 5-HT (10(-6) M) resulted in time-dependent activation ( approximately 2-fold) of JAK2, JAK1, and STAT1, but not STAT3 (maximal at 5 min, returned to baseline by 30 min). |
| 320 | 15601754 | The 5-HT2B receptor agonist BW723C86 and the 5-HT1B receptor agonist CGS12066A (10(-9)-10(-5) M, 5-min stimulation) did not activate the JAK/STAT pathway. |
| 321 | 15601754 | Treatment with the 5-HT2A receptor antagonist ketanserin (10 nM) inhibited JAK2 activation by 5-HT. |
| 322 | 15601754 | Treatment of streptozotocin-induced diabetic rats with ketanserin (5 mg.kg-1.day-1) reduced activation of JAK2 and STAT1 but not STAT3 in endothelium-denuded thoracic aorta in vivo. 5-HT (10(-6) M) treatment resulted in increased cell proliferation and increased DNA synthesis, which were inhibited by the JAK2 inhibitor AG490. |
| 323 | 15601754 | Further studies with apocynin, diphenyleneiodonium chloride, catalase, and virally transfected superoxide dismutase had no effect at either glucose concentration on activation of the JAK/STAT pathway by 5-HT. |
| 324 | 15601754 | Therefore, we conclude that 5-HT activates JAK2, JAK1, and STAT1 via the 5-HT2A receptors in a reactive oxygen species-independent manner under both normal and high glucose conditions. |
| 325 | 15601754 | Previous studies have shown the presence of 5-HT2A, 5-HT2B, and 5-HT1B receptors in vascular smooth muscle cells (VSMCs). |
| 326 | 15601754 | There are currently no data regarding 5-HT2B and 5-HT1B receptor activation of the JAK/STAT pathway in VSMCs and resultant potential alterations in 5-HT signaling in diabetes. |
| 327 | 15601754 | Therefore, we tested the hypothesis that 5-HT differentially activates the JAK/STAT pathway in VSMCs under conditions of normal (5 mM) and high (25 mM) glucose. |
| 328 | 15601754 | Treatment of rat VSMCs with 5-HT (10(-6) M) resulted in time-dependent activation ( approximately 2-fold) of JAK2, JAK1, and STAT1, but not STAT3 (maximal at 5 min, returned to baseline by 30 min). |
| 329 | 15601754 | The 5-HT2B receptor agonist BW723C86 and the 5-HT1B receptor agonist CGS12066A (10(-9)-10(-5) M, 5-min stimulation) did not activate the JAK/STAT pathway. |
| 330 | 15601754 | Treatment with the 5-HT2A receptor antagonist ketanserin (10 nM) inhibited JAK2 activation by 5-HT. |
| 331 | 15601754 | Treatment of streptozotocin-induced diabetic rats with ketanserin (5 mg.kg-1.day-1) reduced activation of JAK2 and STAT1 but not STAT3 in endothelium-denuded thoracic aorta in vivo. 5-HT (10(-6) M) treatment resulted in increased cell proliferation and increased DNA synthesis, which were inhibited by the JAK2 inhibitor AG490. |
| 332 | 15601754 | Further studies with apocynin, diphenyleneiodonium chloride, catalase, and virally transfected superoxide dismutase had no effect at either glucose concentration on activation of the JAK/STAT pathway by 5-HT. |
| 333 | 15601754 | Therefore, we conclude that 5-HT activates JAK2, JAK1, and STAT1 via the 5-HT2A receptors in a reactive oxygen species-independent manner under both normal and high glucose conditions. |
| 334 | 15601754 | Previous studies have shown the presence of 5-HT2A, 5-HT2B, and 5-HT1B receptors in vascular smooth muscle cells (VSMCs). |
| 335 | 15601754 | There are currently no data regarding 5-HT2B and 5-HT1B receptor activation of the JAK/STAT pathway in VSMCs and resultant potential alterations in 5-HT signaling in diabetes. |
| 336 | 15601754 | Therefore, we tested the hypothesis that 5-HT differentially activates the JAK/STAT pathway in VSMCs under conditions of normal (5 mM) and high (25 mM) glucose. |
| 337 | 15601754 | Treatment of rat VSMCs with 5-HT (10(-6) M) resulted in time-dependent activation ( approximately 2-fold) of JAK2, JAK1, and STAT1, but not STAT3 (maximal at 5 min, returned to baseline by 30 min). |
| 338 | 15601754 | The 5-HT2B receptor agonist BW723C86 and the 5-HT1B receptor agonist CGS12066A (10(-9)-10(-5) M, 5-min stimulation) did not activate the JAK/STAT pathway. |
| 339 | 15601754 | Treatment with the 5-HT2A receptor antagonist ketanserin (10 nM) inhibited JAK2 activation by 5-HT. |
| 340 | 15601754 | Treatment of streptozotocin-induced diabetic rats with ketanserin (5 mg.kg-1.day-1) reduced activation of JAK2 and STAT1 but not STAT3 in endothelium-denuded thoracic aorta in vivo. 5-HT (10(-6) M) treatment resulted in increased cell proliferation and increased DNA synthesis, which were inhibited by the JAK2 inhibitor AG490. |
| 341 | 15601754 | Further studies with apocynin, diphenyleneiodonium chloride, catalase, and virally transfected superoxide dismutase had no effect at either glucose concentration on activation of the JAK/STAT pathway by 5-HT. |
| 342 | 15601754 | Therefore, we conclude that 5-HT activates JAK2, JAK1, and STAT1 via the 5-HT2A receptors in a reactive oxygen species-independent manner under both normal and high glucose conditions. |
| 343 | 15601754 | Previous studies have shown the presence of 5-HT2A, 5-HT2B, and 5-HT1B receptors in vascular smooth muscle cells (VSMCs). |
| 344 | 15601754 | There are currently no data regarding 5-HT2B and 5-HT1B receptor activation of the JAK/STAT pathway in VSMCs and resultant potential alterations in 5-HT signaling in diabetes. |
| 345 | 15601754 | Therefore, we tested the hypothesis that 5-HT differentially activates the JAK/STAT pathway in VSMCs under conditions of normal (5 mM) and high (25 mM) glucose. |
| 346 | 15601754 | Treatment of rat VSMCs with 5-HT (10(-6) M) resulted in time-dependent activation ( approximately 2-fold) of JAK2, JAK1, and STAT1, but not STAT3 (maximal at 5 min, returned to baseline by 30 min). |
| 347 | 15601754 | The 5-HT2B receptor agonist BW723C86 and the 5-HT1B receptor agonist CGS12066A (10(-9)-10(-5) M, 5-min stimulation) did not activate the JAK/STAT pathway. |
| 348 | 15601754 | Treatment with the 5-HT2A receptor antagonist ketanserin (10 nM) inhibited JAK2 activation by 5-HT. |
| 349 | 15601754 | Treatment of streptozotocin-induced diabetic rats with ketanserin (5 mg.kg-1.day-1) reduced activation of JAK2 and STAT1 but not STAT3 in endothelium-denuded thoracic aorta in vivo. 5-HT (10(-6) M) treatment resulted in increased cell proliferation and increased DNA synthesis, which were inhibited by the JAK2 inhibitor AG490. |
| 350 | 15601754 | Further studies with apocynin, diphenyleneiodonium chloride, catalase, and virally transfected superoxide dismutase had no effect at either glucose concentration on activation of the JAK/STAT pathway by 5-HT. |
| 351 | 15601754 | Therefore, we conclude that 5-HT activates JAK2, JAK1, and STAT1 via the 5-HT2A receptors in a reactive oxygen species-independent manner under both normal and high glucose conditions. |
| 352 | 15601754 | Previous studies have shown the presence of 5-HT2A, 5-HT2B, and 5-HT1B receptors in vascular smooth muscle cells (VSMCs). |
| 353 | 15601754 | There are currently no data regarding 5-HT2B and 5-HT1B receptor activation of the JAK/STAT pathway in VSMCs and resultant potential alterations in 5-HT signaling in diabetes. |
| 354 | 15601754 | Therefore, we tested the hypothesis that 5-HT differentially activates the JAK/STAT pathway in VSMCs under conditions of normal (5 mM) and high (25 mM) glucose. |
| 355 | 15601754 | Treatment of rat VSMCs with 5-HT (10(-6) M) resulted in time-dependent activation ( approximately 2-fold) of JAK2, JAK1, and STAT1, but not STAT3 (maximal at 5 min, returned to baseline by 30 min). |
| 356 | 15601754 | The 5-HT2B receptor agonist BW723C86 and the 5-HT1B receptor agonist CGS12066A (10(-9)-10(-5) M, 5-min stimulation) did not activate the JAK/STAT pathway. |
| 357 | 15601754 | Treatment with the 5-HT2A receptor antagonist ketanserin (10 nM) inhibited JAK2 activation by 5-HT. |
| 358 | 15601754 | Treatment of streptozotocin-induced diabetic rats with ketanserin (5 mg.kg-1.day-1) reduced activation of JAK2 and STAT1 but not STAT3 in endothelium-denuded thoracic aorta in vivo. 5-HT (10(-6) M) treatment resulted in increased cell proliferation and increased DNA synthesis, which were inhibited by the JAK2 inhibitor AG490. |
| 359 | 15601754 | Further studies with apocynin, diphenyleneiodonium chloride, catalase, and virally transfected superoxide dismutase had no effect at either glucose concentration on activation of the JAK/STAT pathway by 5-HT. |
| 360 | 15601754 | Therefore, we conclude that 5-HT activates JAK2, JAK1, and STAT1 via the 5-HT2A receptors in a reactive oxygen species-independent manner under both normal and high glucose conditions. |
| 361 | 15601754 | Previous studies have shown the presence of 5-HT2A, 5-HT2B, and 5-HT1B receptors in vascular smooth muscle cells (VSMCs). |
| 362 | 15601754 | There are currently no data regarding 5-HT2B and 5-HT1B receptor activation of the JAK/STAT pathway in VSMCs and resultant potential alterations in 5-HT signaling in diabetes. |
| 363 | 15601754 | Therefore, we tested the hypothesis that 5-HT differentially activates the JAK/STAT pathway in VSMCs under conditions of normal (5 mM) and high (25 mM) glucose. |
| 364 | 15601754 | Treatment of rat VSMCs with 5-HT (10(-6) M) resulted in time-dependent activation ( approximately 2-fold) of JAK2, JAK1, and STAT1, but not STAT3 (maximal at 5 min, returned to baseline by 30 min). |
| 365 | 15601754 | The 5-HT2B receptor agonist BW723C86 and the 5-HT1B receptor agonist CGS12066A (10(-9)-10(-5) M, 5-min stimulation) did not activate the JAK/STAT pathway. |
| 366 | 15601754 | Treatment with the 5-HT2A receptor antagonist ketanserin (10 nM) inhibited JAK2 activation by 5-HT. |
| 367 | 15601754 | Treatment of streptozotocin-induced diabetic rats with ketanserin (5 mg.kg-1.day-1) reduced activation of JAK2 and STAT1 but not STAT3 in endothelium-denuded thoracic aorta in vivo. 5-HT (10(-6) M) treatment resulted in increased cell proliferation and increased DNA synthesis, which were inhibited by the JAK2 inhibitor AG490. |
| 368 | 15601754 | Further studies with apocynin, diphenyleneiodonium chloride, catalase, and virally transfected superoxide dismutase had no effect at either glucose concentration on activation of the JAK/STAT pathway by 5-HT. |
| 369 | 15601754 | Therefore, we conclude that 5-HT activates JAK2, JAK1, and STAT1 via the 5-HT2A receptors in a reactive oxygen species-independent manner under both normal and high glucose conditions. |
| 370 | 15601754 | Previous studies have shown the presence of 5-HT2A, 5-HT2B, and 5-HT1B receptors in vascular smooth muscle cells (VSMCs). |
| 371 | 15601754 | There are currently no data regarding 5-HT2B and 5-HT1B receptor activation of the JAK/STAT pathway in VSMCs and resultant potential alterations in 5-HT signaling in diabetes. |
| 372 | 15601754 | Therefore, we tested the hypothesis that 5-HT differentially activates the JAK/STAT pathway in VSMCs under conditions of normal (5 mM) and high (25 mM) glucose. |
| 373 | 15601754 | Treatment of rat VSMCs with 5-HT (10(-6) M) resulted in time-dependent activation ( approximately 2-fold) of JAK2, JAK1, and STAT1, but not STAT3 (maximal at 5 min, returned to baseline by 30 min). |
| 374 | 15601754 | The 5-HT2B receptor agonist BW723C86 and the 5-HT1B receptor agonist CGS12066A (10(-9)-10(-5) M, 5-min stimulation) did not activate the JAK/STAT pathway. |
| 375 | 15601754 | Treatment with the 5-HT2A receptor antagonist ketanserin (10 nM) inhibited JAK2 activation by 5-HT. |
| 376 | 15601754 | Treatment of streptozotocin-induced diabetic rats with ketanserin (5 mg.kg-1.day-1) reduced activation of JAK2 and STAT1 but not STAT3 in endothelium-denuded thoracic aorta in vivo. 5-HT (10(-6) M) treatment resulted in increased cell proliferation and increased DNA synthesis, which were inhibited by the JAK2 inhibitor AG490. |
| 377 | 15601754 | Further studies with apocynin, diphenyleneiodonium chloride, catalase, and virally transfected superoxide dismutase had no effect at either glucose concentration on activation of the JAK/STAT pathway by 5-HT. |
| 378 | 15601754 | Therefore, we conclude that 5-HT activates JAK2, JAK1, and STAT1 via the 5-HT2A receptors in a reactive oxygen species-independent manner under both normal and high glucose conditions. |
| 379 | 15601754 | Previous studies have shown the presence of 5-HT2A, 5-HT2B, and 5-HT1B receptors in vascular smooth muscle cells (VSMCs). |
| 380 | 15601754 | There are currently no data regarding 5-HT2B and 5-HT1B receptor activation of the JAK/STAT pathway in VSMCs and resultant potential alterations in 5-HT signaling in diabetes. |
| 381 | 15601754 | Therefore, we tested the hypothesis that 5-HT differentially activates the JAK/STAT pathway in VSMCs under conditions of normal (5 mM) and high (25 mM) glucose. |
| 382 | 15601754 | Treatment of rat VSMCs with 5-HT (10(-6) M) resulted in time-dependent activation ( approximately 2-fold) of JAK2, JAK1, and STAT1, but not STAT3 (maximal at 5 min, returned to baseline by 30 min). |
| 383 | 15601754 | The 5-HT2B receptor agonist BW723C86 and the 5-HT1B receptor agonist CGS12066A (10(-9)-10(-5) M, 5-min stimulation) did not activate the JAK/STAT pathway. |
| 384 | 15601754 | Treatment with the 5-HT2A receptor antagonist ketanserin (10 nM) inhibited JAK2 activation by 5-HT. |
| 385 | 15601754 | Treatment of streptozotocin-induced diabetic rats with ketanserin (5 mg.kg-1.day-1) reduced activation of JAK2 and STAT1 but not STAT3 in endothelium-denuded thoracic aorta in vivo. 5-HT (10(-6) M) treatment resulted in increased cell proliferation and increased DNA synthesis, which were inhibited by the JAK2 inhibitor AG490. |
| 386 | 15601754 | Further studies with apocynin, diphenyleneiodonium chloride, catalase, and virally transfected superoxide dismutase had no effect at either glucose concentration on activation of the JAK/STAT pathway by 5-HT. |
| 387 | 15601754 | Therefore, we conclude that 5-HT activates JAK2, JAK1, and STAT1 via the 5-HT2A receptors in a reactive oxygen species-independent manner under both normal and high glucose conditions. |
| 388 | 16140162 | In this study, we investigated the effects of acute (7 days) glucose-induced hyperglycemia and sodium acetoacetate (NaAcAc) or ammonium chloride (NH4Cl) induced acidosis on the level of indolamines (5-hydroxytryptamine (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA)) as well as PKC-alpha expression/activity in discrete areas of rat brain. |
| 389 | 16140165 | Clinical observation found that tramadol, mu opioid receptor (MOR) agonist and serotonin (5-HT) reuptake inhibitor, has a hypoglycemic effect in type 2 diabetes patients. |
| 390 | 16140165 | This study showed that tramadol activated a neuronal insulin signaling cascade by increasing the induction of insulin receptor substrate-2 expression in primary cultured neuronal cells while this activation was suppressed by naloxone (MOR inhibitor) and dexamethasone (non-specific inhibitor of MOR and 5-HT receptor, DEX). |
| 391 | 16140165 | Glucose utilization of the cerebral cortex and hypothalamus was enhanced by a 4-week-tramadol administration in 90% pancreatectomized rats, in vivo, as assessed by measurement of glucokinase expression and glycogen deposition via activating insulin signaling cascade such as neuronal cells in vitro. |
| 392 | 16140165 | Clinical observation found that tramadol, mu opioid receptor (MOR) agonist and serotonin (5-HT) reuptake inhibitor, has a hypoglycemic effect in type 2 diabetes patients. |
| 393 | 16140165 | This study showed that tramadol activated a neuronal insulin signaling cascade by increasing the induction of insulin receptor substrate-2 expression in primary cultured neuronal cells while this activation was suppressed by naloxone (MOR inhibitor) and dexamethasone (non-specific inhibitor of MOR and 5-HT receptor, DEX). |
| 394 | 16140165 | Glucose utilization of the cerebral cortex and hypothalamus was enhanced by a 4-week-tramadol administration in 90% pancreatectomized rats, in vivo, as assessed by measurement of glucokinase expression and glycogen deposition via activating insulin signaling cascade such as neuronal cells in vitro. |
| 395 | 16185313 | The effects of tegaserod, a 5-HT receptor agonist, on gastric emptying in a murine model of diabetes mellitus. |
| 396 | 16204433 | Antagonism of the serotonin (5-HT)-2 receptor and insulin sensitivity: implications for atypical antipsychotics. |
| 397 | 16430857 | Brain serotonin (5-hydroxytryptamine; 5-HT) systems contribute to regulate eating behavior and energy homeostasis. 5-HT2C receptors and 5-HT1B receptors have been shown to mediate anorexic effects of 5-HT drugs such as d-fenfluramine, which stimulates 5-HT release and inhibits 5-HT reuptake, and m-chlorophenylpiperazine (mCPP), a 5-HT2C receptor agonist. |
| 398 | 16430857 | Here, we report that 24-h fasting increased the expression of hypothalamic 5-HT2C receptor and 5-HT1B receptor genes in association with increases in plasma active ghrelin levels compared with fed state in mice. |
| 399 | 16430857 | Treatment with mCPP or fenfluramine significantly inhibited the increases in plasma active ghrelin levels. mCPP or fenfluramine significantly increased the expression of hypothalamic pro-opiomelanocortin and cocaine- and amphetamine-regulated transcript genes while having no significant effects on the expression of hypothalamic neuropeptide Y, agouti- related protein, and ghrelin genes. |
| 400 | 16430857 | These results suggest that there is a negative feedback system between brain 5-HT systems and plasma active ghrelin levels in energy homeostasis in mice. |
| 401 | 16430857 | Brain serotonin (5-hydroxytryptamine; 5-HT) systems contribute to regulate eating behavior and energy homeostasis. 5-HT2C receptors and 5-HT1B receptors have been shown to mediate anorexic effects of 5-HT drugs such as d-fenfluramine, which stimulates 5-HT release and inhibits 5-HT reuptake, and m-chlorophenylpiperazine (mCPP), a 5-HT2C receptor agonist. |
| 402 | 16430857 | Here, we report that 24-h fasting increased the expression of hypothalamic 5-HT2C receptor and 5-HT1B receptor genes in association with increases in plasma active ghrelin levels compared with fed state in mice. |
| 403 | 16430857 | Treatment with mCPP or fenfluramine significantly inhibited the increases in plasma active ghrelin levels. mCPP or fenfluramine significantly increased the expression of hypothalamic pro-opiomelanocortin and cocaine- and amphetamine-regulated transcript genes while having no significant effects on the expression of hypothalamic neuropeptide Y, agouti- related protein, and ghrelin genes. |
| 404 | 16430857 | These results suggest that there is a negative feedback system between brain 5-HT systems and plasma active ghrelin levels in energy homeostasis in mice. |
| 405 | 16611151 | Combination therapy like prostaglandin E(1) (PGE(1)) with doxazosin (dox; an alpha-1-blocker) or ketanserin (ketan; a 5-HT(2) antagonist) as well as other pro-erection agents, like Endothelin-1 antagonists, angiotensin II antagonists (valsartan/losartan), adrenomedullin, Rho kinase inhibitors and nitric oxide (NO) donors may be beneficial in the treatment of ED. |
| 406 | 16630608 | The inhibition of electrically induced pressor responses by 5-HT (10 microg/kg/min) in diabetic pithed rats could not be elicited after i.v. treatment with 1H-[1,2,4]Oxadiazolo[4,3-a]quinoxalin-1-one (ODQ) (10 microg/kg), a guanylyl cyclase inhibitor, or N-omega-L-Arginine methyl ester hydrochloride (L-NAME) (10 mg/kg), a nitric oxide synthase (NOS) inhibitor. |
| 407 | 16647108 | The effect of sibutramine (20 mg/kg) on energy expenditure was not inhibited by the non-selective 5-HT receptor antagonist, metergoline (1 mg/kg), or a high dose (20 mg/kg) of the non-selective beta-blocker propranolol, but was blocked by D1 dopamine receptor inhibitor SCH 23390 (0.3 mg/kg). |
| 408 | 16741041 | Six weeks after the onset of diabetes, contractile responses to 0.1-100 nM ET-1 and relaxation responses to 1 nM-10 microM acetylcholine (ACh) in vessels preconstricted (baseline + 60%) with serotonin (5-HT) were assessed by myograph studies in the presence or absence of a nitric oxide synthase (NOS) inhibitor, N-nitro-L-arginine (L-NNA). |
| 409 | 16973729 | Hyperphagia alters expression of hypothalamic 5-HT2C and 5-HT1B receptor genes and plasma des-acyl ghrelin levels in Ay mice. |
| 410 | 16973729 | The central melanocortin (MC) pathway is suggested to mediate satiety signaling downstream of serotonin (5-HT)2C receptors. 5-HT2C receptor mutant mice consume more food, which leads to late-onset obesity and impaired glucose tolerance. |
| 411 | 16973729 | Here, we report that 5-wk-old Ay mice consumed more food in association with decreases in levels of plasma des-acyl ghrelin, but not active ghrelin, and increases in hypothalamic 5-HT2C and 5-HT1B receptor gene expression compared with wild-type mice matched for age and body weight. |
| 412 | 16973729 | Restricted feeding significantly decreased hypothalamic 5-HT2C and 5-HT1B receptor gene expression in association with a reversal of the decreases in plasma des-acyl ghrelin levels in 5-wk-old Ay mice. |
| 413 | 16973729 | Administration of m-chlorophenylpiperazine and fenfluramine, both of which induce anorexic effects via 5-HT2C receptors and/or 5-HT1B receptors, suppressed food intake in 5- and 8-wk-old Ay mice, whereas the anorexic effects were attenuated in food-restricted Ay mice. |
| 414 | 16973729 | These findings suggest that the agouti peptide down-regulates hypothalamic 5-HT2C and 5-HT1B receptor gene expression under restricted feeding conditions, whereas chronic hyperphagia increases the expression of these genes and decreases plasma des-acyl ghrelin levels in Ay mice. |
| 415 | 17097612 | Serotonin (5-hydroxytryptamine; 5-HT) 2A receptors contribute to the effects of 5-HT on platelet aggregation and vascular smooth muscle cell proliferation, and are reportedly involved in decreases in plasma levels of adiponectin, an adipokine, in diabetic subjects. |
| 416 | 17097612 | Here, we report that systemic administration of sarpogrelate, a 5-HT2A receptor antagonist, suppressed appetite and increased hypothalamic pro-opiomelanocortin and cocaine- and amphetamine-regulated transcript, corticotropin releasing hormone, 5-HT2C, and 5-HT1B receptor gene expression. |
| 417 | 17097612 | These results suggest that obesity increases hypothalamic 5-HT2A receptor gene expression, and pharmacologic inactivation of 5-HT2A receptors inhibits overfeeding and obesity in A(y) mice, but did not increase plasma adiponectin levels. |
| 418 | 17218444 | Neither SB242084, a selective 5-HT2C receptor antagonist, nor SB224289, a selective 5-HT1B receptor antagonist, reversed the appetite-suppressing effects of milnacipran. |
| 419 | 17218444 | Moreover, milnacipran significantly increased hypothalamic proopiomelanocortin (POMC) and cocaine- and amphetamine-regulated transcript (CART) mRNA levels, while having no effect on hypothalamic neuropeptide Y, ghrelin, corticotropin-releasing hormone (CRH), and suppressor of cytokine signaling-3 mRNA levels. |
| 420 | 17218444 | Interestingly, milnacipran did not increase plasma corticosterone and blood glucose levels, whereas fenfluramine, which inhibits 5-HT reuptake and stimulates 5-HT release, significantly increased plasma corticosterone and blood glucose levels in association with increased hypothalamic CRH mRNA levels. |
| 421 | 17218444 | These results suggest that inhibition of 5-HT and NA reuptake induces appetite-suppressing effects independent of 5-HT2C and 5-HT1B receptors, and increases hypothalamic POMC and CART gene expression without increasing plasma corticosterone and blood glucose levels in mice. |
| 422 | 17218444 | Neither SB242084, a selective 5-HT2C receptor antagonist, nor SB224289, a selective 5-HT1B receptor antagonist, reversed the appetite-suppressing effects of milnacipran. |
| 423 | 17218444 | Moreover, milnacipran significantly increased hypothalamic proopiomelanocortin (POMC) and cocaine- and amphetamine-regulated transcript (CART) mRNA levels, while having no effect on hypothalamic neuropeptide Y, ghrelin, corticotropin-releasing hormone (CRH), and suppressor of cytokine signaling-3 mRNA levels. |
| 424 | 17218444 | Interestingly, milnacipran did not increase plasma corticosterone and blood glucose levels, whereas fenfluramine, which inhibits 5-HT reuptake and stimulates 5-HT release, significantly increased plasma corticosterone and blood glucose levels in association with increased hypothalamic CRH mRNA levels. |
| 425 | 17218444 | These results suggest that inhibition of 5-HT and NA reuptake induces appetite-suppressing effects independent of 5-HT2C and 5-HT1B receptors, and increases hypothalamic POMC and CART gene expression without increasing plasma corticosterone and blood glucose levels in mice. |
| 426 | 17320057 | The elevated open platform stress-elicited 5-HT secretion was significantly decreased in the PFC of diabetic mice, and this blunted response was normalized by sub-chronic pretreatment with insulin (5 U/kg, s.c., twice daily). |
| 427 | 17397876 | Plasma glucose, insulin, beta-endorphin and adrenaline were assessed after intraperitoneal administration of serotonin. |
| 428 | 17397876 | Serotonin produced hypoglycemic effects without altering plasma insulin and adrenaline levels but increasing beta-endorphin level in STZ-diabetic rats. |
| 429 | 17397876 | Dihydroergotamine (non-selective 5-HT receptor blocker) and pimozide (5-HT(7) receptor blocker) abolished the hypoglycemic effect of serotonin in STZ-diabetic rats. |
| 430 | 17397876 | The results demonstrated that serotonin may activate 5-HT(7) receptor on rat adrenal gland to enhance of beta-endorphin secretion, which then stimulates the opioid receptor to increase peripheral glucose utilization, resulting in decreased plasma glucose levels in STZ-diabetic rats. |
| 431 | 17397876 | Plasma glucose, insulin, beta-endorphin and adrenaline were assessed after intraperitoneal administration of serotonin. |
| 432 | 17397876 | Serotonin produced hypoglycemic effects without altering plasma insulin and adrenaline levels but increasing beta-endorphin level in STZ-diabetic rats. |
| 433 | 17397876 | Dihydroergotamine (non-selective 5-HT receptor blocker) and pimozide (5-HT(7) receptor blocker) abolished the hypoglycemic effect of serotonin in STZ-diabetic rats. |
| 434 | 17397876 | The results demonstrated that serotonin may activate 5-HT(7) receptor on rat adrenal gland to enhance of beta-endorphin secretion, which then stimulates the opioid receptor to increase peripheral glucose utilization, resulting in decreased plasma glucose levels in STZ-diabetic rats. |
| 435 | 17579254 | Blood pressure, glucose, HbA(1C), triglyceride, cholesterol, plasma insulin levels and body weight were measured. |
| 436 | 17579254 | Cumulative concentration-response curves of serotonin (5-hydroxytryptamine; 5-HT) were evaluated before and after 1 h incubations with insulin (10(-7) or 10(-4) U/l), or PIO (10 micromol/l) or insulin plus PIO. |
| 437 | 17579254 | PIO or higher concentration of insulin (10(-4) U/l), each alone, attenuated 5-HT induced contractions in both groups of aortae. |
| 438 | 17579254 | Blood pressure, glucose, HbA(1C), triglyceride, cholesterol, plasma insulin levels and body weight were measured. |
| 439 | 17579254 | Cumulative concentration-response curves of serotonin (5-hydroxytryptamine; 5-HT) were evaluated before and after 1 h incubations with insulin (10(-7) or 10(-4) U/l), or PIO (10 micromol/l) or insulin plus PIO. |
| 440 | 17579254 | PIO or higher concentration of insulin (10(-4) U/l), each alone, attenuated 5-HT induced contractions in both groups of aortae. |
| 441 | 17983585 | We report here that serotonin 2C receptor (5-HT(2C)R) agonists, typically investigated for their anorectic properties, significantly improve glucose tolerance and reduce plasma insulin in murine models of obesity and type 2 diabetes. |
| 442 | 17983585 | We determined that this primary effect on glucose homeostasis requires downstream activation of melanocortin-4 receptors (MC4Rs), but not MC3Rs. |
| 443 | 18403651 | An old dog learns a new trick: regulation of peripheral glucose homeostasis by the serotonin (5-HT)2C receptor. |
| 444 | 18477467 | Serotonin systems upregulate the expression of hypothalamic NUCB2 via 5-HT2C receptors and induce anorexia via a leptin-independent pathway in mice. |
| 445 | 18477467 | NEFA/nucleobindin2 (NUCB2), a novel satiety molecule, is associated with leptin-independent melanocortin signaling in the central nervous system. |
| 446 | 18477467 | Here, we show that systemic administration of m-chlorophenylpiperazine (mCPP), a serotonin 5-HT1B/2C receptor agonist, significantly increased the expression of hypothalamic NUCB2 in wild-type mice. |
| 447 | 18477467 | The increases in hypothalamic NUCB2 expression induced by mCPP were attenuated in 5-HT2C receptor mutant mice. |
| 448 | 18477467 | On the other hand, the expression of hypothalamic NUCB2 and proopiomelanocortin (POMC) was significantly decreased in hyperphagic and non-obese 5-HT2C receptor mutants compared with age-matched wild-type mice. |
| 449 | 18477467 | Interestingly, despite increased expression of hypothalamic POMC, hypothalamic NUCB2 expression was decreased in 5-HT2C receptor mutant mice with heterozygous mutation of beta-endorphin gene. |
| 450 | 18477467 | These findings suggest that 5-HT systems upregulate the expression of hypothalamic NUCB2 via 5-HT2C receptors, and induce anorexia via a leptin-independent pathway in mice. |
| 451 | 18708586 | We have now discovered that activation of 5-HT(2A) receptors in primary aortic smooth muscle cells provides a previously unknown and extremely potent inhibition of tumor necrosis factor (TNF)-alpha-mediated inflammation. 5-HT(2A) receptor stimulation with the agonist (R)-1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane [(R)-DOI] rapidly inhibits a variety of TNF-alpha-mediated proinflammatory markers, including intracellular adhesion molecule 1 (ICAM-1), vascular adhesion molecule 1 (VCAM-1), and interleukin (IL)-6 gene expression, nitric-oxide synthase activity, and nuclear translocation of nuclear factor kappaB, with IC(50) values of only 10 to 20 pM. |
| 452 | 18708586 | Our results indicate that activation of 5-HT(2A) receptors represents a novel, and extraordinarily potent, potential therapeutic avenue for the treatment of disorders involving TNF-alpha-mediated inflammation. |
| 453 | 18708586 | We have now discovered that activation of 5-HT(2A) receptors in primary aortic smooth muscle cells provides a previously unknown and extremely potent inhibition of tumor necrosis factor (TNF)-alpha-mediated inflammation. 5-HT(2A) receptor stimulation with the agonist (R)-1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane [(R)-DOI] rapidly inhibits a variety of TNF-alpha-mediated proinflammatory markers, including intracellular adhesion molecule 1 (ICAM-1), vascular adhesion molecule 1 (VCAM-1), and interleukin (IL)-6 gene expression, nitric-oxide synthase activity, and nuclear translocation of nuclear factor kappaB, with IC(50) values of only 10 to 20 pM. |
| 454 | 18708586 | Our results indicate that activation of 5-HT(2A) receptors represents a novel, and extraordinarily potent, potential therapeutic avenue for the treatment of disorders involving TNF-alpha-mediated inflammation. |
| 455 | 18711746 | Our previous studies have shown that serotonin (5-HT) altered under diabetic condition was accompanied by alterations of protein kinase C-alpha (PKC-alpha) and CaMKII, and those alterations were reversed after insulin administration. |
| 456 | 18711746 | The current study showed that alloxan-induced diabetic animals revealed hyperglycemia and was associated with an increase in the content of 5-HT, PKC-alpha expression and PKC activity (P < 0.05) simultaneously in striatum (ST), midbrain (MB), pons medulla (PM), cerebellum (CB), and cerebral cortex (CCX) from 7 days to 60 days. |
| 457 | 18711746 | Although the 5-HT levels in hippocampus (HC) and hypothalamus (HT) were not altered, the PKC-alpha expression and PKC activity showed increases (P < 0.05) in level in HC. |
| 458 | 18711746 | In contrast, the in vitro study has shown that the 5-HT levels correlated with PKC-alpha expressions as well as PKC activity (P < 0.05) only in ST, MB, and CB either after induction with phorbol 12-myristate 13-acetate (PMA) or blocking with chelerythrine, whereas PM and CCX remained elevated (P < 0.05), implying a regulatory role for PKC-alpha only in ST, MB, and CB. |
| 459 | 18711746 | However, our consecutive studies have shown that the 5-HT level in PM was regulated by p38-mitogen-activated protein kinase (p38-MAPK) both in vivo and in vitro, whereas the 5-HT level in CCX was coregulated by S-100beta by protein-protein interaction with serotonin transporter (SERT) via 8-bromoadenosine 3',5'-cyclic monophosphate sodium salt (8-Br-cAMP)-induced cAMP/PKAII pathway(s). |
| 460 | 18711746 | Our previous studies have shown that serotonin (5-HT) altered under diabetic condition was accompanied by alterations of protein kinase C-alpha (PKC-alpha) and CaMKII, and those alterations were reversed after insulin administration. |
| 461 | 18711746 | The current study showed that alloxan-induced diabetic animals revealed hyperglycemia and was associated with an increase in the content of 5-HT, PKC-alpha expression and PKC activity (P < 0.05) simultaneously in striatum (ST), midbrain (MB), pons medulla (PM), cerebellum (CB), and cerebral cortex (CCX) from 7 days to 60 days. |
| 462 | 18711746 | Although the 5-HT levels in hippocampus (HC) and hypothalamus (HT) were not altered, the PKC-alpha expression and PKC activity showed increases (P < 0.05) in level in HC. |
| 463 | 18711746 | In contrast, the in vitro study has shown that the 5-HT levels correlated with PKC-alpha expressions as well as PKC activity (P < 0.05) only in ST, MB, and CB either after induction with phorbol 12-myristate 13-acetate (PMA) or blocking with chelerythrine, whereas PM and CCX remained elevated (P < 0.05), implying a regulatory role for PKC-alpha only in ST, MB, and CB. |
| 464 | 18711746 | However, our consecutive studies have shown that the 5-HT level in PM was regulated by p38-mitogen-activated protein kinase (p38-MAPK) both in vivo and in vitro, whereas the 5-HT level in CCX was coregulated by S-100beta by protein-protein interaction with serotonin transporter (SERT) via 8-bromoadenosine 3',5'-cyclic monophosphate sodium salt (8-Br-cAMP)-induced cAMP/PKAII pathway(s). |
| 465 | 18711746 | Our previous studies have shown that serotonin (5-HT) altered under diabetic condition was accompanied by alterations of protein kinase C-alpha (PKC-alpha) and CaMKII, and those alterations were reversed after insulin administration. |
| 466 | 18711746 | The current study showed that alloxan-induced diabetic animals revealed hyperglycemia and was associated with an increase in the content of 5-HT, PKC-alpha expression and PKC activity (P < 0.05) simultaneously in striatum (ST), midbrain (MB), pons medulla (PM), cerebellum (CB), and cerebral cortex (CCX) from 7 days to 60 days. |
| 467 | 18711746 | Although the 5-HT levels in hippocampus (HC) and hypothalamus (HT) were not altered, the PKC-alpha expression and PKC activity showed increases (P < 0.05) in level in HC. |
| 468 | 18711746 | In contrast, the in vitro study has shown that the 5-HT levels correlated with PKC-alpha expressions as well as PKC activity (P < 0.05) only in ST, MB, and CB either after induction with phorbol 12-myristate 13-acetate (PMA) or blocking with chelerythrine, whereas PM and CCX remained elevated (P < 0.05), implying a regulatory role for PKC-alpha only in ST, MB, and CB. |
| 469 | 18711746 | However, our consecutive studies have shown that the 5-HT level in PM was regulated by p38-mitogen-activated protein kinase (p38-MAPK) both in vivo and in vitro, whereas the 5-HT level in CCX was coregulated by S-100beta by protein-protein interaction with serotonin transporter (SERT) via 8-bromoadenosine 3',5'-cyclic monophosphate sodium salt (8-Br-cAMP)-induced cAMP/PKAII pathway(s). |
| 470 | 18711746 | Our previous studies have shown that serotonin (5-HT) altered under diabetic condition was accompanied by alterations of protein kinase C-alpha (PKC-alpha) and CaMKII, and those alterations were reversed after insulin administration. |
| 471 | 18711746 | The current study showed that alloxan-induced diabetic animals revealed hyperglycemia and was associated with an increase in the content of 5-HT, PKC-alpha expression and PKC activity (P < 0.05) simultaneously in striatum (ST), midbrain (MB), pons medulla (PM), cerebellum (CB), and cerebral cortex (CCX) from 7 days to 60 days. |
| 472 | 18711746 | Although the 5-HT levels in hippocampus (HC) and hypothalamus (HT) were not altered, the PKC-alpha expression and PKC activity showed increases (P < 0.05) in level in HC. |
| 473 | 18711746 | In contrast, the in vitro study has shown that the 5-HT levels correlated with PKC-alpha expressions as well as PKC activity (P < 0.05) only in ST, MB, and CB either after induction with phorbol 12-myristate 13-acetate (PMA) or blocking with chelerythrine, whereas PM and CCX remained elevated (P < 0.05), implying a regulatory role for PKC-alpha only in ST, MB, and CB. |
| 474 | 18711746 | However, our consecutive studies have shown that the 5-HT level in PM was regulated by p38-mitogen-activated protein kinase (p38-MAPK) both in vivo and in vitro, whereas the 5-HT level in CCX was coregulated by S-100beta by protein-protein interaction with serotonin transporter (SERT) via 8-bromoadenosine 3',5'-cyclic monophosphate sodium salt (8-Br-cAMP)-induced cAMP/PKAII pathway(s). |
| 475 | 18711746 | Our previous studies have shown that serotonin (5-HT) altered under diabetic condition was accompanied by alterations of protein kinase C-alpha (PKC-alpha) and CaMKII, and those alterations were reversed after insulin administration. |
| 476 | 18711746 | The current study showed that alloxan-induced diabetic animals revealed hyperglycemia and was associated with an increase in the content of 5-HT, PKC-alpha expression and PKC activity (P < 0.05) simultaneously in striatum (ST), midbrain (MB), pons medulla (PM), cerebellum (CB), and cerebral cortex (CCX) from 7 days to 60 days. |
| 477 | 18711746 | Although the 5-HT levels in hippocampus (HC) and hypothalamus (HT) were not altered, the PKC-alpha expression and PKC activity showed increases (P < 0.05) in level in HC. |
| 478 | 18711746 | In contrast, the in vitro study has shown that the 5-HT levels correlated with PKC-alpha expressions as well as PKC activity (P < 0.05) only in ST, MB, and CB either after induction with phorbol 12-myristate 13-acetate (PMA) or blocking with chelerythrine, whereas PM and CCX remained elevated (P < 0.05), implying a regulatory role for PKC-alpha only in ST, MB, and CB. |
| 479 | 18711746 | However, our consecutive studies have shown that the 5-HT level in PM was regulated by p38-mitogen-activated protein kinase (p38-MAPK) both in vivo and in vitro, whereas the 5-HT level in CCX was coregulated by S-100beta by protein-protein interaction with serotonin transporter (SERT) via 8-bromoadenosine 3',5'-cyclic monophosphate sodium salt (8-Br-cAMP)-induced cAMP/PKAII pathway(s). |
| 480 | 19721380 | We examined 5-HT receptor subtypes responsible for the 5-HT-induced vasocontraction in the human ITA. |
| 481 | 19721380 | Additionally, we demonstrated that insulin induced internalization of 5-HT(2A) receptors from the plasma membrane in HEK293 cells. |
| 482 | 19721380 | We examined 5-HT receptor subtypes responsible for the 5-HT-induced vasocontraction in the human ITA. |
| 483 | 19721380 | Additionally, we demonstrated that insulin induced internalization of 5-HT(2A) receptors from the plasma membrane in HEK293 cells. |
| 484 | 19859528 | While serotonin (5-HT) co-localization with insulin in granules of pancreatic beta-cells was demonstrated more than three decades ago, its physiological role in the etiology of diabetes is still unclear. |
| 485 | 19859528 | We combined biochemical and electrophysiological analyses of mice selectively deficient in peripheral tryptophan hydroxylase (Tph1-/-) and 5-HT to show that intracellular 5-HT regulates insulin secretion. |
| 486 | 19859528 | We found that these mice are diabetic and have an impaired insulin secretion due to the lack of 5-HT in the pancreas. |
| 487 | 19859528 | The pharmacological restoration of peripheral 5-HT levels rescued the impaired insulin secretion in vivo. |
| 488 | 19859528 | In elucidating the underlying mechanism further, we demonstrate the covalent coupling of 5-HT by transglutaminases during insulin exocytosis to two key players in insulin secretion, the small GTPases Rab3a and Rab27a. |
| 489 | 19859528 | Our results demonstrate that 5-HT regulates insulin secretion by serotonylation of GTPases within pancreatic beta-cells and suggest that intracellular 5-HT functions in various microenvironments via this mechanism in concert with the known receptor-mediated signaling. |
| 490 | 19859528 | While serotonin (5-HT) co-localization with insulin in granules of pancreatic beta-cells was demonstrated more than three decades ago, its physiological role in the etiology of diabetes is still unclear. |
| 491 | 19859528 | We combined biochemical and electrophysiological analyses of mice selectively deficient in peripheral tryptophan hydroxylase (Tph1-/-) and 5-HT to show that intracellular 5-HT regulates insulin secretion. |
| 492 | 19859528 | We found that these mice are diabetic and have an impaired insulin secretion due to the lack of 5-HT in the pancreas. |
| 493 | 19859528 | The pharmacological restoration of peripheral 5-HT levels rescued the impaired insulin secretion in vivo. |
| 494 | 19859528 | In elucidating the underlying mechanism further, we demonstrate the covalent coupling of 5-HT by transglutaminases during insulin exocytosis to two key players in insulin secretion, the small GTPases Rab3a and Rab27a. |
| 495 | 19859528 | Our results demonstrate that 5-HT regulates insulin secretion by serotonylation of GTPases within pancreatic beta-cells and suggest that intracellular 5-HT functions in various microenvironments via this mechanism in concert with the known receptor-mediated signaling. |
| 496 | 19859528 | While serotonin (5-HT) co-localization with insulin in granules of pancreatic beta-cells was demonstrated more than three decades ago, its physiological role in the etiology of diabetes is still unclear. |
| 497 | 19859528 | We combined biochemical and electrophysiological analyses of mice selectively deficient in peripheral tryptophan hydroxylase (Tph1-/-) and 5-HT to show that intracellular 5-HT regulates insulin secretion. |
| 498 | 19859528 | We found that these mice are diabetic and have an impaired insulin secretion due to the lack of 5-HT in the pancreas. |
| 499 | 19859528 | The pharmacological restoration of peripheral 5-HT levels rescued the impaired insulin secretion in vivo. |
| 500 | 19859528 | In elucidating the underlying mechanism further, we demonstrate the covalent coupling of 5-HT by transglutaminases during insulin exocytosis to two key players in insulin secretion, the small GTPases Rab3a and Rab27a. |
| 501 | 19859528 | Our results demonstrate that 5-HT regulates insulin secretion by serotonylation of GTPases within pancreatic beta-cells and suggest that intracellular 5-HT functions in various microenvironments via this mechanism in concert with the known receptor-mediated signaling. |
| 502 | 19859528 | While serotonin (5-HT) co-localization with insulin in granules of pancreatic beta-cells was demonstrated more than three decades ago, its physiological role in the etiology of diabetes is still unclear. |
| 503 | 19859528 | We combined biochemical and electrophysiological analyses of mice selectively deficient in peripheral tryptophan hydroxylase (Tph1-/-) and 5-HT to show that intracellular 5-HT regulates insulin secretion. |
| 504 | 19859528 | We found that these mice are diabetic and have an impaired insulin secretion due to the lack of 5-HT in the pancreas. |
| 505 | 19859528 | The pharmacological restoration of peripheral 5-HT levels rescued the impaired insulin secretion in vivo. |
| 506 | 19859528 | In elucidating the underlying mechanism further, we demonstrate the covalent coupling of 5-HT by transglutaminases during insulin exocytosis to two key players in insulin secretion, the small GTPases Rab3a and Rab27a. |
| 507 | 19859528 | Our results demonstrate that 5-HT regulates insulin secretion by serotonylation of GTPases within pancreatic beta-cells and suggest that intracellular 5-HT functions in various microenvironments via this mechanism in concert with the known receptor-mediated signaling. |
| 508 | 19859528 | While serotonin (5-HT) co-localization with insulin in granules of pancreatic beta-cells was demonstrated more than three decades ago, its physiological role in the etiology of diabetes is still unclear. |
| 509 | 19859528 | We combined biochemical and electrophysiological analyses of mice selectively deficient in peripheral tryptophan hydroxylase (Tph1-/-) and 5-HT to show that intracellular 5-HT regulates insulin secretion. |
| 510 | 19859528 | We found that these mice are diabetic and have an impaired insulin secretion due to the lack of 5-HT in the pancreas. |
| 511 | 19859528 | The pharmacological restoration of peripheral 5-HT levels rescued the impaired insulin secretion in vivo. |
| 512 | 19859528 | In elucidating the underlying mechanism further, we demonstrate the covalent coupling of 5-HT by transglutaminases during insulin exocytosis to two key players in insulin secretion, the small GTPases Rab3a and Rab27a. |
| 513 | 19859528 | Our results demonstrate that 5-HT regulates insulin secretion by serotonylation of GTPases within pancreatic beta-cells and suggest that intracellular 5-HT functions in various microenvironments via this mechanism in concert with the known receptor-mediated signaling. |
| 514 | 19859528 | While serotonin (5-HT) co-localization with insulin in granules of pancreatic beta-cells was demonstrated more than three decades ago, its physiological role in the etiology of diabetes is still unclear. |
| 515 | 19859528 | We combined biochemical and electrophysiological analyses of mice selectively deficient in peripheral tryptophan hydroxylase (Tph1-/-) and 5-HT to show that intracellular 5-HT regulates insulin secretion. |
| 516 | 19859528 | We found that these mice are diabetic and have an impaired insulin secretion due to the lack of 5-HT in the pancreas. |
| 517 | 19859528 | The pharmacological restoration of peripheral 5-HT levels rescued the impaired insulin secretion in vivo. |
| 518 | 19859528 | In elucidating the underlying mechanism further, we demonstrate the covalent coupling of 5-HT by transglutaminases during insulin exocytosis to two key players in insulin secretion, the small GTPases Rab3a and Rab27a. |
| 519 | 19859528 | Our results demonstrate that 5-HT regulates insulin secretion by serotonylation of GTPases within pancreatic beta-cells and suggest that intracellular 5-HT functions in various microenvironments via this mechanism in concert with the known receptor-mediated signaling. |
| 520 | 20170713 | The present study was carried out to find the effects of Aegle marmelose leaf extract and insulin alone and in combination with pyridoxine on the cerebellar 5-HT through 5-HT(2A) receptor subtype, gene expression studies on the status of antioxidants-superoxide dismutase (SOD), glutathione peroxidase (GPx), 5-HT(2A) and 5-HT transporter (5-HTT) and immunohistochemical studies in streptozotocin induced diabetic rats. 5-HT and 5-HT(2A) receptor binding parameters, B(max) and K(d), showed a significant decrease (p<0.001) in the cerebellum of diabetic rats compared to control. |
| 521 | 20170713 | Gene expression studies of SOD, GPx, 5-HT(2A) and 5-HTT in cerebellum showed a significant down regulation (p<0.001) in diabetic rats compared to control. |
| 522 | 20170713 | Pyridoxine treated alone and in combination with insulin, A. marmelose to diabetic rats reversed the B(max), K(d) of 5-HT, 5-HT(2A) and the gene expression of SOD, GPx, 5-HT(2A) and 5-HTT in cerebellum to near control. |
| 523 | 20170713 | The gene expression of 5-HT(2A) and 5-HTT were confirmed by immunohistochemical studies. |
| 524 | 20170713 | Our results suggest that pyridoxine treated alone and in combination with insulin and A. marmelose has a role in the regulation of insulin synthesis and release, normalizing diabetic related oxidative stress and neurodegeneration affecting the motor ability of an individual by serotonergic receptors through 5-HT(2A) function. |
| 525 | 20170713 | The present study was carried out to find the effects of Aegle marmelose leaf extract and insulin alone and in combination with pyridoxine on the cerebellar 5-HT through 5-HT(2A) receptor subtype, gene expression studies on the status of antioxidants-superoxide dismutase (SOD), glutathione peroxidase (GPx), 5-HT(2A) and 5-HT transporter (5-HTT) and immunohistochemical studies in streptozotocin induced diabetic rats. 5-HT and 5-HT(2A) receptor binding parameters, B(max) and K(d), showed a significant decrease (p<0.001) in the cerebellum of diabetic rats compared to control. |
| 526 | 20170713 | Gene expression studies of SOD, GPx, 5-HT(2A) and 5-HTT in cerebellum showed a significant down regulation (p<0.001) in diabetic rats compared to control. |
| 527 | 20170713 | Pyridoxine treated alone and in combination with insulin, A. marmelose to diabetic rats reversed the B(max), K(d) of 5-HT, 5-HT(2A) and the gene expression of SOD, GPx, 5-HT(2A) and 5-HTT in cerebellum to near control. |
| 528 | 20170713 | The gene expression of 5-HT(2A) and 5-HTT were confirmed by immunohistochemical studies. |
| 529 | 20170713 | Our results suggest that pyridoxine treated alone and in combination with insulin and A. marmelose has a role in the regulation of insulin synthesis and release, normalizing diabetic related oxidative stress and neurodegeneration affecting the motor ability of an individual by serotonergic receptors through 5-HT(2A) function. |
| 530 | 20170713 | The present study was carried out to find the effects of Aegle marmelose leaf extract and insulin alone and in combination with pyridoxine on the cerebellar 5-HT through 5-HT(2A) receptor subtype, gene expression studies on the status of antioxidants-superoxide dismutase (SOD), glutathione peroxidase (GPx), 5-HT(2A) and 5-HT transporter (5-HTT) and immunohistochemical studies in streptozotocin induced diabetic rats. 5-HT and 5-HT(2A) receptor binding parameters, B(max) and K(d), showed a significant decrease (p<0.001) in the cerebellum of diabetic rats compared to control. |
| 531 | 20170713 | Gene expression studies of SOD, GPx, 5-HT(2A) and 5-HTT in cerebellum showed a significant down regulation (p<0.001) in diabetic rats compared to control. |
| 532 | 20170713 | Pyridoxine treated alone and in combination with insulin, A. marmelose to diabetic rats reversed the B(max), K(d) of 5-HT, 5-HT(2A) and the gene expression of SOD, GPx, 5-HT(2A) and 5-HTT in cerebellum to near control. |
| 533 | 20170713 | The gene expression of 5-HT(2A) and 5-HTT were confirmed by immunohistochemical studies. |
| 534 | 20170713 | Our results suggest that pyridoxine treated alone and in combination with insulin and A. marmelose has a role in the regulation of insulin synthesis and release, normalizing diabetic related oxidative stress and neurodegeneration affecting the motor ability of an individual by serotonergic receptors through 5-HT(2A) function. |
| 535 | 20170713 | The present study was carried out to find the effects of Aegle marmelose leaf extract and insulin alone and in combination with pyridoxine on the cerebellar 5-HT through 5-HT(2A) receptor subtype, gene expression studies on the status of antioxidants-superoxide dismutase (SOD), glutathione peroxidase (GPx), 5-HT(2A) and 5-HT transporter (5-HTT) and immunohistochemical studies in streptozotocin induced diabetic rats. 5-HT and 5-HT(2A) receptor binding parameters, B(max) and K(d), showed a significant decrease (p<0.001) in the cerebellum of diabetic rats compared to control. |
| 536 | 20170713 | Gene expression studies of SOD, GPx, 5-HT(2A) and 5-HTT in cerebellum showed a significant down regulation (p<0.001) in diabetic rats compared to control. |
| 537 | 20170713 | Pyridoxine treated alone and in combination with insulin, A. marmelose to diabetic rats reversed the B(max), K(d) of 5-HT, 5-HT(2A) and the gene expression of SOD, GPx, 5-HT(2A) and 5-HTT in cerebellum to near control. |
| 538 | 20170713 | The gene expression of 5-HT(2A) and 5-HTT were confirmed by immunohistochemical studies. |
| 539 | 20170713 | Our results suggest that pyridoxine treated alone and in combination with insulin and A. marmelose has a role in the regulation of insulin synthesis and release, normalizing diabetic related oxidative stress and neurodegeneration affecting the motor ability of an individual by serotonergic receptors through 5-HT(2A) function. |
| 540 | 20170713 | The present study was carried out to find the effects of Aegle marmelose leaf extract and insulin alone and in combination with pyridoxine on the cerebellar 5-HT through 5-HT(2A) receptor subtype, gene expression studies on the status of antioxidants-superoxide dismutase (SOD), glutathione peroxidase (GPx), 5-HT(2A) and 5-HT transporter (5-HTT) and immunohistochemical studies in streptozotocin induced diabetic rats. 5-HT and 5-HT(2A) receptor binding parameters, B(max) and K(d), showed a significant decrease (p<0.001) in the cerebellum of diabetic rats compared to control. |
| 541 | 20170713 | Gene expression studies of SOD, GPx, 5-HT(2A) and 5-HTT in cerebellum showed a significant down regulation (p<0.001) in diabetic rats compared to control. |
| 542 | 20170713 | Pyridoxine treated alone and in combination with insulin, A. marmelose to diabetic rats reversed the B(max), K(d) of 5-HT, 5-HT(2A) and the gene expression of SOD, GPx, 5-HT(2A) and 5-HTT in cerebellum to near control. |
| 543 | 20170713 | The gene expression of 5-HT(2A) and 5-HTT were confirmed by immunohistochemical studies. |
| 544 | 20170713 | Our results suggest that pyridoxine treated alone and in combination with insulin and A. marmelose has a role in the regulation of insulin synthesis and release, normalizing diabetic related oxidative stress and neurodegeneration affecting the motor ability of an individual by serotonergic receptors through 5-HT(2A) function. |
| 545 | 20219524 | We investigated the effects of serotonin (5-HT) on voltage-dependent K(+) (Kv) channel activity, vasoconstriction, 5-HT receptor expression levels, and the involvement of protein kinase C (PKC) in mesenteric arteries of Otsuka Long-Evans Tokushima fatty (OLETF) rats compared with Long-Evans Tokushima Otsuka (LETO) rats. |
| 546 | 20219524 | The expression level of 5-HT(2A), but not 5-HT(2B), receptor and the expression levels of total PKC, PKCbeta, and PKCepsilon, but not PKCalpha, were higher in the mesenteric arteries of OLETF rats compared with LETO rats. |
| 547 | 20219524 | The enhanced expression of 5-HT(2A) receptor together with PKCbeta may promote mesenteric vasoconstriction and increase vascular resistance in OLETF rats. |
| 548 | 20219524 | We investigated the effects of serotonin (5-HT) on voltage-dependent K(+) (Kv) channel activity, vasoconstriction, 5-HT receptor expression levels, and the involvement of protein kinase C (PKC) in mesenteric arteries of Otsuka Long-Evans Tokushima fatty (OLETF) rats compared with Long-Evans Tokushima Otsuka (LETO) rats. |
| 549 | 20219524 | The expression level of 5-HT(2A), but not 5-HT(2B), receptor and the expression levels of total PKC, PKCbeta, and PKCepsilon, but not PKCalpha, were higher in the mesenteric arteries of OLETF rats compared with LETO rats. |
| 550 | 20219524 | The enhanced expression of 5-HT(2A) receptor together with PKCbeta may promote mesenteric vasoconstriction and increase vascular resistance in OLETF rats. |
| 551 | 20219524 | We investigated the effects of serotonin (5-HT) on voltage-dependent K(+) (Kv) channel activity, vasoconstriction, 5-HT receptor expression levels, and the involvement of protein kinase C (PKC) in mesenteric arteries of Otsuka Long-Evans Tokushima fatty (OLETF) rats compared with Long-Evans Tokushima Otsuka (LETO) rats. |
| 552 | 20219524 | The expression level of 5-HT(2A), but not 5-HT(2B), receptor and the expression levels of total PKC, PKCbeta, and PKCepsilon, but not PKCalpha, were higher in the mesenteric arteries of OLETF rats compared with LETO rats. |
| 553 | 20219524 | The enhanced expression of 5-HT(2A) receptor together with PKCbeta may promote mesenteric vasoconstriction and increase vascular resistance in OLETF rats. |
| 554 | 20531396 | Here, we show, in diabetic neuropathic rats, an alteration of the antihyperalgesic effect induced by stimulation of 5-HT(2A) receptors, which are known to mediate SSRI-induced analgesia. 5-HT(2A) receptor density was not changed in the spinal cord of diabetic rats, whereas postsynaptic density protein-95 (PSD-95), one of the PSD-95/disc large suppressor/zonula occludens-1 (PDZ) domain containing proteins interacting with these receptors, was upregulated. |
| 555 | 20531396 | Its effects likely resulted from an increase in receptor responsiveness, because it revealed functional 5-HT(2A) receptor-operated Ca(2+) responses in neurons, an effect mimicked by knockdown of PSD-95. |
| 556 | 20531396 | Here, we show, in diabetic neuropathic rats, an alteration of the antihyperalgesic effect induced by stimulation of 5-HT(2A) receptors, which are known to mediate SSRI-induced analgesia. 5-HT(2A) receptor density was not changed in the spinal cord of diabetic rats, whereas postsynaptic density protein-95 (PSD-95), one of the PSD-95/disc large suppressor/zonula occludens-1 (PDZ) domain containing proteins interacting with these receptors, was upregulated. |
| 557 | 20531396 | Its effects likely resulted from an increase in receptor responsiveness, because it revealed functional 5-HT(2A) receptor-operated Ca(2+) responses in neurons, an effect mimicked by knockdown of PSD-95. |
| 558 | 20581837 | Increasing insulin resistance in the mother maintains nutrient flow to the growing fetus, whereas prolactin and placental lactogen counterbalance this resistance and prevent maternal hyperglycemia by driving expansion of the maternal population of insulin-producing beta cells. |
| 559 | 20581837 | Inhibition of serotonin synthesis by dietary tryptophan restriction or Tph inhibition blocked beta cell expansion and induced glucose intolerance in pregnant mice without affecting insulin sensitivity. |
| 560 | 20581837 | Expression of the G alpha(q)-linked serotonin receptor 5-hydroxytryptamine receptor-2b (Htr2b) in maternal islets increased during pregnancy and normalized just before parturition, whereas expression of the G alpha(i)-linked receptor Htr1d increased at the end of pregnancy and postpartum. |
| 561 | 20655360 | The present study was carried out to find the role of insulin in combination with pyridoxine on the concentrations of 5-HT and 5-HIAA, 5-HT receptor binding, 5-HTT gene expression and immunohistochemistry studies in the cerebral cortex and brainstem of streptozotocin induced diabetic rats. 5-HT content showed a significant decrease with a significant increase in 5-HIAA in cerebral cortex (p<0.01) and brain stem (p<0.001) in diabetic rats. 5-HT receptor binding parameters, B(max) and K(d), showed a significant decrease (p<0.001) in diabetic rats in cerebral cortex whereas in brainstem it showed a significant increase (p<0.001) compared to control. |
| 562 | 20655360 | Insulin and pyridoxine treatment to diabetic rats reversed the 5-HT content, B(max), K(d) and gene expression of 5-HTT confirmed by immunohistochemistry studies in cerebral cortex and brainstem to near control. |
| 563 | 20655360 | The present study was carried out to find the role of insulin in combination with pyridoxine on the concentrations of 5-HT and 5-HIAA, 5-HT receptor binding, 5-HTT gene expression and immunohistochemistry studies in the cerebral cortex and brainstem of streptozotocin induced diabetic rats. 5-HT content showed a significant decrease with a significant increase in 5-HIAA in cerebral cortex (p<0.01) and brain stem (p<0.001) in diabetic rats. 5-HT receptor binding parameters, B(max) and K(d), showed a significant decrease (p<0.001) in diabetic rats in cerebral cortex whereas in brainstem it showed a significant increase (p<0.001) compared to control. |
| 564 | 20655360 | Insulin and pyridoxine treatment to diabetic rats reversed the 5-HT content, B(max), K(d) and gene expression of 5-HTT confirmed by immunohistochemistry studies in cerebral cortex and brainstem to near control. |
| 565 | 21403818 | Peripheral 5-HT1A and 5-HT7 serotonergic receptors modulate parasympathetic neurotransmission in long-term diabetic rats. |
| 566 | 21403818 | Pretreatment with 5-HT(1) antagonist methiothepin blocked the stimulatory and inhibitory effect of 5-CT, whereas pimozide, 5-HT(7) antagonist, only abolished 5-CT inhibitory action. |
| 567 | 21403818 | In conclusion, long-term diabetes elicits changes in the subtype of the 5-HT receptor involved in modulation of vagally induced bradycardia. |
| 568 | 21403818 | Activation of the 5-HT(1A) receptors induces enhancement, whereas attenuation is due to 5-HT(7) receptor activation. |
| 569 | 21403818 | Peripheral 5-HT1A and 5-HT7 serotonergic receptors modulate parasympathetic neurotransmission in long-term diabetic rats. |
| 570 | 21403818 | Pretreatment with 5-HT(1) antagonist methiothepin blocked the stimulatory and inhibitory effect of 5-CT, whereas pimozide, 5-HT(7) antagonist, only abolished 5-CT inhibitory action. |
| 571 | 21403818 | In conclusion, long-term diabetes elicits changes in the subtype of the 5-HT receptor involved in modulation of vagally induced bradycardia. |
| 572 | 21403818 | Activation of the 5-HT(1A) receptors induces enhancement, whereas attenuation is due to 5-HT(7) receptor activation. |
| 573 | 21403818 | Peripheral 5-HT1A and 5-HT7 serotonergic receptors modulate parasympathetic neurotransmission in long-term diabetic rats. |
| 574 | 21403818 | Pretreatment with 5-HT(1) antagonist methiothepin blocked the stimulatory and inhibitory effect of 5-CT, whereas pimozide, 5-HT(7) antagonist, only abolished 5-CT inhibitory action. |
| 575 | 21403818 | In conclusion, long-term diabetes elicits changes in the subtype of the 5-HT receptor involved in modulation of vagally induced bradycardia. |
| 576 | 21403818 | Activation of the 5-HT(1A) receptors induces enhancement, whereas attenuation is due to 5-HT(7) receptor activation. |
| 577 | 21697998 | Application of crude water extract of Morus alba resulted in amelioration of the alterations of maternal serum glucose, LDL, HDL, total cholesterol and creatine phosphokinase activity as well as retinal neurotransmitters including acetylcholine (ACE), adrenaline (AD), nor-adrenaline (NAD), serotonin (5-HT), histamine (HS), dopamine (DA) and gamma amino butyric acid (GABA). |
| 578 | 21821002 | RhoA/ROCK pathway is activated by various G-protein-coupled receptor agonists and consequently induces phosphorylation of myosin phosphatase target subunit 1 (MYPT1), a subunit of myosin light chain phosphatase (MLCP), which inhibits MLCP activity. |
| 579 | 21821002 | In the resting state of the vessels, total tissue protein levels of 5-HT(2A) receptor, 5-HT(1B) receptor, RhoA, ROCK1, and ROCK2 did not differ between NDM and DM groups. |
| 580 | 21836641 | Association of variations in TPH1 and HTR2B with gestational weight gain and measures of obesity. |
| 581 | 21836641 | Recently, it has been reported that 5-hydroxytryptamine receptor 2B (Htr2b) and tryptophan hydroxylase 1 (Tph1) play major role in β-cell proliferation in mouse during pregnancy. |
| 582 | 21836641 | We investigated the genetic association of HTR2B and TPH1 with risk of gestational diabetes mellitus (GDM) and measures of obesity, in 869 Korean GDM women and carefully selected 632 nondiabetic control subjects. |
| 583 | 21836641 | Six single-nucleotide polymorphisms (SNPs) in HTR2B and ten SNPs in TPH1 were selected for genotyping according to their tagging status. |
| 584 | 21836641 | Genetic variants in HTR2B and TPH1 were not associated with the risk of GDM. |
| 585 | 21836641 | Although genetic variants in HTR2B and TPH1 were not associated with risk of GDM, we found significant association of these variants with measures of obesity. |
| 586 | 21836641 | Association of variations in TPH1 and HTR2B with gestational weight gain and measures of obesity. |
| 587 | 21836641 | Recently, it has been reported that 5-hydroxytryptamine receptor 2B (Htr2b) and tryptophan hydroxylase 1 (Tph1) play major role in β-cell proliferation in mouse during pregnancy. |
| 588 | 21836641 | We investigated the genetic association of HTR2B and TPH1 with risk of gestational diabetes mellitus (GDM) and measures of obesity, in 869 Korean GDM women and carefully selected 632 nondiabetic control subjects. |
| 589 | 21836641 | Six single-nucleotide polymorphisms (SNPs) in HTR2B and ten SNPs in TPH1 were selected for genotyping according to their tagging status. |
| 590 | 21836641 | Genetic variants in HTR2B and TPH1 were not associated with the risk of GDM. |
| 591 | 21836641 | Although genetic variants in HTR2B and TPH1 were not associated with risk of GDM, we found significant association of these variants with measures of obesity. |
| 592 | 21836641 | Association of variations in TPH1 and HTR2B with gestational weight gain and measures of obesity. |
| 593 | 21836641 | Recently, it has been reported that 5-hydroxytryptamine receptor 2B (Htr2b) and tryptophan hydroxylase 1 (Tph1) play major role in β-cell proliferation in mouse during pregnancy. |
| 594 | 21836641 | We investigated the genetic association of HTR2B and TPH1 with risk of gestational diabetes mellitus (GDM) and measures of obesity, in 869 Korean GDM women and carefully selected 632 nondiabetic control subjects. |
| 595 | 21836641 | Six single-nucleotide polymorphisms (SNPs) in HTR2B and ten SNPs in TPH1 were selected for genotyping according to their tagging status. |
| 596 | 21836641 | Genetic variants in HTR2B and TPH1 were not associated with the risk of GDM. |
| 597 | 21836641 | Although genetic variants in HTR2B and TPH1 were not associated with risk of GDM, we found significant association of these variants with measures of obesity. |
| 598 | 21836641 | Association of variations in TPH1 and HTR2B with gestational weight gain and measures of obesity. |
| 599 | 21836641 | Recently, it has been reported that 5-hydroxytryptamine receptor 2B (Htr2b) and tryptophan hydroxylase 1 (Tph1) play major role in β-cell proliferation in mouse during pregnancy. |
| 600 | 21836641 | We investigated the genetic association of HTR2B and TPH1 with risk of gestational diabetes mellitus (GDM) and measures of obesity, in 869 Korean GDM women and carefully selected 632 nondiabetic control subjects. |
| 601 | 21836641 | Six single-nucleotide polymorphisms (SNPs) in HTR2B and ten SNPs in TPH1 were selected for genotyping according to their tagging status. |
| 602 | 21836641 | Genetic variants in HTR2B and TPH1 were not associated with the risk of GDM. |
| 603 | 21836641 | Although genetic variants in HTR2B and TPH1 were not associated with risk of GDM, we found significant association of these variants with measures of obesity. |
| 604 | 21836641 | Association of variations in TPH1 and HTR2B with gestational weight gain and measures of obesity. |
| 605 | 21836641 | Recently, it has been reported that 5-hydroxytryptamine receptor 2B (Htr2b) and tryptophan hydroxylase 1 (Tph1) play major role in β-cell proliferation in mouse during pregnancy. |
| 606 | 21836641 | We investigated the genetic association of HTR2B and TPH1 with risk of gestational diabetes mellitus (GDM) and measures of obesity, in 869 Korean GDM women and carefully selected 632 nondiabetic control subjects. |
| 607 | 21836641 | Six single-nucleotide polymorphisms (SNPs) in HTR2B and ten SNPs in TPH1 were selected for genotyping according to their tagging status. |
| 608 | 21836641 | Genetic variants in HTR2B and TPH1 were not associated with the risk of GDM. |
| 609 | 21836641 | Although genetic variants in HTR2B and TPH1 were not associated with risk of GDM, we found significant association of these variants with measures of obesity. |
| 610 | 21836641 | Association of variations in TPH1 and HTR2B with gestational weight gain and measures of obesity. |
| 611 | 21836641 | Recently, it has been reported that 5-hydroxytryptamine receptor 2B (Htr2b) and tryptophan hydroxylase 1 (Tph1) play major role in β-cell proliferation in mouse during pregnancy. |
| 612 | 21836641 | We investigated the genetic association of HTR2B and TPH1 with risk of gestational diabetes mellitus (GDM) and measures of obesity, in 869 Korean GDM women and carefully selected 632 nondiabetic control subjects. |
| 613 | 21836641 | Six single-nucleotide polymorphisms (SNPs) in HTR2B and ten SNPs in TPH1 were selected for genotyping according to their tagging status. |
| 614 | 21836641 | Genetic variants in HTR2B and TPH1 were not associated with the risk of GDM. |
| 615 | 21836641 | Although genetic variants in HTR2B and TPH1 were not associated with risk of GDM, we found significant association of these variants with measures of obesity. |
| 616 | 22028447 | Heparin-binding EGF-like growth factor (HB-EGF) mediates 5-HT-induced insulin resistance through activation of EGF receptor-ERK1/2-mTOR pathway. |
| 617 | 22028447 | Although an inverse correlation between insulin sensitivity and the level of Gq/11-coupled receptor agonists, such as endothelin-1, thrombin, and 5-hydroxytryptamine (5-HT), has been reported, its precise mechanism remains unclear. |
| 618 | 22028447 | In this report, we provide evidence that 5-HT induced production of heparin-binding epidermal growth factor-like growth factor (HB-EGF) and caused insulin resistance in 3T3-L1 adipocytes, primary adipocytes, and C2C12 myotubes. |
| 619 | 22028447 | In 3T3-L1 adipocytes, 5-HT stimulated HB-EGF production by promoting metalloproteinase-dependent shedding of transmembrane protein pro-HB-EGF. |
| 620 | 22028447 | HB-EGF then bound and tyrosine-phosphorylated EGF receptors, which activated the mammalian target of rapamycin pathway through ERK1/2 phosphorylation. |
| 621 | 22028447 | Mammalian target of rapamycin activation caused serine phosphorylation of insulin receptor substrate-1, which attenuated insulin-stimulated tyrosine phosphorylation of insulin receptor substrate-1 and glucose uptake. |
| 622 | 22028447 | Pharmacological inhibition of either Gq/11-coupled receptors or metalloproteinases, as well as either inhibition or knockdown of HB-EGF or Gαq/11, restored insulin signal transduction impaired by 5-HT. |
| 623 | 22028447 | Inhibition of metalloproteinase activity also abolished HB-EGF production and subsequent EGF receptor activation by other Gq/11-coupled receptor agonists known to cause insulin resistance, such as endothelin-1 and thrombin. |
| 624 | 22028447 | These results suggest that transactivation of the EGF receptor through HB-EGF processing plays a pivotal role in 5-HT-induced insulin resistance. |
| 625 | 22028447 | Heparin-binding EGF-like growth factor (HB-EGF) mediates 5-HT-induced insulin resistance through activation of EGF receptor-ERK1/2-mTOR pathway. |
| 626 | 22028447 | Although an inverse correlation between insulin sensitivity and the level of Gq/11-coupled receptor agonists, such as endothelin-1, thrombin, and 5-hydroxytryptamine (5-HT), has been reported, its precise mechanism remains unclear. |
| 627 | 22028447 | In this report, we provide evidence that 5-HT induced production of heparin-binding epidermal growth factor-like growth factor (HB-EGF) and caused insulin resistance in 3T3-L1 adipocytes, primary adipocytes, and C2C12 myotubes. |
| 628 | 22028447 | In 3T3-L1 adipocytes, 5-HT stimulated HB-EGF production by promoting metalloproteinase-dependent shedding of transmembrane protein pro-HB-EGF. |
| 629 | 22028447 | HB-EGF then bound and tyrosine-phosphorylated EGF receptors, which activated the mammalian target of rapamycin pathway through ERK1/2 phosphorylation. |
| 630 | 22028447 | Mammalian target of rapamycin activation caused serine phosphorylation of insulin receptor substrate-1, which attenuated insulin-stimulated tyrosine phosphorylation of insulin receptor substrate-1 and glucose uptake. |
| 631 | 22028447 | Pharmacological inhibition of either Gq/11-coupled receptors or metalloproteinases, as well as either inhibition or knockdown of HB-EGF or Gαq/11, restored insulin signal transduction impaired by 5-HT. |
| 632 | 22028447 | Inhibition of metalloproteinase activity also abolished HB-EGF production and subsequent EGF receptor activation by other Gq/11-coupled receptor agonists known to cause insulin resistance, such as endothelin-1 and thrombin. |
| 633 | 22028447 | These results suggest that transactivation of the EGF receptor through HB-EGF processing plays a pivotal role in 5-HT-induced insulin resistance. |
| 634 | 22028447 | Heparin-binding EGF-like growth factor (HB-EGF) mediates 5-HT-induced insulin resistance through activation of EGF receptor-ERK1/2-mTOR pathway. |
| 635 | 22028447 | Although an inverse correlation between insulin sensitivity and the level of Gq/11-coupled receptor agonists, such as endothelin-1, thrombin, and 5-hydroxytryptamine (5-HT), has been reported, its precise mechanism remains unclear. |
| 636 | 22028447 | In this report, we provide evidence that 5-HT induced production of heparin-binding epidermal growth factor-like growth factor (HB-EGF) and caused insulin resistance in 3T3-L1 adipocytes, primary adipocytes, and C2C12 myotubes. |
| 637 | 22028447 | In 3T3-L1 adipocytes, 5-HT stimulated HB-EGF production by promoting metalloproteinase-dependent shedding of transmembrane protein pro-HB-EGF. |
| 638 | 22028447 | HB-EGF then bound and tyrosine-phosphorylated EGF receptors, which activated the mammalian target of rapamycin pathway through ERK1/2 phosphorylation. |
| 639 | 22028447 | Mammalian target of rapamycin activation caused serine phosphorylation of insulin receptor substrate-1, which attenuated insulin-stimulated tyrosine phosphorylation of insulin receptor substrate-1 and glucose uptake. |
| 640 | 22028447 | Pharmacological inhibition of either Gq/11-coupled receptors or metalloproteinases, as well as either inhibition or knockdown of HB-EGF or Gαq/11, restored insulin signal transduction impaired by 5-HT. |
| 641 | 22028447 | Inhibition of metalloproteinase activity also abolished HB-EGF production and subsequent EGF receptor activation by other Gq/11-coupled receptor agonists known to cause insulin resistance, such as endothelin-1 and thrombin. |
| 642 | 22028447 | These results suggest that transactivation of the EGF receptor through HB-EGF processing plays a pivotal role in 5-HT-induced insulin resistance. |
| 643 | 22028447 | Heparin-binding EGF-like growth factor (HB-EGF) mediates 5-HT-induced insulin resistance through activation of EGF receptor-ERK1/2-mTOR pathway. |
| 644 | 22028447 | Although an inverse correlation between insulin sensitivity and the level of Gq/11-coupled receptor agonists, such as endothelin-1, thrombin, and 5-hydroxytryptamine (5-HT), has been reported, its precise mechanism remains unclear. |
| 645 | 22028447 | In this report, we provide evidence that 5-HT induced production of heparin-binding epidermal growth factor-like growth factor (HB-EGF) and caused insulin resistance in 3T3-L1 adipocytes, primary adipocytes, and C2C12 myotubes. |
| 646 | 22028447 | In 3T3-L1 adipocytes, 5-HT stimulated HB-EGF production by promoting metalloproteinase-dependent shedding of transmembrane protein pro-HB-EGF. |
| 647 | 22028447 | HB-EGF then bound and tyrosine-phosphorylated EGF receptors, which activated the mammalian target of rapamycin pathway through ERK1/2 phosphorylation. |
| 648 | 22028447 | Mammalian target of rapamycin activation caused serine phosphorylation of insulin receptor substrate-1, which attenuated insulin-stimulated tyrosine phosphorylation of insulin receptor substrate-1 and glucose uptake. |
| 649 | 22028447 | Pharmacological inhibition of either Gq/11-coupled receptors or metalloproteinases, as well as either inhibition or knockdown of HB-EGF or Gαq/11, restored insulin signal transduction impaired by 5-HT. |
| 650 | 22028447 | Inhibition of metalloproteinase activity also abolished HB-EGF production and subsequent EGF receptor activation by other Gq/11-coupled receptor agonists known to cause insulin resistance, such as endothelin-1 and thrombin. |
| 651 | 22028447 | These results suggest that transactivation of the EGF receptor through HB-EGF processing plays a pivotal role in 5-HT-induced insulin resistance. |
| 652 | 22028447 | Heparin-binding EGF-like growth factor (HB-EGF) mediates 5-HT-induced insulin resistance through activation of EGF receptor-ERK1/2-mTOR pathway. |
| 653 | 22028447 | Although an inverse correlation between insulin sensitivity and the level of Gq/11-coupled receptor agonists, such as endothelin-1, thrombin, and 5-hydroxytryptamine (5-HT), has been reported, its precise mechanism remains unclear. |
| 654 | 22028447 | In this report, we provide evidence that 5-HT induced production of heparin-binding epidermal growth factor-like growth factor (HB-EGF) and caused insulin resistance in 3T3-L1 adipocytes, primary adipocytes, and C2C12 myotubes. |
| 655 | 22028447 | In 3T3-L1 adipocytes, 5-HT stimulated HB-EGF production by promoting metalloproteinase-dependent shedding of transmembrane protein pro-HB-EGF. |
| 656 | 22028447 | HB-EGF then bound and tyrosine-phosphorylated EGF receptors, which activated the mammalian target of rapamycin pathway through ERK1/2 phosphorylation. |
| 657 | 22028447 | Mammalian target of rapamycin activation caused serine phosphorylation of insulin receptor substrate-1, which attenuated insulin-stimulated tyrosine phosphorylation of insulin receptor substrate-1 and glucose uptake. |
| 658 | 22028447 | Pharmacological inhibition of either Gq/11-coupled receptors or metalloproteinases, as well as either inhibition or knockdown of HB-EGF or Gαq/11, restored insulin signal transduction impaired by 5-HT. |
| 659 | 22028447 | Inhibition of metalloproteinase activity also abolished HB-EGF production and subsequent EGF receptor activation by other Gq/11-coupled receptor agonists known to cause insulin resistance, such as endothelin-1 and thrombin. |
| 660 | 22028447 | These results suggest that transactivation of the EGF receptor through HB-EGF processing plays a pivotal role in 5-HT-induced insulin resistance. |
| 661 | 22028447 | Heparin-binding EGF-like growth factor (HB-EGF) mediates 5-HT-induced insulin resistance through activation of EGF receptor-ERK1/2-mTOR pathway. |
| 662 | 22028447 | Although an inverse correlation between insulin sensitivity and the level of Gq/11-coupled receptor agonists, such as endothelin-1, thrombin, and 5-hydroxytryptamine (5-HT), has been reported, its precise mechanism remains unclear. |
| 663 | 22028447 | In this report, we provide evidence that 5-HT induced production of heparin-binding epidermal growth factor-like growth factor (HB-EGF) and caused insulin resistance in 3T3-L1 adipocytes, primary adipocytes, and C2C12 myotubes. |
| 664 | 22028447 | In 3T3-L1 adipocytes, 5-HT stimulated HB-EGF production by promoting metalloproteinase-dependent shedding of transmembrane protein pro-HB-EGF. |
| 665 | 22028447 | HB-EGF then bound and tyrosine-phosphorylated EGF receptors, which activated the mammalian target of rapamycin pathway through ERK1/2 phosphorylation. |
| 666 | 22028447 | Mammalian target of rapamycin activation caused serine phosphorylation of insulin receptor substrate-1, which attenuated insulin-stimulated tyrosine phosphorylation of insulin receptor substrate-1 and glucose uptake. |
| 667 | 22028447 | Pharmacological inhibition of either Gq/11-coupled receptors or metalloproteinases, as well as either inhibition or knockdown of HB-EGF or Gαq/11, restored insulin signal transduction impaired by 5-HT. |
| 668 | 22028447 | Inhibition of metalloproteinase activity also abolished HB-EGF production and subsequent EGF receptor activation by other Gq/11-coupled receptor agonists known to cause insulin resistance, such as endothelin-1 and thrombin. |
| 669 | 22028447 | These results suggest that transactivation of the EGF receptor through HB-EGF processing plays a pivotal role in 5-HT-induced insulin resistance. |
| 670 | 22160540 | Glucose in the gut lumen activates gut endocrine cells to release 5-HT, glucagon-like peptide 1/2 (GLP-1/2), and glucose-dependent insulinotropic polypeptide (GIP), which act to change gastrointestinal function and regulate postprandial plasma glucose. |
| 671 | 22160540 | Immunoreactivity for GLP-1, but not GIP, was significantly reduced in RD and 3MD compared with PD rats (P < 0.01). |
| 672 | 22570547 | It has much greater affinity for 5-HT(7) subtype receptors than other atypical antipsychotics. |
| 673 | 22948792 | The inhibitory effect of infusion of α-methyl 5-HT (5 µg/kg/min) was abolished in the presence of indomethacin (2 mg/kg), a non-selective cyclooxygenase (COX) inhibitor, or FR 122047 (1.5 mg/kg) or nimesulide (1.5 mg/kg), two selective COX-1 and COX-2 inhibitors, respectively, in long-term-diabetic pithed rats. |
| 674 | 22948792 | Our results indicate that 5-HT inhibition of the pressor responses induced by electrical stimulation is mediated both by the NO and COX pathways in long-term-diabetic rats. |
| 675 | 22948792 | The inhibitory effect of infusion of α-methyl 5-HT (5 µg/kg/min) was abolished in the presence of indomethacin (2 mg/kg), a non-selective cyclooxygenase (COX) inhibitor, or FR 122047 (1.5 mg/kg) or nimesulide (1.5 mg/kg), two selective COX-1 and COX-2 inhibitors, respectively, in long-term-diabetic pithed rats. |
| 676 | 22948792 | Our results indicate that 5-HT inhibition of the pressor responses induced by electrical stimulation is mediated both by the NO and COX pathways in long-term-diabetic rats. |
| 677 | 22975078 | Activation of Akt through 5-HT2A receptor ameliorates serotonin-induced degradation of insulin receptor substrate-1 in adipocytes. |
| 678 | 22975078 | In this study, we investigate the mechanism of insulin desensitization caused by 5-HT. |
| 679 | 22975078 | In 3T3-L1 adipocytes, 5-HT treatment induced the translocation of insulin receptor substrate-1 (IRS-1) from low density microsome (LDM), the important intracellular compartment for its functions, to cytosol, inducing IRS-1 ubiquitination and degradation. |
| 680 | 22975078 | Moreover, inhibition of 5-HT-stimulated Akt activation by either ketanserin (a specific 5-HT2A receptor antagonist) or knocking-down the expression of 5-HT2A receptor promoted 5-HT-stimulated IRS-1 dissociation from 14-3-3β in LDM, leading to drastic ubiquitination. |
| 681 | 22975078 | Interestingly, sarpogrelate, another antagonist of 5-HT2A receptor, protected IRS-1 from degradation through activation of Akt. |
| 682 | 22975078 | This implicates the importance of Akt activation in extending IRS-1 life span through maintaining their optimal sub-location into adipocytes. |
| 683 | 22975078 | Taken together, this study suggest that activation of Akt may be able to compensate the adverse effects of 5-HT by stabilizing IRS-1 in LDM. |
| 684 | 22975078 | Activation of Akt through 5-HT2A receptor ameliorates serotonin-induced degradation of insulin receptor substrate-1 in adipocytes. |
| 685 | 22975078 | In this study, we investigate the mechanism of insulin desensitization caused by 5-HT. |
| 686 | 22975078 | In 3T3-L1 adipocytes, 5-HT treatment induced the translocation of insulin receptor substrate-1 (IRS-1) from low density microsome (LDM), the important intracellular compartment for its functions, to cytosol, inducing IRS-1 ubiquitination and degradation. |
| 687 | 22975078 | Moreover, inhibition of 5-HT-stimulated Akt activation by either ketanserin (a specific 5-HT2A receptor antagonist) or knocking-down the expression of 5-HT2A receptor promoted 5-HT-stimulated IRS-1 dissociation from 14-3-3β in LDM, leading to drastic ubiquitination. |
| 688 | 22975078 | Interestingly, sarpogrelate, another antagonist of 5-HT2A receptor, protected IRS-1 from degradation through activation of Akt. |
| 689 | 22975078 | This implicates the importance of Akt activation in extending IRS-1 life span through maintaining their optimal sub-location into adipocytes. |
| 690 | 22975078 | Taken together, this study suggest that activation of Akt may be able to compensate the adverse effects of 5-HT by stabilizing IRS-1 in LDM. |
| 691 | 22975078 | Activation of Akt through 5-HT2A receptor ameliorates serotonin-induced degradation of insulin receptor substrate-1 in adipocytes. |
| 692 | 22975078 | In this study, we investigate the mechanism of insulin desensitization caused by 5-HT. |
| 693 | 22975078 | In 3T3-L1 adipocytes, 5-HT treatment induced the translocation of insulin receptor substrate-1 (IRS-1) from low density microsome (LDM), the important intracellular compartment for its functions, to cytosol, inducing IRS-1 ubiquitination and degradation. |
| 694 | 22975078 | Moreover, inhibition of 5-HT-stimulated Akt activation by either ketanserin (a specific 5-HT2A receptor antagonist) or knocking-down the expression of 5-HT2A receptor promoted 5-HT-stimulated IRS-1 dissociation from 14-3-3β in LDM, leading to drastic ubiquitination. |
| 695 | 22975078 | Interestingly, sarpogrelate, another antagonist of 5-HT2A receptor, protected IRS-1 from degradation through activation of Akt. |
| 696 | 22975078 | This implicates the importance of Akt activation in extending IRS-1 life span through maintaining their optimal sub-location into adipocytes. |
| 697 | 22975078 | Taken together, this study suggest that activation of Akt may be able to compensate the adverse effects of 5-HT by stabilizing IRS-1 in LDM. |
| 698 | 22975078 | Activation of Akt through 5-HT2A receptor ameliorates serotonin-induced degradation of insulin receptor substrate-1 in adipocytes. |
| 699 | 22975078 | In this study, we investigate the mechanism of insulin desensitization caused by 5-HT. |
| 700 | 22975078 | In 3T3-L1 adipocytes, 5-HT treatment induced the translocation of insulin receptor substrate-1 (IRS-1) from low density microsome (LDM), the important intracellular compartment for its functions, to cytosol, inducing IRS-1 ubiquitination and degradation. |
| 701 | 22975078 | Moreover, inhibition of 5-HT-stimulated Akt activation by either ketanserin (a specific 5-HT2A receptor antagonist) or knocking-down the expression of 5-HT2A receptor promoted 5-HT-stimulated IRS-1 dissociation from 14-3-3β in LDM, leading to drastic ubiquitination. |
| 702 | 22975078 | Interestingly, sarpogrelate, another antagonist of 5-HT2A receptor, protected IRS-1 from degradation through activation of Akt. |
| 703 | 22975078 | This implicates the importance of Akt activation in extending IRS-1 life span through maintaining their optimal sub-location into adipocytes. |
| 704 | 22975078 | Taken together, this study suggest that activation of Akt may be able to compensate the adverse effects of 5-HT by stabilizing IRS-1 in LDM. |
| 705 | 23085101 | In adipocytes, GDS signals through the Htr2b receptor to favor lipolysis by increasing phosphorylation and activity of hormone-sensitive lipase. |
| 706 | 23085101 | In hepatocytes, GDS signaling through Htr2b promotes gluconeogenesis by enhancing activity of two rate-limiting gluconeogenic enzymes, FBPase and G6Pase. |
| 707 | 23085101 | In adipocytes, GDS signals through the Htr2b receptor to favor lipolysis by increasing phosphorylation and activity of hormone-sensitive lipase. |
| 708 | 23085101 | In hepatocytes, GDS signaling through Htr2b promotes gluconeogenesis by enhancing activity of two rate-limiting gluconeogenic enzymes, FBPase and G6Pase. |
| 709 | 23327507 | Olanzapine is a thienobenzodiazepine that blocks especially the serontonin (5-hydroxytryptamine [5-HT]) 5-HT2A and the dopamine D2 receptors as well as muscarinic (M1), histamine (H1), 5-HT2C, 5-HT3 to 5-HT6, adrenergic (α(l)), and D4 receptors. |
| 710 | 23349838 | Serotonin receptor 2C and insulin secretion. |
| 711 | 23349838 | High plasma levels of serotonin (5-hydroxytryptamine; 5-HT) have been reported in T2DM patients, though the potential effect on insulin secretion is unclear. |
| 712 | 23349838 | However, it is known that the 5-HT receptor 2C (5-HT(2C)R) agonist, mCPP, decreases plasma insulin concentration in mice. |
| 713 | 23349838 | As such, we aimed to investigate the expression of the 5-HT(2C)R in pancreatic islets of diabetic mice and the role of 5-HT(2C)R signaling in insulin secretion from pancreatic β-cells. |
| 714 | 23349838 | Furthermore, treatment with a 5-HT(2C)R antagonist (SB242084) increased insulin secretion from pancreatic islets isolated from db/db mice in a dose-dependent manner, but had no effect in islets from control mice. |
| 715 | 23349838 | We found that mCPP significantly inhibited insulin secretion in Min-6 cells and isolated islets in a dose-dependent manner, which could be reversed by SB242084 or RNA interference against 5-HT(2C)R. |
| 716 | 23349838 | We also treated Min-6 cells with palmitic acid for 24 h, and found that the expression of 5-HT(2C)R increased in a dose-dependent manner; furthermore, the inhibition of insulin secretion in Min-6 cells induced by palmitic acid could be reversed by SB242084 or RNA interference against 5-HT(2C)R. |
| 717 | 23349838 | Taken together, our data suggests that increased expression of 5-HT(2C)R in pancreatic β-cells might inhibit insulin secretion. |
| 718 | 23349838 | Serotonin receptor 2C and insulin secretion. |
| 719 | 23349838 | High plasma levels of serotonin (5-hydroxytryptamine; 5-HT) have been reported in T2DM patients, though the potential effect on insulin secretion is unclear. |
| 720 | 23349838 | However, it is known that the 5-HT receptor 2C (5-HT(2C)R) agonist, mCPP, decreases plasma insulin concentration in mice. |
| 721 | 23349838 | As such, we aimed to investigate the expression of the 5-HT(2C)R in pancreatic islets of diabetic mice and the role of 5-HT(2C)R signaling in insulin secretion from pancreatic β-cells. |
| 722 | 23349838 | Furthermore, treatment with a 5-HT(2C)R antagonist (SB242084) increased insulin secretion from pancreatic islets isolated from db/db mice in a dose-dependent manner, but had no effect in islets from control mice. |
| 723 | 23349838 | We found that mCPP significantly inhibited insulin secretion in Min-6 cells and isolated islets in a dose-dependent manner, which could be reversed by SB242084 or RNA interference against 5-HT(2C)R. |
| 724 | 23349838 | We also treated Min-6 cells with palmitic acid for 24 h, and found that the expression of 5-HT(2C)R increased in a dose-dependent manner; furthermore, the inhibition of insulin secretion in Min-6 cells induced by palmitic acid could be reversed by SB242084 or RNA interference against 5-HT(2C)R. |
| 725 | 23349838 | Taken together, our data suggests that increased expression of 5-HT(2C)R in pancreatic β-cells might inhibit insulin secretion. |
| 726 | 23349838 | Serotonin receptor 2C and insulin secretion. |
| 727 | 23349838 | High plasma levels of serotonin (5-hydroxytryptamine; 5-HT) have been reported in T2DM patients, though the potential effect on insulin secretion is unclear. |
| 728 | 23349838 | However, it is known that the 5-HT receptor 2C (5-HT(2C)R) agonist, mCPP, decreases plasma insulin concentration in mice. |
| 729 | 23349838 | As such, we aimed to investigate the expression of the 5-HT(2C)R in pancreatic islets of diabetic mice and the role of 5-HT(2C)R signaling in insulin secretion from pancreatic β-cells. |
| 730 | 23349838 | Furthermore, treatment with a 5-HT(2C)R antagonist (SB242084) increased insulin secretion from pancreatic islets isolated from db/db mice in a dose-dependent manner, but had no effect in islets from control mice. |
| 731 | 23349838 | We found that mCPP significantly inhibited insulin secretion in Min-6 cells and isolated islets in a dose-dependent manner, which could be reversed by SB242084 or RNA interference against 5-HT(2C)R. |
| 732 | 23349838 | We also treated Min-6 cells with palmitic acid for 24 h, and found that the expression of 5-HT(2C)R increased in a dose-dependent manner; furthermore, the inhibition of insulin secretion in Min-6 cells induced by palmitic acid could be reversed by SB242084 or RNA interference against 5-HT(2C)R. |
| 733 | 23349838 | Taken together, our data suggests that increased expression of 5-HT(2C)R in pancreatic β-cells might inhibit insulin secretion. |
| 734 | 23349838 | Serotonin receptor 2C and insulin secretion. |
| 735 | 23349838 | High plasma levels of serotonin (5-hydroxytryptamine; 5-HT) have been reported in T2DM patients, though the potential effect on insulin secretion is unclear. |
| 736 | 23349838 | However, it is known that the 5-HT receptor 2C (5-HT(2C)R) agonist, mCPP, decreases plasma insulin concentration in mice. |
| 737 | 23349838 | As such, we aimed to investigate the expression of the 5-HT(2C)R in pancreatic islets of diabetic mice and the role of 5-HT(2C)R signaling in insulin secretion from pancreatic β-cells. |
| 738 | 23349838 | Furthermore, treatment with a 5-HT(2C)R antagonist (SB242084) increased insulin secretion from pancreatic islets isolated from db/db mice in a dose-dependent manner, but had no effect in islets from control mice. |
| 739 | 23349838 | We found that mCPP significantly inhibited insulin secretion in Min-6 cells and isolated islets in a dose-dependent manner, which could be reversed by SB242084 or RNA interference against 5-HT(2C)R. |
| 740 | 23349838 | We also treated Min-6 cells with palmitic acid for 24 h, and found that the expression of 5-HT(2C)R increased in a dose-dependent manner; furthermore, the inhibition of insulin secretion in Min-6 cells induced by palmitic acid could be reversed by SB242084 or RNA interference against 5-HT(2C)R. |
| 741 | 23349838 | Taken together, our data suggests that increased expression of 5-HT(2C)R in pancreatic β-cells might inhibit insulin secretion. |
| 742 | 23349838 | Serotonin receptor 2C and insulin secretion. |
| 743 | 23349838 | High plasma levels of serotonin (5-hydroxytryptamine; 5-HT) have been reported in T2DM patients, though the potential effect on insulin secretion is unclear. |
| 744 | 23349838 | However, it is known that the 5-HT receptor 2C (5-HT(2C)R) agonist, mCPP, decreases plasma insulin concentration in mice. |
| 745 | 23349838 | As such, we aimed to investigate the expression of the 5-HT(2C)R in pancreatic islets of diabetic mice and the role of 5-HT(2C)R signaling in insulin secretion from pancreatic β-cells. |
| 746 | 23349838 | Furthermore, treatment with a 5-HT(2C)R antagonist (SB242084) increased insulin secretion from pancreatic islets isolated from db/db mice in a dose-dependent manner, but had no effect in islets from control mice. |
| 747 | 23349838 | We found that mCPP significantly inhibited insulin secretion in Min-6 cells and isolated islets in a dose-dependent manner, which could be reversed by SB242084 or RNA interference against 5-HT(2C)R. |
| 748 | 23349838 | We also treated Min-6 cells with palmitic acid for 24 h, and found that the expression of 5-HT(2C)R increased in a dose-dependent manner; furthermore, the inhibition of insulin secretion in Min-6 cells induced by palmitic acid could be reversed by SB242084 or RNA interference against 5-HT(2C)R. |
| 749 | 23349838 | Taken together, our data suggests that increased expression of 5-HT(2C)R in pancreatic β-cells might inhibit insulin secretion. |
| 750 | 23349838 | Serotonin receptor 2C and insulin secretion. |
| 751 | 23349838 | High plasma levels of serotonin (5-hydroxytryptamine; 5-HT) have been reported in T2DM patients, though the potential effect on insulin secretion is unclear. |
| 752 | 23349838 | However, it is known that the 5-HT receptor 2C (5-HT(2C)R) agonist, mCPP, decreases plasma insulin concentration in mice. |
| 753 | 23349838 | As such, we aimed to investigate the expression of the 5-HT(2C)R in pancreatic islets of diabetic mice and the role of 5-HT(2C)R signaling in insulin secretion from pancreatic β-cells. |
| 754 | 23349838 | Furthermore, treatment with a 5-HT(2C)R antagonist (SB242084) increased insulin secretion from pancreatic islets isolated from db/db mice in a dose-dependent manner, but had no effect in islets from control mice. |
| 755 | 23349838 | We found that mCPP significantly inhibited insulin secretion in Min-6 cells and isolated islets in a dose-dependent manner, which could be reversed by SB242084 or RNA interference against 5-HT(2C)R. |
| 756 | 23349838 | We also treated Min-6 cells with palmitic acid for 24 h, and found that the expression of 5-HT(2C)R increased in a dose-dependent manner; furthermore, the inhibition of insulin secretion in Min-6 cells induced by palmitic acid could be reversed by SB242084 or RNA interference against 5-HT(2C)R. |
| 757 | 23349838 | Taken together, our data suggests that increased expression of 5-HT(2C)R in pancreatic β-cells might inhibit insulin secretion. |
| 758 | 23349838 | Serotonin receptor 2C and insulin secretion. |
| 759 | 23349838 | High plasma levels of serotonin (5-hydroxytryptamine; 5-HT) have been reported in T2DM patients, though the potential effect on insulin secretion is unclear. |
| 760 | 23349838 | However, it is known that the 5-HT receptor 2C (5-HT(2C)R) agonist, mCPP, decreases plasma insulin concentration in mice. |
| 761 | 23349838 | As such, we aimed to investigate the expression of the 5-HT(2C)R in pancreatic islets of diabetic mice and the role of 5-HT(2C)R signaling in insulin secretion from pancreatic β-cells. |
| 762 | 23349838 | Furthermore, treatment with a 5-HT(2C)R antagonist (SB242084) increased insulin secretion from pancreatic islets isolated from db/db mice in a dose-dependent manner, but had no effect in islets from control mice. |
| 763 | 23349838 | We found that mCPP significantly inhibited insulin secretion in Min-6 cells and isolated islets in a dose-dependent manner, which could be reversed by SB242084 or RNA interference against 5-HT(2C)R. |
| 764 | 23349838 | We also treated Min-6 cells with palmitic acid for 24 h, and found that the expression of 5-HT(2C)R increased in a dose-dependent manner; furthermore, the inhibition of insulin secretion in Min-6 cells induced by palmitic acid could be reversed by SB242084 or RNA interference against 5-HT(2C)R. |
| 765 | 23349838 | Taken together, our data suggests that increased expression of 5-HT(2C)R in pancreatic β-cells might inhibit insulin secretion. |
| 766 | 23995651 | The vasoconstrictive effects of 5-HT are mediated by 5-HT1B and 5-HT2A receptors located on the membrane of smooth muscle cells, except in the intracranial arteries which constrict only through 5-HT1B receptors. 5-HT also acts as vasodilator because it releases nitric oxide from endothelial cells. |
| 767 | 23995651 | This response is dominantly mediated by 5-HT1B receptors but not by 5-HT2A receptors. |