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PMID |
Sentence |
1 |
10480603
|
The effects of corticotropin-releasing factor (CRF) on the intracellular concentration of Ca2+ were studied in isolated single beta-cells of the rat islet.
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2 |
10480603
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Immunohistochemical staining using CRF-receptor antibodies revealed the presence of both type 1 (CRF-R1) and type 2 (CRF-R2) receptors for CRF in the majority of islet cells.
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3 |
10480603
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These results suggest that in single beta-cells of rat islets, CRF, through its own receptor, potentiates Ca2+ influx through the L-type Ca2+ channel by activation of the cAMP/protein kinase A signaling pathway.
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4 |
10822340
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Treatment of rats or monkeys with the novel CRH receptor type 1 (CRH-R1) antagonist antalarmin inhibits the HPA and/or the SA/SS axes.
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5 |
10822340
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Expression of CRH, ACTH, CRH type I and type II receptor mRNA were analyzed by reverse-transcription (RT) PCR.
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6 |
10822340
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ACTH, CRH, and CRH-R1 and CRH-R2 mRNAs were expressed in the human adrenal as determined by RT-PCR.
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7 |
10822340
|
CRH, ACTH, and both CRH-R1 and CRH-R2 mRNAs are expressed in the adult human adrenal gland.
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8 |
10822340
|
This effect is blocked by antalarmin, a selective CRH-R1 receptor antagonist, suggesting that CRH-R1 receptors are involved in an intraadrenal CRH/ACTH control system in humans.
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9 |
10822340
|
Treatment of rats or monkeys with the novel CRH receptor type 1 (CRH-R1) antagonist antalarmin inhibits the HPA and/or the SA/SS axes.
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10 |
10822340
|
Expression of CRH, ACTH, CRH type I and type II receptor mRNA were analyzed by reverse-transcription (RT) PCR.
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11 |
10822340
|
ACTH, CRH, and CRH-R1 and CRH-R2 mRNAs were expressed in the human adrenal as determined by RT-PCR.
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12 |
10822340
|
CRH, ACTH, and both CRH-R1 and CRH-R2 mRNAs are expressed in the adult human adrenal gland.
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13 |
10822340
|
This effect is blocked by antalarmin, a selective CRH-R1 receptor antagonist, suggesting that CRH-R1 receptors are involved in an intraadrenal CRH/ACTH control system in humans.
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14 |
10822340
|
Treatment of rats or monkeys with the novel CRH receptor type 1 (CRH-R1) antagonist antalarmin inhibits the HPA and/or the SA/SS axes.
|
15 |
10822340
|
Expression of CRH, ACTH, CRH type I and type II receptor mRNA were analyzed by reverse-transcription (RT) PCR.
|
16 |
10822340
|
ACTH, CRH, and CRH-R1 and CRH-R2 mRNAs were expressed in the human adrenal as determined by RT-PCR.
|
17 |
10822340
|
CRH, ACTH, and both CRH-R1 and CRH-R2 mRNAs are expressed in the adult human adrenal gland.
|
18 |
10822340
|
This effect is blocked by antalarmin, a selective CRH-R1 receptor antagonist, suggesting that CRH-R1 receptors are involved in an intraadrenal CRH/ACTH control system in humans.
|
19 |
10822340
|
Treatment of rats or monkeys with the novel CRH receptor type 1 (CRH-R1) antagonist antalarmin inhibits the HPA and/or the SA/SS axes.
|
20 |
10822340
|
Expression of CRH, ACTH, CRH type I and type II receptor mRNA were analyzed by reverse-transcription (RT) PCR.
|
21 |
10822340
|
ACTH, CRH, and CRH-R1 and CRH-R2 mRNAs were expressed in the human adrenal as determined by RT-PCR.
|
22 |
10822340
|
CRH, ACTH, and both CRH-R1 and CRH-R2 mRNAs are expressed in the adult human adrenal gland.
|
23 |
10822340
|
This effect is blocked by antalarmin, a selective CRH-R1 receptor antagonist, suggesting that CRH-R1 receptors are involved in an intraadrenal CRH/ACTH control system in humans.
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24 |
11738619
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CRHR1 Receptor binding and lipophilicity of pyrrolopyrimidines, potential nonpeptide corticotropin-releasing hormone type 1 receptor antagonists.
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25 |
11738619
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A series of compounds related to N-butyl-N-ethyl[2,5,6-trimethyl-7-(2,4,6-trimethylphenyl)pyrrolo[2,3-d]pyrimidin-4-yl]amine (1, antalarmin) have been prepared and evaluated for their CRHR1 binding affinity as the initial step in the development of selective high affinity hydrophilic nonpeptide corticotropin-releasing hormone type 1 receptor (CRHR1) antagonists.
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26 |
11738619
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CRHR1 Receptor binding and lipophilicity of pyrrolopyrimidines, potential nonpeptide corticotropin-releasing hormone type 1 receptor antagonists.
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27 |
11738619
|
A series of compounds related to N-butyl-N-ethyl[2,5,6-trimethyl-7-(2,4,6-trimethylphenyl)pyrrolo[2,3-d]pyrimidin-4-yl]amine (1, antalarmin) have been prepared and evaluated for their CRHR1 binding affinity as the initial step in the development of selective high affinity hydrophilic nonpeptide corticotropin-releasing hormone type 1 receptor (CRHR1) antagonists.
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28 |
12606499
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Three more groups underwent pretreatment with corticosterone, adrenocorticotrophic hormone (ACTH), or corticotrophin-releasing hormone (CRH) mirroring the glucocorticoid response of the hypoglycemic group.
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29 |
12606499
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CRH- (and insulin-treated) animals showed markedly reduced epinephrine responses (CRH 1,276 +/- 404 pg/ml, controls 3,559 +/- 563 pg/ml; P < 0.05).
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30 |
12606499
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The addition of a CRH receptor 1 (CRHr1) antagonist to the antecedent CRH reversed the subsequent suppression of epinephrine.
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31 |
12606499
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These findings suggest that CRH acting via CRHr1 plays an important role in the sympathoadrenal downregulation seen in this rodent model of antecedent hypoglycemia; this action is not mediated via activation of the hypothalamic-pituitary-adrenal axis.
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32 |
12606499
|
Three more groups underwent pretreatment with corticosterone, adrenocorticotrophic hormone (ACTH), or corticotrophin-releasing hormone (CRH) mirroring the glucocorticoid response of the hypoglycemic group.
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33 |
12606499
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CRH- (and insulin-treated) animals showed markedly reduced epinephrine responses (CRH 1,276 +/- 404 pg/ml, controls 3,559 +/- 563 pg/ml; P < 0.05).
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34 |
12606499
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The addition of a CRH receptor 1 (CRHr1) antagonist to the antecedent CRH reversed the subsequent suppression of epinephrine.
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35 |
12606499
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These findings suggest that CRH acting via CRHr1 plays an important role in the sympathoadrenal downregulation seen in this rodent model of antecedent hypoglycemia; this action is not mediated via activation of the hypothalamic-pituitary-adrenal axis.
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36 |
14764822
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We characterized the expression of CRH receptors 1 and 2 and CRH-like peptides stresscopin and urocortin in human adipose tissue in comparison with other peripheral tissues, adrenal, and heart.
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37 |
14764822
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CRH-R1:CRH-R2 ratio varied according to fat-depot type; whereas CRH-R1 expression was higher in sc fat than in visceral fat, the opposite was true for CRH-R2.
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38 |
14764822
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Adipose tissue also expressed urocortin and stresscopin, the predominant ligands of peripheral CRH-R2.
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39 |
14764822
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CRH down-regulated CRH-R1 and CRH-R2 mRNA expression in isolated adipocytes.
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40 |
14764822
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We characterized the expression of CRH receptors 1 and 2 and CRH-like peptides stresscopin and urocortin in human adipose tissue in comparison with other peripheral tissues, adrenal, and heart.
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41 |
14764822
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CRH-R1:CRH-R2 ratio varied according to fat-depot type; whereas CRH-R1 expression was higher in sc fat than in visceral fat, the opposite was true for CRH-R2.
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42 |
14764822
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Adipose tissue also expressed urocortin and stresscopin, the predominant ligands of peripheral CRH-R2.
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43 |
14764822
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CRH down-regulated CRH-R1 and CRH-R2 mRNA expression in isolated adipocytes.
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44 |
15356091
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CRP levels correlated with non-HDL cholesterol levels (r = 0.16, P = 0.0236) and the CRF (r = 0.18, P = 0.14), but not with levels of HDL or TG.
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45 |
16199893
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Mouse models of adrenal cortical dysfunction, such as the targeted disruption of the 21-hydroxylase- or the CRHR1 genes, show alterations in chromaffin cell function, while disruption of tyrosine hydroxylase, a key enzyme in catecholamine synthesis, impairs adrenal cortical function.
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46 |
16741581
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The corticotrophin-releasing factor (CRF) family of neuropeptides and their receptors (CRFR1 and CRFR2) play a critical role in regulating the neuroendocrine stress response.
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47 |
16741581
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Here we show in the Sprague-Dawley rat that direct in vivo application to the ventromedial hypothalamus (VMH), a key glucose-sensing region, of urocortin I (UCN I), an endogenous CRFR2 agonist, suppressed (approximately 55-60%), whereas CRF, a predominantly CRFR1 agonist, amplified (approximately 50-70%) CRR to hypoglycemia.
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48 |
16741581
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Our data suggest that regulation of the CRR is largely determined by the interaction between CRFR2-mediated suppression and CRFR1-mediated activation in the VMH.
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49 |
16741581
|
The corticotrophin-releasing factor (CRF) family of neuropeptides and their receptors (CRFR1 and CRFR2) play a critical role in regulating the neuroendocrine stress response.
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50 |
16741581
|
Here we show in the Sprague-Dawley rat that direct in vivo application to the ventromedial hypothalamus (VMH), a key glucose-sensing region, of urocortin I (UCN I), an endogenous CRFR2 agonist, suppressed (approximately 55-60%), whereas CRF, a predominantly CRFR1 agonist, amplified (approximately 50-70%) CRR to hypoglycemia.
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51 |
16741581
|
Our data suggest that regulation of the CRR is largely determined by the interaction between CRFR2-mediated suppression and CRFR1-mediated activation in the VMH.
|
52 |
16741581
|
The corticotrophin-releasing factor (CRF) family of neuropeptides and their receptors (CRFR1 and CRFR2) play a critical role in regulating the neuroendocrine stress response.
|
53 |
16741581
|
Here we show in the Sprague-Dawley rat that direct in vivo application to the ventromedial hypothalamus (VMH), a key glucose-sensing region, of urocortin I (UCN I), an endogenous CRFR2 agonist, suppressed (approximately 55-60%), whereas CRF, a predominantly CRFR1 agonist, amplified (approximately 50-70%) CRR to hypoglycemia.
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54 |
16741581
|
Our data suggest that regulation of the CRR is largely determined by the interaction between CRFR2-mediated suppression and CRFR1-mediated activation in the VMH.
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55 |
17400798
|
CRF(1) receptor blockade increased uncoupling protein-1 mRNA levels in interscapular brown adipose tissue of obese rats.
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56 |
17437246
|
Gastric inhibitory polypeptide (GIP, or glucose-dependent insulinotropic polypeptide) is a 42-amino acid incretin hormone moderating glucose-induced insulin secretion.
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57 |
17437246
|
We have studied the structure of GIP(1-30)NH2 and built a model of its G-protein coupled receptor (GPCR).
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58 |
17437246
|
GIP(1-30)NH2 has all the structural features of peptides belonging to family B1 GPCRs, which are characterized by a coil at the N-terminal and a long C-terminal alpha-helix with or without a break.
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59 |
17437246
|
A model of the seven transmembrane (TM) helices of the GIP receptor (GIPR) has been built on the principles of comparative protein modeling, using the crystal structure of bovine rhodopsin as a template.
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60 |
17437246
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The N-terminal domain of GIPR has been constructed from the NMR structure of the N-terminal of corticoptropin releasing factor receptor (CRFR), a family B1 GCPR.
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61 |
17437246
|
On the basis of the experimental data available for some members of family B1 GPCRs, four pairs of constraints between GIP(1-30)NH2 and its receptor were used in the FTDOCK program, to build the complete model of the GIP(1-30)NH2:GIPR complex.
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62 |
17437246
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This work is the first complete model at the atomic level of GIP(1-30)NH2 and of the complex with its GPCR.
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63 |
19026699
|
Based on the reported anti-inflammatory and anti-stress responses by corticotropin-releasing factor (CRF) receptor signaling, endogenous CRF receptor agonists, CRF, urocortin (UCN) I and its related peptides, may play protective roles against cardiovascular stresses via the CRF receptor signaling.
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64 |
19026699
|
In addition, due to the possible involvement of CRF receptor signaling in the effects of statin on endothelial cells, the effects of pitavastatin on the expression of UCN-related peptides in HAECs were also evaluated.
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65 |
19026699
|
HAECs expressed all UCNs, CRF type 1 receptor (CRF-R1), and CRF type 2 (CRF-R2)alpha and CRF-R2beta mRNAs.
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66 |
19026699
|
Real time PCR analysis revealed that UCN I mRNA was down-regulated, whereas UCN II mRNA was up-regulated by tumor necrosis factor (TNF)-alpha.
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67 |
19026699
|
Selective blockade of CRF-R1 resulted in significant increase in TNF-alpha-induced expression of vascular adhesion molecule-1 at mRNA level and E-selectin at mRNA and protein levels.
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68 |
19026699
|
On the contrary, UCN II, CRF-R1, and CRF-R2 mRNAs were markedly increased by co-incubation of pitavastatin and TNF-alpha.
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69 |
19026699
|
These facts indicate that CRF-R1 signaling may have protective role against TNF-alpha-induced vascular inflammation.
|
70 |
19026699
|
In addition, because of up-regulation of CRF-R1 mRNA by pitavastatin with or without TNF-alpha, CRF-R1 may be involved in the vasoprotective effects of pitavastatin.
|
71 |
19026699
|
Based on the reported anti-inflammatory and anti-stress responses by corticotropin-releasing factor (CRF) receptor signaling, endogenous CRF receptor agonists, CRF, urocortin (UCN) I and its related peptides, may play protective roles against cardiovascular stresses via the CRF receptor signaling.
|
72 |
19026699
|
In addition, due to the possible involvement of CRF receptor signaling in the effects of statin on endothelial cells, the effects of pitavastatin on the expression of UCN-related peptides in HAECs were also evaluated.
|
73 |
19026699
|
HAECs expressed all UCNs, CRF type 1 receptor (CRF-R1), and CRF type 2 (CRF-R2)alpha and CRF-R2beta mRNAs.
|
74 |
19026699
|
Real time PCR analysis revealed that UCN I mRNA was down-regulated, whereas UCN II mRNA was up-regulated by tumor necrosis factor (TNF)-alpha.
|
75 |
19026699
|
Selective blockade of CRF-R1 resulted in significant increase in TNF-alpha-induced expression of vascular adhesion molecule-1 at mRNA level and E-selectin at mRNA and protein levels.
|
76 |
19026699
|
On the contrary, UCN II, CRF-R1, and CRF-R2 mRNAs were markedly increased by co-incubation of pitavastatin and TNF-alpha.
|
77 |
19026699
|
These facts indicate that CRF-R1 signaling may have protective role against TNF-alpha-induced vascular inflammation.
|
78 |
19026699
|
In addition, because of up-regulation of CRF-R1 mRNA by pitavastatin with or without TNF-alpha, CRF-R1 may be involved in the vasoprotective effects of pitavastatin.
|
79 |
19026699
|
Based on the reported anti-inflammatory and anti-stress responses by corticotropin-releasing factor (CRF) receptor signaling, endogenous CRF receptor agonists, CRF, urocortin (UCN) I and its related peptides, may play protective roles against cardiovascular stresses via the CRF receptor signaling.
|
80 |
19026699
|
In addition, due to the possible involvement of CRF receptor signaling in the effects of statin on endothelial cells, the effects of pitavastatin on the expression of UCN-related peptides in HAECs were also evaluated.
|
81 |
19026699
|
HAECs expressed all UCNs, CRF type 1 receptor (CRF-R1), and CRF type 2 (CRF-R2)alpha and CRF-R2beta mRNAs.
|
82 |
19026699
|
Real time PCR analysis revealed that UCN I mRNA was down-regulated, whereas UCN II mRNA was up-regulated by tumor necrosis factor (TNF)-alpha.
|
83 |
19026699
|
Selective blockade of CRF-R1 resulted in significant increase in TNF-alpha-induced expression of vascular adhesion molecule-1 at mRNA level and E-selectin at mRNA and protein levels.
|
84 |
19026699
|
On the contrary, UCN II, CRF-R1, and CRF-R2 mRNAs were markedly increased by co-incubation of pitavastatin and TNF-alpha.
|
85 |
19026699
|
These facts indicate that CRF-R1 signaling may have protective role against TNF-alpha-induced vascular inflammation.
|
86 |
19026699
|
In addition, because of up-regulation of CRF-R1 mRNA by pitavastatin with or without TNF-alpha, CRF-R1 may be involved in the vasoprotective effects of pitavastatin.
|
87 |
19026699
|
Based on the reported anti-inflammatory and anti-stress responses by corticotropin-releasing factor (CRF) receptor signaling, endogenous CRF receptor agonists, CRF, urocortin (UCN) I and its related peptides, may play protective roles against cardiovascular stresses via the CRF receptor signaling.
|
88 |
19026699
|
In addition, due to the possible involvement of CRF receptor signaling in the effects of statin on endothelial cells, the effects of pitavastatin on the expression of UCN-related peptides in HAECs were also evaluated.
|
89 |
19026699
|
HAECs expressed all UCNs, CRF type 1 receptor (CRF-R1), and CRF type 2 (CRF-R2)alpha and CRF-R2beta mRNAs.
|
90 |
19026699
|
Real time PCR analysis revealed that UCN I mRNA was down-regulated, whereas UCN II mRNA was up-regulated by tumor necrosis factor (TNF)-alpha.
|
91 |
19026699
|
Selective blockade of CRF-R1 resulted in significant increase in TNF-alpha-induced expression of vascular adhesion molecule-1 at mRNA level and E-selectin at mRNA and protein levels.
|
92 |
19026699
|
On the contrary, UCN II, CRF-R1, and CRF-R2 mRNAs were markedly increased by co-incubation of pitavastatin and TNF-alpha.
|
93 |
19026699
|
These facts indicate that CRF-R1 signaling may have protective role against TNF-alpha-induced vascular inflammation.
|
94 |
19026699
|
In addition, because of up-regulation of CRF-R1 mRNA by pitavastatin with or without TNF-alpha, CRF-R1 may be involved in the vasoprotective effects of pitavastatin.
|
95 |
19026699
|
Based on the reported anti-inflammatory and anti-stress responses by corticotropin-releasing factor (CRF) receptor signaling, endogenous CRF receptor agonists, CRF, urocortin (UCN) I and its related peptides, may play protective roles against cardiovascular stresses via the CRF receptor signaling.
|
96 |
19026699
|
In addition, due to the possible involvement of CRF receptor signaling in the effects of statin on endothelial cells, the effects of pitavastatin on the expression of UCN-related peptides in HAECs were also evaluated.
|
97 |
19026699
|
HAECs expressed all UCNs, CRF type 1 receptor (CRF-R1), and CRF type 2 (CRF-R2)alpha and CRF-R2beta mRNAs.
|
98 |
19026699
|
Real time PCR analysis revealed that UCN I mRNA was down-regulated, whereas UCN II mRNA was up-regulated by tumor necrosis factor (TNF)-alpha.
|
99 |
19026699
|
Selective blockade of CRF-R1 resulted in significant increase in TNF-alpha-induced expression of vascular adhesion molecule-1 at mRNA level and E-selectin at mRNA and protein levels.
|
100 |
19026699
|
On the contrary, UCN II, CRF-R1, and CRF-R2 mRNAs were markedly increased by co-incubation of pitavastatin and TNF-alpha.
|
101 |
19026699
|
These facts indicate that CRF-R1 signaling may have protective role against TNF-alpha-induced vascular inflammation.
|
102 |
19026699
|
In addition, because of up-regulation of CRF-R1 mRNA by pitavastatin with or without TNF-alpha, CRF-R1 may be involved in the vasoprotective effects of pitavastatin.
|
103 |
20472052
|
We evaluated arginine vasopressin (AVP), glucocorticoid receptor (GR), and corticotropin-releasing hormone (CRH) expression with immunohistochemistry (IHC), immunofluorescence, real-time PCR, and Western blot analysis in each treatment group 7 weeks post ADX to assess HPA axis regulatory patterns in connection with type 2 diabetes.
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104 |
20472052
|
Additionally, mRNA expression of AVP and CRH receptors (V1aR, V1bR, CRHR1, and CRHR2) was also measured and adrenocorticotropin hormone (ACTH) immunoreactivity was surveyed by IHC to add to data regarding the regulatory mechanism.
|
105 |
20472052
|
Without the negative feedback system of corticosterone, CRH is highly enhanced and may primarily combine with CRHR1 to stimulate negative feedback through ACTH in the pituitary gland in type 2 diabetic rats with long-term ADX.
|
106 |
20472052
|
We evaluated arginine vasopressin (AVP), glucocorticoid receptor (GR), and corticotropin-releasing hormone (CRH) expression with immunohistochemistry (IHC), immunofluorescence, real-time PCR, and Western blot analysis in each treatment group 7 weeks post ADX to assess HPA axis regulatory patterns in connection with type 2 diabetes.
|
107 |
20472052
|
Additionally, mRNA expression of AVP and CRH receptors (V1aR, V1bR, CRHR1, and CRHR2) was also measured and adrenocorticotropin hormone (ACTH) immunoreactivity was surveyed by IHC to add to data regarding the regulatory mechanism.
|
108 |
20472052
|
Without the negative feedback system of corticosterone, CRH is highly enhanced and may primarily combine with CRHR1 to stimulate negative feedback through ACTH in the pituitary gland in type 2 diabetic rats with long-term ADX.
|
109 |
21777182
|
Beside the large family A (rhodopsin-like receptors) and family C GPCR (metabotropic glutamate receptors), the small family B1 GPCR (secretin-like receptors) includes important receptors such as vasoactive intestinal peptide receptors (VPAC), pituitary adenylyl cyclase activating peptide receptor (PAC1R), secretin receptor (SECR), growth hormone releasing factor receptor (GRFR), glucagon receptor (GCGR), glucagon like-peptide 1 and 2 receptors (GLPR), gastric inhibitory peptide receptor (GIPR), parathyroid hormone receptors (PTHR), calcitonin receptors (CTR) and corticotropin-releasing factor receptors (CRFR).
|
110 |
21825133
|
Corticotropin-releasing hormone (CRH) and growth hormone-releasing hormone (GHRH), primarily characterized as neuroregulators of the hypothalamic-pituitary-adrenal axis, directly influence tissue-specific receptor-systems for CRH and GHRH in the endocrine pancreas.
|
111 |
21825133
|
Here, we demonstrate the expression of mRNA for CRH and CRH-receptor type 1 (CRHR1) and of protein for CRHR1 in rat and human pancreatic islets and rat insulinoma cells.
|
112 |
21825133
|
Activation of CRHR1 and GHRH-receptor significantly increased cell proliferation and reduced cell apoptosis.
|
113 |
21825133
|
CRH stimulated both cellular content and release of insulin in rat islet and insulinoma cells.
|
114 |
21825133
|
Quantitative real-time PCR revealed that stimulation of CRHR1 and GHRH-receptor affects the metabolism of insulinoma cells by down-regulating 11β-HSD-1 and up-regulating 11β-HSD-2.
|
115 |
21825133
|
Similarly, activation of CRHR1 resulted in reduced cortisol levels, indicating either decreased 11β-HSD-1 enzyme activity or increased 11β-HSD-2 enzyme activity; thus, activation of CRHR1 alters the glucocorticoid balance toward the inactive form.
|
116 |
21825133
|
Agonists of CRHR1 and GHRH-receptor, therefore, may play an important role as novel therapeutic tools in the treatment of diabetes mellitus.
|
117 |
21825133
|
Corticotropin-releasing hormone (CRH) and growth hormone-releasing hormone (GHRH), primarily characterized as neuroregulators of the hypothalamic-pituitary-adrenal axis, directly influence tissue-specific receptor-systems for CRH and GHRH in the endocrine pancreas.
|
118 |
21825133
|
Here, we demonstrate the expression of mRNA for CRH and CRH-receptor type 1 (CRHR1) and of protein for CRHR1 in rat and human pancreatic islets and rat insulinoma cells.
|
119 |
21825133
|
Activation of CRHR1 and GHRH-receptor significantly increased cell proliferation and reduced cell apoptosis.
|
120 |
21825133
|
CRH stimulated both cellular content and release of insulin in rat islet and insulinoma cells.
|
121 |
21825133
|
Quantitative real-time PCR revealed that stimulation of CRHR1 and GHRH-receptor affects the metabolism of insulinoma cells by down-regulating 11β-HSD-1 and up-regulating 11β-HSD-2.
|
122 |
21825133
|
Similarly, activation of CRHR1 resulted in reduced cortisol levels, indicating either decreased 11β-HSD-1 enzyme activity or increased 11β-HSD-2 enzyme activity; thus, activation of CRHR1 alters the glucocorticoid balance toward the inactive form.
|
123 |
21825133
|
Agonists of CRHR1 and GHRH-receptor, therefore, may play an important role as novel therapeutic tools in the treatment of diabetes mellitus.
|
124 |
21825133
|
Corticotropin-releasing hormone (CRH) and growth hormone-releasing hormone (GHRH), primarily characterized as neuroregulators of the hypothalamic-pituitary-adrenal axis, directly influence tissue-specific receptor-systems for CRH and GHRH in the endocrine pancreas.
|
125 |
21825133
|
Here, we demonstrate the expression of mRNA for CRH and CRH-receptor type 1 (CRHR1) and of protein for CRHR1 in rat and human pancreatic islets and rat insulinoma cells.
|
126 |
21825133
|
Activation of CRHR1 and GHRH-receptor significantly increased cell proliferation and reduced cell apoptosis.
|
127 |
21825133
|
CRH stimulated both cellular content and release of insulin in rat islet and insulinoma cells.
|
128 |
21825133
|
Quantitative real-time PCR revealed that stimulation of CRHR1 and GHRH-receptor affects the metabolism of insulinoma cells by down-regulating 11β-HSD-1 and up-regulating 11β-HSD-2.
|
129 |
21825133
|
Similarly, activation of CRHR1 resulted in reduced cortisol levels, indicating either decreased 11β-HSD-1 enzyme activity or increased 11β-HSD-2 enzyme activity; thus, activation of CRHR1 alters the glucocorticoid balance toward the inactive form.
|
130 |
21825133
|
Agonists of CRHR1 and GHRH-receptor, therefore, may play an important role as novel therapeutic tools in the treatment of diabetes mellitus.
|
131 |
21825133
|
Corticotropin-releasing hormone (CRH) and growth hormone-releasing hormone (GHRH), primarily characterized as neuroregulators of the hypothalamic-pituitary-adrenal axis, directly influence tissue-specific receptor-systems for CRH and GHRH in the endocrine pancreas.
|
132 |
21825133
|
Here, we demonstrate the expression of mRNA for CRH and CRH-receptor type 1 (CRHR1) and of protein for CRHR1 in rat and human pancreatic islets and rat insulinoma cells.
|
133 |
21825133
|
Activation of CRHR1 and GHRH-receptor significantly increased cell proliferation and reduced cell apoptosis.
|
134 |
21825133
|
CRH stimulated both cellular content and release of insulin in rat islet and insulinoma cells.
|
135 |
21825133
|
Quantitative real-time PCR revealed that stimulation of CRHR1 and GHRH-receptor affects the metabolism of insulinoma cells by down-regulating 11β-HSD-1 and up-regulating 11β-HSD-2.
|
136 |
21825133
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Similarly, activation of CRHR1 resulted in reduced cortisol levels, indicating either decreased 11β-HSD-1 enzyme activity or increased 11β-HSD-2 enzyme activity; thus, activation of CRHR1 alters the glucocorticoid balance toward the inactive form.
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137 |
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Agonists of CRHR1 and GHRH-receptor, therefore, may play an important role as novel therapeutic tools in the treatment of diabetes mellitus.
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138 |
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Corticotropin-releasing hormone (CRH) and growth hormone-releasing hormone (GHRH), primarily characterized as neuroregulators of the hypothalamic-pituitary-adrenal axis, directly influence tissue-specific receptor-systems for CRH and GHRH in the endocrine pancreas.
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Here, we demonstrate the expression of mRNA for CRH and CRH-receptor type 1 (CRHR1) and of protein for CRHR1 in rat and human pancreatic islets and rat insulinoma cells.
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Activation of CRHR1 and GHRH-receptor significantly increased cell proliferation and reduced cell apoptosis.
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CRH stimulated both cellular content and release of insulin in rat islet and insulinoma cells.
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142 |
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Quantitative real-time PCR revealed that stimulation of CRHR1 and GHRH-receptor affects the metabolism of insulinoma cells by down-regulating 11β-HSD-1 and up-regulating 11β-HSD-2.
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143 |
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Similarly, activation of CRHR1 resulted in reduced cortisol levels, indicating either decreased 11β-HSD-1 enzyme activity or increased 11β-HSD-2 enzyme activity; thus, activation of CRHR1 alters the glucocorticoid balance toward the inactive form.
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144 |
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Agonists of CRHR1 and GHRH-receptor, therefore, may play an important role as novel therapeutic tools in the treatment of diabetes mellitus.
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145 |
23834894
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Stress-induced anorexia in A(y)/a mice was independent of pathways involving hypothalamic-pituitary-adrenal axis activity and hypothalamic orexigenic neuropeptide (agouti-related peptide and neuropeptide Y) gene expressions and corticotrophin-releasing factor type 1 receptor (CRFR1).
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Hypothalamic CRFR2 is known to mediate anorectic signals from CRF-related peptides.
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