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PMID |
Sentence |
1 |
9264049
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LHRH receptors and LHRH receptor-bearing cells in pituitaries of streptozocin diabetic male rats.
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2 |
9264049
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Possible causes for the gonadotrope disorders may be low hypothalamic LHRH secretion alone or combined with reduced (a) number of LHRH receptor sites, or (b) receptor to ligand affinity, or (c) of LHRH receptor-bearing cells.
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3 |
9264049
|
To clarify this question we determined by saturation and competition binding Bmax, KD and KA of the LHRH receptor sites and counted the receptor-bearing cells in pituitary glands of control and STZ-diabetic adult male rats.
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4 |
9264049
|
The number of LHRH receptor-bearing cells in diabetic animals was increased.
|
5 |
9264049
|
We conclude that the reduced LH secretion from the diabetic pituitary gland might be due to a reduced number of LHRH receptor sites in the pituitary gland.
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6 |
9264049
|
LHRH receptors and LHRH receptor-bearing cells in pituitaries of streptozocin diabetic male rats.
|
7 |
9264049
|
Possible causes for the gonadotrope disorders may be low hypothalamic LHRH secretion alone or combined with reduced (a) number of LHRH receptor sites, or (b) receptor to ligand affinity, or (c) of LHRH receptor-bearing cells.
|
8 |
9264049
|
To clarify this question we determined by saturation and competition binding Bmax, KD and KA of the LHRH receptor sites and counted the receptor-bearing cells in pituitary glands of control and STZ-diabetic adult male rats.
|
9 |
9264049
|
The number of LHRH receptor-bearing cells in diabetic animals was increased.
|
10 |
9264049
|
We conclude that the reduced LH secretion from the diabetic pituitary gland might be due to a reduced number of LHRH receptor sites in the pituitary gland.
|
11 |
9264049
|
LHRH receptors and LHRH receptor-bearing cells in pituitaries of streptozocin diabetic male rats.
|
12 |
9264049
|
Possible causes for the gonadotrope disorders may be low hypothalamic LHRH secretion alone or combined with reduced (a) number of LHRH receptor sites, or (b) receptor to ligand affinity, or (c) of LHRH receptor-bearing cells.
|
13 |
9264049
|
To clarify this question we determined by saturation and competition binding Bmax, KD and KA of the LHRH receptor sites and counted the receptor-bearing cells in pituitary glands of control and STZ-diabetic adult male rats.
|
14 |
9264049
|
The number of LHRH receptor-bearing cells in diabetic animals was increased.
|
15 |
9264049
|
We conclude that the reduced LH secretion from the diabetic pituitary gland might be due to a reduced number of LHRH receptor sites in the pituitary gland.
|
16 |
9264049
|
LHRH receptors and LHRH receptor-bearing cells in pituitaries of streptozocin diabetic male rats.
|
17 |
9264049
|
Possible causes for the gonadotrope disorders may be low hypothalamic LHRH secretion alone or combined with reduced (a) number of LHRH receptor sites, or (b) receptor to ligand affinity, or (c) of LHRH receptor-bearing cells.
|
18 |
9264049
|
To clarify this question we determined by saturation and competition binding Bmax, KD and KA of the LHRH receptor sites and counted the receptor-bearing cells in pituitary glands of control and STZ-diabetic adult male rats.
|
19 |
9264049
|
The number of LHRH receptor-bearing cells in diabetic animals was increased.
|
20 |
9264049
|
We conclude that the reduced LH secretion from the diabetic pituitary gland might be due to a reduced number of LHRH receptor sites in the pituitary gland.
|
21 |
9264049
|
LHRH receptors and LHRH receptor-bearing cells in pituitaries of streptozocin diabetic male rats.
|
22 |
9264049
|
Possible causes for the gonadotrope disorders may be low hypothalamic LHRH secretion alone or combined with reduced (a) number of LHRH receptor sites, or (b) receptor to ligand affinity, or (c) of LHRH receptor-bearing cells.
|
23 |
9264049
|
To clarify this question we determined by saturation and competition binding Bmax, KD and KA of the LHRH receptor sites and counted the receptor-bearing cells in pituitary glands of control and STZ-diabetic adult male rats.
|
24 |
9264049
|
The number of LHRH receptor-bearing cells in diabetic animals was increased.
|
25 |
9264049
|
We conclude that the reduced LH secretion from the diabetic pituitary gland might be due to a reduced number of LHRH receptor sites in the pituitary gland.
|
26 |
9439932
|
Involvement of gamma amino butyric acid (GABA) in the postnatal function of the GnRH pulse generator as determined on the basis of GnRH and GnRH-receptor gene expression in the hypothalamus and the pituitary.
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27 |
12959992
|
To test whether the increased incidence of diabetes in castrated male NOD mice is related to an increase in GnRH activity, we treated castrated male NOD mice with Antide, a GnRH receptor antagonist, to determine the effect on the incidence and timing of onset of diabetes.
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28 |
15226417
|
Essential role of the homeodomain for pituitary homeobox 1 activation of mouse gonadotropin-releasing hormone receptor gene expression through interactions with c-Jun and DNA.
|
29 |
15226417
|
Pituitary homeobox 1 (Pitx-1) has been shown to activate pituitary-specific gene expression by direct DNA binding and/or protein-protein interaction with other transcription factors.
|
30 |
15226417
|
We hypothesized that Pitx-1 might also dictate tissue-specific expression of the mouse GnRHR (mGnRHR) gene in a similar manner.
|
31 |
15226417
|
Pitx-1 activated the mGnRHR gene promoter, and transactivation was localized to sequences between -308 and -264.
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32 |
15226417
|
This region includes an activating protein 1 (AP-1) site, which was previously shown to be important for mGnRHR gene expression.
|
33 |
15226417
|
Further characterization indicated that an intact AP-1 site was required for full Pitx-1 responsiveness.
|
34 |
15226417
|
Furthermore, Pitx-1 and AP-1 were synergistic in the activation of the mGnRHR gene promoter.
|
35 |
15226417
|
Pitx-1 interacted directly with c-Jun, and the HD was sufficient for this interaction.
|
36 |
15226417
|
While the point mutation in the Pitx-1 HD did not affect interaction with c-Jun, deletion of the HD eliminated the interaction.
|
37 |
15226417
|
Taken together, our studies indicate that Pitx-1 can direct transactivation of the mGnRHR gene, in part by DNA binding and in part by an action of Pitx-1 as a cofactor for AP-1, augmenting AP-1 activity through a novel protein-protein interaction between c-Jun and the HD of Pitx-1.
|
38 |
15226417
|
Essential role of the homeodomain for pituitary homeobox 1 activation of mouse gonadotropin-releasing hormone receptor gene expression through interactions with c-Jun and DNA.
|
39 |
15226417
|
Pituitary homeobox 1 (Pitx-1) has been shown to activate pituitary-specific gene expression by direct DNA binding and/or protein-protein interaction with other transcription factors.
|
40 |
15226417
|
We hypothesized that Pitx-1 might also dictate tissue-specific expression of the mouse GnRHR (mGnRHR) gene in a similar manner.
|
41 |
15226417
|
Pitx-1 activated the mGnRHR gene promoter, and transactivation was localized to sequences between -308 and -264.
|
42 |
15226417
|
This region includes an activating protein 1 (AP-1) site, which was previously shown to be important for mGnRHR gene expression.
|
43 |
15226417
|
Further characterization indicated that an intact AP-1 site was required for full Pitx-1 responsiveness.
|
44 |
15226417
|
Furthermore, Pitx-1 and AP-1 were synergistic in the activation of the mGnRHR gene promoter.
|
45 |
15226417
|
Pitx-1 interacted directly with c-Jun, and the HD was sufficient for this interaction.
|
46 |
15226417
|
While the point mutation in the Pitx-1 HD did not affect interaction with c-Jun, deletion of the HD eliminated the interaction.
|
47 |
15226417
|
Taken together, our studies indicate that Pitx-1 can direct transactivation of the mGnRHR gene, in part by DNA binding and in part by an action of Pitx-1 as a cofactor for AP-1, augmenting AP-1 activity through a novel protein-protein interaction between c-Jun and the HD of Pitx-1.
|
48 |
15226417
|
Essential role of the homeodomain for pituitary homeobox 1 activation of mouse gonadotropin-releasing hormone receptor gene expression through interactions with c-Jun and DNA.
|
49 |
15226417
|
Pituitary homeobox 1 (Pitx-1) has been shown to activate pituitary-specific gene expression by direct DNA binding and/or protein-protein interaction with other transcription factors.
|
50 |
15226417
|
We hypothesized that Pitx-1 might also dictate tissue-specific expression of the mouse GnRHR (mGnRHR) gene in a similar manner.
|
51 |
15226417
|
Pitx-1 activated the mGnRHR gene promoter, and transactivation was localized to sequences between -308 and -264.
|
52 |
15226417
|
This region includes an activating protein 1 (AP-1) site, which was previously shown to be important for mGnRHR gene expression.
|
53 |
15226417
|
Further characterization indicated that an intact AP-1 site was required for full Pitx-1 responsiveness.
|
54 |
15226417
|
Furthermore, Pitx-1 and AP-1 were synergistic in the activation of the mGnRHR gene promoter.
|
55 |
15226417
|
Pitx-1 interacted directly with c-Jun, and the HD was sufficient for this interaction.
|
56 |
15226417
|
While the point mutation in the Pitx-1 HD did not affect interaction with c-Jun, deletion of the HD eliminated the interaction.
|
57 |
15226417
|
Taken together, our studies indicate that Pitx-1 can direct transactivation of the mGnRHR gene, in part by DNA binding and in part by an action of Pitx-1 as a cofactor for AP-1, augmenting AP-1 activity through a novel protein-protein interaction between c-Jun and the HD of Pitx-1.
|
58 |
15226417
|
Essential role of the homeodomain for pituitary homeobox 1 activation of mouse gonadotropin-releasing hormone receptor gene expression through interactions with c-Jun and DNA.
|
59 |
15226417
|
Pituitary homeobox 1 (Pitx-1) has been shown to activate pituitary-specific gene expression by direct DNA binding and/or protein-protein interaction with other transcription factors.
|
60 |
15226417
|
We hypothesized that Pitx-1 might also dictate tissue-specific expression of the mouse GnRHR (mGnRHR) gene in a similar manner.
|
61 |
15226417
|
Pitx-1 activated the mGnRHR gene promoter, and transactivation was localized to sequences between -308 and -264.
|
62 |
15226417
|
This region includes an activating protein 1 (AP-1) site, which was previously shown to be important for mGnRHR gene expression.
|
63 |
15226417
|
Further characterization indicated that an intact AP-1 site was required for full Pitx-1 responsiveness.
|
64 |
15226417
|
Furthermore, Pitx-1 and AP-1 were synergistic in the activation of the mGnRHR gene promoter.
|
65 |
15226417
|
Pitx-1 interacted directly with c-Jun, and the HD was sufficient for this interaction.
|
66 |
15226417
|
While the point mutation in the Pitx-1 HD did not affect interaction with c-Jun, deletion of the HD eliminated the interaction.
|
67 |
15226417
|
Taken together, our studies indicate that Pitx-1 can direct transactivation of the mGnRHR gene, in part by DNA binding and in part by an action of Pitx-1 as a cofactor for AP-1, augmenting AP-1 activity through a novel protein-protein interaction between c-Jun and the HD of Pitx-1.
|
68 |
15226417
|
Essential role of the homeodomain for pituitary homeobox 1 activation of mouse gonadotropin-releasing hormone receptor gene expression through interactions with c-Jun and DNA.
|
69 |
15226417
|
Pituitary homeobox 1 (Pitx-1) has been shown to activate pituitary-specific gene expression by direct DNA binding and/or protein-protein interaction with other transcription factors.
|
70 |
15226417
|
We hypothesized that Pitx-1 might also dictate tissue-specific expression of the mouse GnRHR (mGnRHR) gene in a similar manner.
|
71 |
15226417
|
Pitx-1 activated the mGnRHR gene promoter, and transactivation was localized to sequences between -308 and -264.
|
72 |
15226417
|
This region includes an activating protein 1 (AP-1) site, which was previously shown to be important for mGnRHR gene expression.
|
73 |
15226417
|
Further characterization indicated that an intact AP-1 site was required for full Pitx-1 responsiveness.
|
74 |
15226417
|
Furthermore, Pitx-1 and AP-1 were synergistic in the activation of the mGnRHR gene promoter.
|
75 |
15226417
|
Pitx-1 interacted directly with c-Jun, and the HD was sufficient for this interaction.
|
76 |
15226417
|
While the point mutation in the Pitx-1 HD did not affect interaction with c-Jun, deletion of the HD eliminated the interaction.
|
77 |
15226417
|
Taken together, our studies indicate that Pitx-1 can direct transactivation of the mGnRHR gene, in part by DNA binding and in part by an action of Pitx-1 as a cofactor for AP-1, augmenting AP-1 activity through a novel protein-protein interaction between c-Jun and the HD of Pitx-1.
|
78 |
15226417
|
Essential role of the homeodomain for pituitary homeobox 1 activation of mouse gonadotropin-releasing hormone receptor gene expression through interactions with c-Jun and DNA.
|
79 |
15226417
|
Pituitary homeobox 1 (Pitx-1) has been shown to activate pituitary-specific gene expression by direct DNA binding and/or protein-protein interaction with other transcription factors.
|
80 |
15226417
|
We hypothesized that Pitx-1 might also dictate tissue-specific expression of the mouse GnRHR (mGnRHR) gene in a similar manner.
|
81 |
15226417
|
Pitx-1 activated the mGnRHR gene promoter, and transactivation was localized to sequences between -308 and -264.
|
82 |
15226417
|
This region includes an activating protein 1 (AP-1) site, which was previously shown to be important for mGnRHR gene expression.
|
83 |
15226417
|
Further characterization indicated that an intact AP-1 site was required for full Pitx-1 responsiveness.
|
84 |
15226417
|
Furthermore, Pitx-1 and AP-1 were synergistic in the activation of the mGnRHR gene promoter.
|
85 |
15226417
|
Pitx-1 interacted directly with c-Jun, and the HD was sufficient for this interaction.
|
86 |
15226417
|
While the point mutation in the Pitx-1 HD did not affect interaction with c-Jun, deletion of the HD eliminated the interaction.
|
87 |
15226417
|
Taken together, our studies indicate that Pitx-1 can direct transactivation of the mGnRHR gene, in part by DNA binding and in part by an action of Pitx-1 as a cofactor for AP-1, augmenting AP-1 activity through a novel protein-protein interaction between c-Jun and the HD of Pitx-1.
|
88 |
15232060
|
The FSH-beta and GnRH-receptor genes are up-regulated by pituitary activin and down-regulated by pituitary follistatin, and circulating inhibin disrupts this local regulation by functioning as an endogenous competitor of the activin receptor.
|
89 |
15232060
|
There is evidence that the intra-pituitary regulation of FSH-beta and GnRH-receptor gene expression may activate pubertal maturation in male rats.
|
90 |
15232060
|
The FSH-beta and GnRH-receptor genes are up-regulated by pituitary activin and down-regulated by pituitary follistatin, and circulating inhibin disrupts this local regulation by functioning as an endogenous competitor of the activin receptor.
|
91 |
15232060
|
There is evidence that the intra-pituitary regulation of FSH-beta and GnRH-receptor gene expression may activate pubertal maturation in male rats.
|
92 |
15319828
|
Inhibin, activin, and follistatin were first identified as gonadal hormones that could exert selective effects on follicle-stimulating hormone (FSH) secretion without affecting luteinizing hormone (LH).
|
93 |
15319828
|
Although the primary source of inhibin remains the gonad, both activin and follistatin are produced in extragonadal tissues and can exert effects on FSH through an autocrine-paracrine mechanism.
|
94 |
15319828
|
Second, activin up-regulates gonadotropin-releasing hormone receptor (GnRHR) gene expression, leading to alterations in the synthesis and release of both gonadotropins in response to GnRH.
|
95 |
15319828
|
Third, activin can stimulate GnRH release from GnRH neurons in the hypothalamus and thereby affect FSH and LH secretion.
|
96 |
15319828
|
Both inhibin and follistatin can negatively regulate these effects by preventing activin binding to the activin receptor at the cell membrane and blocking activation of downstream signal transduction pathways.
|
97 |
15319828
|
This review concentrates on the mechanisms through which inhibin, activin, and follistatin regulate the gonadotropins.
|
98 |
15319828
|
The mechanisms of inhibin and activin signaling are also reported, with particular attention to developments in our understanding of inhibin receptor action and activin-induced transcriptional regulation of the FSHbeta gene promoter.
|
99 |
17985235
|
Interactions between TNF and GnRH.
|
100 |
17985235
|
Tumour necrosis factor (TNF) ligand members and their associated TNF receptor (TNFR) superfamilies have many diverse physiological roles.
|
101 |
17985235
|
The cellular signalling machinery used by TNFRs to achieve their many cellular responses are discussed, as is the gonadotrophin-releasing hormone (GnRH) receptor signalling mechanisms.
|
102 |
17985235
|
These interactions between TNF, GnRH and gonadotrophs are discussed.
|
103 |
18463157
|
Idiopathic hypogonadotropic hypogonadism (IHH) and Kallmann syndrome (KS) are clinically and genetically heterogeneous disorders caused by a deficiency of gonadotrophin-releasing hormone (GnRH).
|
104 |
18463157
|
Mutations in three genes--KAL1, GNRHR and FGFR1--account for 15-20% of all causes of IHH/KS.
|
105 |
18463157
|
Fifty-four IHH/KS patients were studied for KAL1 deletions and 100 were studied for an autosomal panel of FGFR1, GNRH1, GNRHR, GPR54 and NELF gene deletions.
|
106 |
18463157
|
Our results indicate approximately 12% of KS males have KAL1 deletions, but intragenic deletions of the FGFR1, GNRH1, GNRHR, GPR54 and NELF genes are uncommon in IHH/KS.
|
107 |
18463157
|
Idiopathic hypogonadotropic hypogonadism (IHH) and Kallmann syndrome (KS) are clinically and genetically heterogeneous disorders caused by a deficiency of gonadotrophin-releasing hormone (GnRH).
|
108 |
18463157
|
Mutations in three genes--KAL1, GNRHR and FGFR1--account for 15-20% of all causes of IHH/KS.
|
109 |
18463157
|
Fifty-four IHH/KS patients were studied for KAL1 deletions and 100 were studied for an autosomal panel of FGFR1, GNRH1, GNRHR, GPR54 and NELF gene deletions.
|
110 |
18463157
|
Our results indicate approximately 12% of KS males have KAL1 deletions, but intragenic deletions of the FGFR1, GNRH1, GNRHR, GPR54 and NELF genes are uncommon in IHH/KS.
|
111 |
18463157
|
Idiopathic hypogonadotropic hypogonadism (IHH) and Kallmann syndrome (KS) are clinically and genetically heterogeneous disorders caused by a deficiency of gonadotrophin-releasing hormone (GnRH).
|
112 |
18463157
|
Mutations in three genes--KAL1, GNRHR and FGFR1--account for 15-20% of all causes of IHH/KS.
|
113 |
18463157
|
Fifty-four IHH/KS patients were studied for KAL1 deletions and 100 were studied for an autosomal panel of FGFR1, GNRH1, GNRHR, GPR54 and NELF gene deletions.
|
114 |
18463157
|
Our results indicate approximately 12% of KS males have KAL1 deletions, but intragenic deletions of the FGFR1, GNRH1, GNRHR, GPR54 and NELF genes are uncommon in IHH/KS.
|
115 |
18499748
|
The gonadotropin-releasing hormone (GnRH) neuronal population is normal in size and distribution in GnRH-deficient and GnRH receptor-mutant hypogonadal mice.
|
116 |
18499748
|
In addition to pituitary gonadotrope stimulation, activity of GnRH through its receptor (GnRHR) has been suggested to include autocrine regulation of the GnRH neuron.
|
117 |
18499748
|
Two hypogonadal mouse strains, the Gnrh1 mutant (hpg) mice and Gnrhr mutant mice were used to investigate the potential role of GnRH signaling in the proper development and maintenance of GnRH neurons.
|
118 |
18499748
|
Similarly, adult mice deficient in functional GnRHR possessed a full complement of GnRH neurons in the basal forebrain that was indistinguishable from the distribution of GnRH neurons in their wild-type counterparts.
|
119 |
18499748
|
The gonadotropin-releasing hormone (GnRH) neuronal population is normal in size and distribution in GnRH-deficient and GnRH receptor-mutant hypogonadal mice.
|
120 |
18499748
|
In addition to pituitary gonadotrope stimulation, activity of GnRH through its receptor (GnRHR) has been suggested to include autocrine regulation of the GnRH neuron.
|
121 |
18499748
|
Two hypogonadal mouse strains, the Gnrh1 mutant (hpg) mice and Gnrhr mutant mice were used to investigate the potential role of GnRH signaling in the proper development and maintenance of GnRH neurons.
|
122 |
18499748
|
Similarly, adult mice deficient in functional GnRHR possessed a full complement of GnRH neurons in the basal forebrain that was indistinguishable from the distribution of GnRH neurons in their wild-type counterparts.
|
123 |
18499748
|
The gonadotropin-releasing hormone (GnRH) neuronal population is normal in size and distribution in GnRH-deficient and GnRH receptor-mutant hypogonadal mice.
|
124 |
18499748
|
In addition to pituitary gonadotrope stimulation, activity of GnRH through its receptor (GnRHR) has been suggested to include autocrine regulation of the GnRH neuron.
|
125 |
18499748
|
Two hypogonadal mouse strains, the Gnrh1 mutant (hpg) mice and Gnrhr mutant mice were used to investigate the potential role of GnRH signaling in the proper development and maintenance of GnRH neurons.
|
126 |
18499748
|
Similarly, adult mice deficient in functional GnRHR possessed a full complement of GnRH neurons in the basal forebrain that was indistinguishable from the distribution of GnRH neurons in their wild-type counterparts.
|
127 |
18499748
|
The gonadotropin-releasing hormone (GnRH) neuronal population is normal in size and distribution in GnRH-deficient and GnRH receptor-mutant hypogonadal mice.
|
128 |
18499748
|
In addition to pituitary gonadotrope stimulation, activity of GnRH through its receptor (GnRHR) has been suggested to include autocrine regulation of the GnRH neuron.
|
129 |
18499748
|
Two hypogonadal mouse strains, the Gnrh1 mutant (hpg) mice and Gnrhr mutant mice were used to investigate the potential role of GnRH signaling in the proper development and maintenance of GnRH neurons.
|
130 |
18499748
|
Similarly, adult mice deficient in functional GnRHR possessed a full complement of GnRH neurons in the basal forebrain that was indistinguishable from the distribution of GnRH neurons in their wild-type counterparts.
|
131 |
19282386
|
The GnRH receptor (GnRHR) responds to pulsatile GnRH signals to coordinate pituitary gonadotropin synthesis and secretion.
|
132 |
19669946
|
Our experiment investigated the mRNA expression of intestinal gonadotropin-releasing hormone (GnRH), proglucagon (PG), and glucagon-like peptide 1 receptor (GLP-1R) in the jejunum, ileum, and colon of rats fed with high-fat diet and Goto-Kakizaki (GK) rats and revealed the physiological role of intestinal GnRH.
|
133 |
19669946
|
However, the GnRH receptor (GnRHR) and GLP-1R mRNA levels did not differ significantly between HCh and control.
|
134 |
19669946
|
The GnRH, PG, and GLP-1R mRNA levels in GK rats were lower, respectively, than those in control rats, while the GnRHR levels did not differ significantly between GK rats and control rats.
|
135 |
19669946
|
There were no difference in GnRH, PG, GnRHR, and GLP-1R mRNA levels in the ileum and colon tissue between HCh and control rats.
|
136 |
19669946
|
The GnRH mRNA levels of GK rats were lower than those in control rats; however, the PG, GLP-1R, and GnRHR levels did not differ significantly between GK and control rats.
|
137 |
19669946
|
The GnRH level in the jejunum showed a significant effect on blood glucose level, while the PG level in the jejunum showed a significant effect on insulin level.
|
138 |
19669946
|
This may imply that, compared with the ileum and colon, the jejunum had greater impact on glucose metabolism; furthermore, GnRH might interact with intestinal GLP-1 and GLP-2 through the paracrine and autocrine ways and then regulate glucose metabolism and insulin secretion.
|
139 |
19669946
|
Our experiment investigated the mRNA expression of intestinal gonadotropin-releasing hormone (GnRH), proglucagon (PG), and glucagon-like peptide 1 receptor (GLP-1R) in the jejunum, ileum, and colon of rats fed with high-fat diet and Goto-Kakizaki (GK) rats and revealed the physiological role of intestinal GnRH.
|
140 |
19669946
|
However, the GnRH receptor (GnRHR) and GLP-1R mRNA levels did not differ significantly between HCh and control.
|
141 |
19669946
|
The GnRH, PG, and GLP-1R mRNA levels in GK rats were lower, respectively, than those in control rats, while the GnRHR levels did not differ significantly between GK rats and control rats.
|
142 |
19669946
|
There were no difference in GnRH, PG, GnRHR, and GLP-1R mRNA levels in the ileum and colon tissue between HCh and control rats.
|
143 |
19669946
|
The GnRH mRNA levels of GK rats were lower than those in control rats; however, the PG, GLP-1R, and GnRHR levels did not differ significantly between GK and control rats.
|
144 |
19669946
|
The GnRH level in the jejunum showed a significant effect on blood glucose level, while the PG level in the jejunum showed a significant effect on insulin level.
|
145 |
19669946
|
This may imply that, compared with the ileum and colon, the jejunum had greater impact on glucose metabolism; furthermore, GnRH might interact with intestinal GLP-1 and GLP-2 through the paracrine and autocrine ways and then regulate glucose metabolism and insulin secretion.
|
146 |
19669946
|
Our experiment investigated the mRNA expression of intestinal gonadotropin-releasing hormone (GnRH), proglucagon (PG), and glucagon-like peptide 1 receptor (GLP-1R) in the jejunum, ileum, and colon of rats fed with high-fat diet and Goto-Kakizaki (GK) rats and revealed the physiological role of intestinal GnRH.
|
147 |
19669946
|
However, the GnRH receptor (GnRHR) and GLP-1R mRNA levels did not differ significantly between HCh and control.
|
148 |
19669946
|
The GnRH, PG, and GLP-1R mRNA levels in GK rats were lower, respectively, than those in control rats, while the GnRHR levels did not differ significantly between GK rats and control rats.
|
149 |
19669946
|
There were no difference in GnRH, PG, GnRHR, and GLP-1R mRNA levels in the ileum and colon tissue between HCh and control rats.
|
150 |
19669946
|
The GnRH mRNA levels of GK rats were lower than those in control rats; however, the PG, GLP-1R, and GnRHR levels did not differ significantly between GK and control rats.
|
151 |
19669946
|
The GnRH level in the jejunum showed a significant effect on blood glucose level, while the PG level in the jejunum showed a significant effect on insulin level.
|
152 |
19669946
|
This may imply that, compared with the ileum and colon, the jejunum had greater impact on glucose metabolism; furthermore, GnRH might interact with intestinal GLP-1 and GLP-2 through the paracrine and autocrine ways and then regulate glucose metabolism and insulin secretion.
|
153 |
19669946
|
Our experiment investigated the mRNA expression of intestinal gonadotropin-releasing hormone (GnRH), proglucagon (PG), and glucagon-like peptide 1 receptor (GLP-1R) in the jejunum, ileum, and colon of rats fed with high-fat diet and Goto-Kakizaki (GK) rats and revealed the physiological role of intestinal GnRH.
|
154 |
19669946
|
However, the GnRH receptor (GnRHR) and GLP-1R mRNA levels did not differ significantly between HCh and control.
|
155 |
19669946
|
The GnRH, PG, and GLP-1R mRNA levels in GK rats were lower, respectively, than those in control rats, while the GnRHR levels did not differ significantly between GK rats and control rats.
|
156 |
19669946
|
There were no difference in GnRH, PG, GnRHR, and GLP-1R mRNA levels in the ileum and colon tissue between HCh and control rats.
|
157 |
19669946
|
The GnRH mRNA levels of GK rats were lower than those in control rats; however, the PG, GLP-1R, and GnRHR levels did not differ significantly between GK and control rats.
|
158 |
19669946
|
The GnRH level in the jejunum showed a significant effect on blood glucose level, while the PG level in the jejunum showed a significant effect on insulin level.
|
159 |
19669946
|
This may imply that, compared with the ileum and colon, the jejunum had greater impact on glucose metabolism; furthermore, GnRH might interact with intestinal GLP-1 and GLP-2 through the paracrine and autocrine ways and then regulate glucose metabolism and insulin secretion.
|
160 |
21191111
|
PACAP increases alpha-subunit (Cga) and Lhb mRNAs, and it stimulates the transcription of follistatin (Fst) that, in turn, restrains activin signaling to repress Fshb and gonadotropin-releasing hormone-receptor (Gnrhr) expression as well as other activin-responsive genes.
|
161 |
21191111
|
At birth, pituitary PACAP declines and pituitary follistatin levels decrease, which together with increased gonadotropin-releasing hormone secretion allow Gnrhr and Fshb to increase and facilitate activation of the newborn gonads.
|
162 |
21191111
|
Changes in Adcyap1 expression levels in the adult pituitary may contribute to the selective rise in follicle-stimulating hormone (FSH) from age 20-30 days to the midcycle surge and to the secondary increase in FSH that occurs before estrus.
|
163 |
21191111
|
PACAP increases alpha-subunit (Cga) and Lhb mRNAs, and it stimulates the transcription of follistatin (Fst) that, in turn, restrains activin signaling to repress Fshb and gonadotropin-releasing hormone-receptor (Gnrhr) expression as well as other activin-responsive genes.
|
164 |
21191111
|
At birth, pituitary PACAP declines and pituitary follistatin levels decrease, which together with increased gonadotropin-releasing hormone secretion allow Gnrhr and Fshb to increase and facilitate activation of the newborn gonads.
|
165 |
21191111
|
Changes in Adcyap1 expression levels in the adult pituitary may contribute to the selective rise in follicle-stimulating hormone (FSH) from age 20-30 days to the midcycle surge and to the secondary increase in FSH that occurs before estrus.
|