Preparing your results

Our searching services are busy right now. Your search will reload in five seconds.

X
Forgot Password

If you have forgotten your password you can enter your email here and get a temporary password sent to your email.

Growth hormone receptor regulates β cell hyperplasia and glucose-stimulated insulin secretion in obese mice.

http://www.ncbi.nlm.nih.gov/pubmed/21555853

Insulin, growth hormone (GH), and insulin-like growth factor-1 (IGF-1) play key roles in the regulation of β cell growth and function. Although β cells express the GH receptor, the direct effects of GH on β cells remain largely unknown. Here we have employed a rat insulin II promoter-driven (RIP-driven) Cre recombinase to disrupt the GH receptor in β cells (βGHRKO). βGHRKO mice fed a standard chow diet exhibited impaired glucose-stimulated insulin secretion but had no changes in β cell mass. When challenged with a high-fat diet, βGHRKO mice showed evidence of a β cell secretory defect, with further deterioration of glucose homeostasis indicated by their altered glucose tolerance and blunted glucose-stimulated insulin secretion. Interestingly, βGHRKO mice were impaired in β cell hyperplasia in response to a high-fat diet, with decreased β cell proliferation and overall reduced β cell mass. Therefore, GH receptor plays critical roles in glucose-stimulated insulin secretion and β cell compensation in response to a high-fat diet.

Pubmed ID: 21555853 RIS Download

Mesh terms: Animal Feed | Animals | Cell Division | Dietary Fats | Female | Gene Knockdown Techniques | Glucose | Glucose Intolerance | Hyperplasia | Insulin | Islets of Langerhans | Male | Mice | Mice, Inbred C57BL | Mice, Knockout | Mice, Transgenic | Obesity | Organ Specificity | Rats | Receptors, Somatotropin | STAT5 Transcription Factor

Research resources used in this publication

None found

Research tools detected in this publication

None found

Data used in this publication

None found

Associated grants

  • Agency: NIDDK NIH HHS, Id: P60 DK020541

Publication data is provided by the National Library of Medicine ® and PubMed ®. Data is retrieved from PubMed ® on a weekly schedule. For terms and conditions see the National Library of Medicine Terms and Conditions.