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

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


  • Wu Y
  • Liu C
  • Sun H
  • Vijayakumar A
  • Giglou PR
  • Qiao R
  • Oppenheimer J
  • Yakar S
  • LeRoith D


The Journal of clinical investigation

Publication Data

June 2, 2011

Associated Grants

  • Agency: NIDDK NIH HHS, Id: P60 DK020541

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