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Suppression of FAT/CD36 mRNA by human growth hormone in pancreatic β-cells

Louise T Dalgaard1, Peter Thams, Louise W Gaarn

  • 1Department of Biomedical Sciences, University of Copenhagen, Copenhagen, Denmark. ltd@ruc.dk

Biochemical and Biophysical Research Communications
|June 18, 2011
PubMed

Insights

Human growth hormone (hGH) protects pancreatic beta cells from fatty acid damage by reducing FAT/CD36. This improves insulin secretion, offering a potential therapeutic strategy for type 2 diabetes.

Area of Science:

  • Endocrinology
  • Molecular Biology
  • Diabetes Research

Background:

  • Fatty acid-induced damage to pancreatic beta cells contributes to type 2 diabetes.
  • Lactogens, including human growth hormone (hGH), enhance beta cell survival through STAT5 activation, but their specific molecular targets remain unclear.

Purpose of the Study:

  • To investigate the impact of hGH on the expression of fatty acid transport and binding proteins in pancreatic beta cells.
  • To correlate these changes with beta cell survival following fatty acid exposure.

Main Methods:

  • Quantitative analysis of mRNA levels for various fatty acid-related proteins.
  • RNA interference (RNAi) to target FAT/CD36.
  • Manipulation of STAT5 signaling pathways (constitutively active and dominant-negative forms).
  • Measurement of palmitate uptake and insulin secretion.

Main Results:

  • hGH significantly reduced mRNA levels of FAT/CD36 but did not affect GPR40, FASN, FABP2, FATP1, or FATP4.
  • Silencing FAT/CD36 using RNAi decreased fatty acid-induced apoptosis.
  • STAT5 activation mimicked hGH's effect on FAT/CD36, but STAT5 inhibition did not block hGH's action, suggesting indirect STAT5 involvement.
  • hGH-induced reduction in FAT/CD36 correlated with decreased palmitate uptake and improved glucose-stimulated insulin secretion.

Conclusions:

  • hGH protects pancreatic beta cells from fatty acid-induced damage by downregulating FAT/CD36 expression.
  • This mechanism involves reduced fatty acid uptake and improved insulin secretion, suggesting a protective role for hGH in diabetes.

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