Adiponectin increases insulin content and cell proliferation in MIN6 cells via PPAR gamma-dependent and PPAR gamma-independent mechanisms

Rao, J. R., Keating, D. J., Chen, C. and Parkington, H. C. (2012) Adiponectin increases insulin content and cell proliferation in MIN6 cells via PPAR gamma-dependent and PPAR gamma-independent mechanisms. Diabetes Obesity & Metabolism, 14 11: 983-989.


Author Rao, J. R.
Keating, D. J.
Chen, C.
Parkington, H. C.
Title Adiponectin increases insulin content and cell proliferation in MIN6 cells via PPAR gamma-dependent and PPAR gamma-independent mechanisms
Journal name Diabetes Obesity & Metabolism  (ERA 2012 Listed)    (ERA 2010 Rank B)   Check publisher's open access policy
Publication date 2012-11
Sub-type Article
DOI 10.1111/j.1463-1326.2012.01626.x
Volume number 14
Issue number 11
ISSN 1462-8902; 1463-1326
Start page 983
End page 989
Total pages 7
Place of publication Chichester, West Sussex, United Kingdom
Publisher Wiley-Blackwell
Collection year 2013
Language eng
Formatted abstract Aims: Adiponectin is an important adipokine whose levels are decreased in obesity despite increases in adipocyte mass. Studies in animal models implicate adiponectin as an insulin sensitizer in skeletal muscle and liver. Thiazolidinediones (TZDs) are insulin sensitizers and ligands for peroxisome proliferator-activated γ receptors (PPARγ) and these receptors are expressed in β cells where their activation promotes cell survival. We hypothesize that adiponectin promotes β cell survival by activating PPARγ.

Methods: We used MIN6 cells to investigate the effect of adiponectin on PPARγ expression, β-cell proliferation, insulin synthesis and insulin secretion.

Results: We demonstrate that MIN6 cells contain adiponectin receptors and that adiponectin activates PPARγ mRNA and protein expression. This increase in PPARγ expression is blocked by the PPARγ antagonist, GW9662, indicating a transcriptional feedback loop involving PPARγ activation of itself. Adiponectin causes a significant increase in insulin content and secretion and this occurs also via PPARγ activation due to the inhibitory effect of GW9662. Adiponectin also promotes MIN6 cell proliferation, however, this effect is independent of PPARγ activation.

Conclusions: Our results identify novel roles for the adipokine, adiponectin, in β-cells function. Adiponectin upregulates PPARγ expression, insulin content and insulin secretion through PPARγ-dependent mechanisms. Reductions in circulating adiponectin levels in obese individuals could therefore result in negative effects on β-cell function and this may have direct relevance to β-cell dysfunction in type 2 diabetes.
Keyword Adiponectin
MIN6 cells
PPARĪ³
Q-Index Code C1
Q-Index Status Confirmed Code
Institutional Status UQ
Additional Notes Article first published online: 7 June 2012.

Document type: Journal Article
Sub-type: Article
Collections: Official 2013 Collection
School of Biomedical Sciences Publications
 
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