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Ja-Young Kim, Esther van de Wall, Mathieu Laplante, Anthony Azzara, Maria E. Trujillo, Susanna M. Hofmann, Todd Schraw, Jorge L. Durand, Hua Li, Guangyu Li, Linda A. Jelicks, Mark F. Mehler, David Y. Hui, Yves Deshaies, Gerald I. Shulman, Gary J. Schwartz, Philipp E. Scherer
J Clin Invest. 2007;
117(9):2621
doi:10.1172/JCI31021
Abstract |
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E
xcess caloric intake can lead to insulin resistance. The underlying reasons are
complex but likely related to ectopic lipid deposition in nonadipose tissue. We
hypothesized that the inability to appropriately expand subcutaneous adipose tissue
may be an underlying reason for insulin resistance and β cell failure.
Mice lacking leptin while overexpressing adiponectin showed normalized glucose and
insulin levels and dramatically improved glucose as well as positively affected
serum triglyceride levels. Therefore, modestly increasing the levels of circulating
full-length adiponectin completely rescued the diabetic phenotype in
ob/ob mice. They displayed increased expression of
PPARγ target genes and a reduction in macrophage infiltration in adipose
tissue and systemic inflammation. As a result, the transgenic mice were morbidly
obese, with significantly higher levels of adipose tissue than their
ob/ob littermates, leading to an interesting dichotomy of
increased fat mass associated with improvement in insulin sensitivity. Based on
these data, we propose that adiponectin acts as a peripheral
“starvation” signal promoting the storage of triglycerides
preferentially in adipose tissue. As a consequence, reduced triglyceride levels in
the liver and muscle convey improved systemic insulin sensitivity. These mice
therefore represent what we believe is a novel model of morbid obesity associated
with an improved metabolic profile.
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