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Tracy Hampton, PhD

JAMA. 2007;298:1506.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

A novel model of morbid obesity associated with an improved metabolic profile may help explain why not all obese people are diabetic, according to a study led by scientists at the University of Texas Southwestern Medical Center, in Dallas (Kim JY et al. J Clin Invest. doi:10.1172/jci31021 [published online ahead of print August 23, 2007]). The study found that obese mice with an abundance of the hormone adiponectin and a lack of another hormone, leptin, do not develop insulin resistance. While adiponectin controls sensitivity to insulin, leptin curbs appetite.

Noting the interesting dichotomy of increased fat mass occurring alongside improved insulin sensitivity in these transgenic mice, the investigators 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 lead to improved systemic insulin sensitivity.

The study's results . . . [Full Text of this Article]