Since the discovery of the satiety factor leptin, it has been clear that fat should be regarded not solely as a storage site for lipids, but also as an endocrine tissue. The discovery of resistin and Acrp30 extended this finding and showed that multiple hormones secreted by adipocytes can profoundly alter energy metabolism in various tissues. Here, Combs and colleagues elucidate the primary metabolic effect of the latter hormone, also known as adiponectin. From earlier work, it appears that Acrp30 can sensitize animals to insulin?s effects on the liver and muscle; Combs et al. now find that when healthy mice are maintained for short periods at constant blood glucose and insulin levels, the presence of exogenous Acrp30 decreases hepatic glucose production. In particular, the authors show that glucose-6-phosphatase (G6Pase), an enzyme critical for hepatic glucose release, is less active in animals treated with exogenous Acrp30. At least during the 90-minute test period, this hormone has no appreciable effect on other aspects of energy metabolism, such as the rate of glucose consumption. Interestingly, Combs et al. show that mRNAs for G6Pase and a related gluconeogenic enzyme decline in the liver of Acrp30-treated animals. However, the effect on G6Pase activity seen in their physiological measurements probably occurs too quickly to be explained by a suppression of G6Pase transcription. Rather, this observation hints that Acrp30 exerts additional, long-term effects on energy metabolism by altering patterns of gene expression in the liver, and possibly in other target tissues as well.

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Contact: John Ashkenas
scied@the-jci.org
416-946-7593
Journal of Clinical Investigation
12-Dec-2001

Page: 1
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