AICAR prevents fat gain following the cessation of voluntary physical activity

Abstract

The transition from physical activity to inactivity is associated with drastic increases in 'catch-up' fat that in turn foster the development of many obesity-associated maladies. We tested if 5-Aminoimidazole-4-carboxamide ribonucleotide (AICAR) treatment would prevent gains in body fat following the sudden transition from a physically active state to an inactive state by locking a voluntary running wheel. Male, Wistar rats were either sedentary (SED), or given wheel access for 4 weeks, at which time rats with wheels continued running (RUN), either had their wheel locked (WL), or had WL with daily AICAR injection (WL + AICAR) for 1 week. RUN and WL + AICAR prevented gains in body fat compared to SED and WL (P < 0.001). Cyclin A1 mRNA, a marker of cell proliferation, was decreased in omental (OMAT), but not subcutaneous (SAT) adipose tissue, in RUN and WL + AICAR compared to SED and WL (P < 0.05). Both cyclin A1 mRNA and protein positively associated with gains in fat mass (P < 0.05). Cyclin A1 mRNA in OMAT, but not SAT, negatively correlated with p-AMPK levels (P < 0.05). Differences in fat gain and OMAT mRNA and protein levels were independent of changes in food intake and in differences in select hypothalamic mRNAs. These findings suggest that AICAR treatment prevents acute gains in adipose tissue following physical inactivity to levels of rats that continuously run, and that together continuous physical activity and AICAR could, at least initially under these conditions, exert similar inhibitory effects on adipogenesis in a depot-specific manner.

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