Resveratrol suppresses body mass gain in a seasonal non-human primate model of obesity

Resveratrol reduced the seasonal body-mass gain by concomitantly decreasing energy intake by 13% and increasing resting metabolic rate by 29%. Resveratrol supplementation inhibited the depth of daily torpor, an important energy-saving process in this primate. The daily amount of locomotor activity remained unchanged. Except for an increase in the glucose-dependent insulinotropic polypeptide, a gut hormone known to promote mobilization of fat stores, no major change in satiety hormone plasma levels was observed under resveratrol supplementation.These results suggest that in a non-human primate, resveratrol reduces body-mass gain by increasing satiety and resting metabolic rate, and by inhibiting torpor expression. The measured anorectic gut hormones did not seem to play a major role in these observations.Obesity stems from a prolonged imbalance between the level of energy intake and energy expenditure, with the resultant surplus being stored as lipids predominantly in adipose tissue, but also in muscle and liver tissue, triggering features of the metabolic syndrome. Understanding the factors which regulate both energy intake and expenditure, such as environmental/lifestyle manipulations or pharmaceuticals, is an important step towards developing obesity treatments.The physiological benefits of resveratrol (3,4',5-trihydroxystilbene or RSV), a natural polyphenol, are currently under intensive investigation. Resveratrol is produced by plants in response to infection by the pathogen Botrytis cinerea [1]. It is also induced in response to a variety of stress conditions (climate, exposure to ozone, sunlight and heavy metals) [2]. Presently, it has been detected in more than 70 plant species, including grapes, peanuts, berries and pines [2]. Resveratrol is able to activate nicotinamide adenosine dinucleotide-dependent deacetylase SIRT1 (Silent mating type Information Regulation 2 homologue Type 1), one of the seven mammalian sirtuins [3,4] involved in glucose homeostasis a