Fat can not only be unsightly, but if it’s sitting on your belly, may also contribute to overproduction of signaling hormones called adipokines, which are linked to metabolic changes that can worsen health.
New research from Aarhus University has found that abdominal adipose tissue extracted from overweight adults, and then exposed to resveratrol, exhibited reduced adipokine production. According to these authors, “small interfering molecules such as resveratrol are, in this matter, hypothesized to possess beneficial effects and might improve the metabolic profile in human obesity.”
The scientists obtained the abdominal adipose tissue via liposuction from seven women and one man, ages 43-55, who had body mass indexes categorized as overweight. All subjects were Caucasian, healthy and not on any medication that could confound the results.
Because previous studies in rodents have shown that calorie restriction reduces production of adipokines by activating an enzyme called Sirtuin 1, the scientists had hypothesized that resveratrol may act similarly. Resveratrol is well-known as a potent Sirtuin 1 activator.
This most recent in vitro study, published in International Journal of Obesity, suggests that regular dietary intake of resveratrol may guard against the metabolic changes that occur when there is excess fat on the body – as it has with rodents and monkeys.
Resveratrol is a phytoalexin (a plant-produced antimicrobial substance) found in small amounts, most notably, in red wine, as well as in other common foods such as grapes, peanuts, and chocolate. The most concentrated natural source is the Japanese Knotweed (Polyganum cuspidatum).
Resveratrol gained scientific interest after it demonstrated effects similar to calorie restriction in slowing the rate of aging and increasing the lifespan in a number of species including nematode worms, mice, and rhesus monkeys. In addition, resveratrol protects overfed mice from weight gain and lemurs from seasonal weight gain.
Source: Olholm J, Paulsen SK, Cullberg KB, Richelsen B, Pedersen SB. Int J Obes (Lond) 2010;34:1546-53.