Resveratrol stimulates release of adiponectin; a hormone involved with weight (fat) loss, liver protection, and decreased risk of metabolic syndrome
There are several hormones and neurotransmitters that have noteworthy effects on appetite and eating behavior, and as a result are of much interest with respect to weight gain (or loss) and obesity. The hormone adiponectin is produced exclusively in adipose tissue, i.e. fat, and hence the name. Unsurprisingly, adiponectin is involved in a number of metabolic processes, such as glucose regulation and the metabolism (burning) of fat for energy production. Levels of adiponectin are inversely correlated with body fat percentage; the greater the percentage of body fat - the lower the level adiponectin. The hormone plays a role in the suppression of the metabolic derangements that may result in type 2 diabetes, obesity, atherosclerosis, non-alcoholic fatty liver disease and having a low level is an independent risk factor for developing metabolic syndrome.
Researchers at the University of Pennsylvania School of Medicine have established in an animal model that the hormone adiponectin secreted by fat tissue acts in the brain to reduce body weight. Adiponectin can cause weight loss by raising metabolic rate while not affecting appetite. When adiponectin, which is involved in glucose and lipid metabolism, was introduced into the cerebrospinal fluid of normal mice, they showed no changes in food intake, but their metabolism rose. "The animal burns off more calories, so over time loses weight," explains [lead author Rexford] Ahima. From just about the same time researchers found high levels of adiponectin in human milk; this might explain the known association between breastfeeding and reduced risk of obesity later in life.
In this new study researchers from the University of Texas Health Science Center at San Antonio used Resveratrol on adipocytes (fat cells used in research known as 3T3-L1). Resveratrol improved the level of adiponectin in the fat cells. Generally Resveratrol is thought to work through effects on a life extending enzyme known as SIRT1 but in this case it worked because it stimulated FOXO1 activity. FOXO1 is involved with carbohydrate metabolism, insulin activity, and longevity. The study is published online ahead of print in the October 27th, 2010 edition of the Journal of Biological Chemistry.