A compound found in red wine, grapes and other fruits, and similar in structure to resveratrol, is able to block cellular processes that allow fat cells to develop, opening a door to a potential method to control obesity, according to a Purdue University study.
While similar in structure to resveratrol — the compound found in red wine, grapes and peanuts that is thought to combat cancer, heart disease and neurodegenerative diseases — piceatannol might be an important weapon against obesity. Resveratrol is converted to piceatannol in humans after consumption.
“Piceatannol actually alters the timing of gene expressions, gene functions and insulin action during adipogenesis, the process in which early stage fat cells become mature fat cells,” Kim said. “In the presence of piceatannol, you can see delay or complete inhibition of adipogenesis.”
Over a period of 10 days or more, immature fat cells, called preadipocytes, go through several stages to become mature fat cells, or adipocytes.
“These precursor cells, even though they have not accumulated lipids, have the potential to become fat cells,” Kim said. “We consider that adipogenesis is an important molecular target to delay or prevent fat cell accumulation and, hopefully, body fat mass gain.”
Kim found that piceatannol binds to insulin receptors of immature fat cells in the first stage of adipogenesis, blocking insulin’s ability to control cell cycles and activate genes that carry out further stages of fat cell formation. Piceatannol essentially blocks the pathways necessary for immature fat cells to mature and grow.
Piceatannol is one of several compounds being studied in Kim’s laboratory for its health benefits, and it is also present in different amounts in red grape seeds and skin, blueberries, passion fruit, and other fruits.
Kim would like to confirm his current finding, which is based on a cell culture system, using an animal model of obesity. His future work would also include determining methods for protecting piceatannol from degrading so that concentrations large enough would be available in the bloodstream to stop adipogenesis or body fat gain.
“We need to work on improving the stability and solubility of piceatannol to create a biological effect,” Kim said.
The Purdue Research Foundation funded the work.
Story Source:
The above story is reprinted from materials provided by Purdue University. The original article was written by Brian Wallheimer.
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Journal Reference:
- J. Y. Kwon, S. G. Seo, Y.-S. Heo, S. Yue, J.-X. Cheng, K. W. Lee, K.-H. Kim. Piceatannol, Natural Polyphenolic Stilbene, Inhibits Adipogenesis via Modulation of Mitotic Clonal Expansion and Insulin Receptor-dependent Insulin Signaling in Early Phase of Differentiation. Journal of Biological Chemistry, 2012; 287 (14): 11566 DOI: 10.1074/jbc.M111.259721
Fitoterapia. 2009 Oct 25. [Epub ahead of print]
Berberine inhibits adipogenesis in high-fat diet-induced obesity mice.
Department of Pharmaceutical Sciences, College of Pharmacy, South Dakota State University, Brookings, SD 57007, USA.
Our previous studies illustrated that berberine inhibited adipogenesis in murine-derived 3T3-L1 preadipocytes and human white preadipocytes. In this study, the effects of berberine on the adipogenesis of high-fat diet-induced obesity (FD) or normal diet (ND) mice and possible transcriptional impact are investigated. The results demonstrated that in FD mice, berberine reduced mouse weight gain and food intake and serum glucose, triglyceride, and total cholesterol levels accompanied with a down-regulation of PPARgamma expression and an up-regulation of GATA-3 expression. Berberine had no adverse effects on ND mice. These encouraging findings suggest that berberine has excellent pharmacological potential to prevent obesity.
PMID: 19861153
Our previous studies illustrated that berberine inhibited adipogenesis in murine-derived 3T3-L1 preadipocytes and human white preadipocytes.
The results demonstrated that in FD mice, berberine reduced mouse weight gain and food intake and serum glucose, triglyceride, and total cholesterol levels accompanied with a down-regulation of PPARgamma expression and an up-regulation of GATA-3 expression.
