Effect of Resveratrol on Mitochondrial Activity in Differentiated Mature Adipocytes

• Published in: International journal of morphology 2015-09, Vol.33 (3), p.1085-1092
• Main Authors: Noriega-González, J. E, Chirino, Y. I, Mata-Miranda, M. M, Vázquez-Zapién, G. J, Sánchez-Monroy, V
• Format: Article
• Language: English
• Subjects: ANATOMY & MORPHOLOGY
• ISSN: 0717-9502; 0717-9502
• DOI: 10.4067/S0717-95022015000300044

Obesity has reached epidemic proportions, the World Health Organization (WHO) estimates that there are more than 1,000 million overweight adults world-wide. Furthermore, obesity is characterized as an overgrowth of white adipose tissue as a result of adipocyte hypertrophy and hyperplasia. Mitochondria is considered the source of energy within the adipocyte, since it contains the molecular machinery, and it is involved in a large number of metabolic pathways, besides the transformation of chemical energy into adenosine triphosphate. Mitochondria shortage and adipocyte dysfunction result in an excessive accumulation of triacylglycerol in the cytoplasm, which determines an imbalance between energy production and energy expenditure. Resveratrol (RSV) is a polyphenol found in different plants and its effects have been associated with mitochondrial biogenesis. An adipogenesis in vitro model (3T3-L1 preadipocytes) was used, and these cells were differentiated into mature adipocytes. Subsequently the effect of RSV on the adipocytes morphology, the lipid content and mitochondrial activity was evaluated using microscopic and flow cytometry techniques. The effect of RSV on differentiated mature adipocytes, was characterized by the decrease in lipid content and the consequently declination of the mitochondrial activity. 3T3-L1 preadipocytes retained the differentiation ability until passage 18. The RSV at doses of 25 and 50 µM for 48 hours in differentiated mature adipocytes promoted the decreased in lipid content probably due to an increase in mitochondrial activity in the early hours of RSV exposure, causing the consequently declination of mitochondrial activity at the end of 48 hours.