High fat diet-induced obesity modifies the methylation pattern of leptin promoter in rats

• Published in: Journal of physiology and biochemistry 2009-03, Vol.65 (1), p.1-9
• Main Authors: Milagro, F. I., Campión, J., García-Díaz, D. F., Goyenechea, E., Paternain, L., Martínez, J. A.
• Format: Article
• Language: English
• Subjects: Animal Physiology; Animals; Biomedical and Life Sciences; Biomedicine; CpG Islands - genetics; Dietary Fats - pharmacology; DNA Methylation - drug effects; Human Physiology; Leptin - genetics; Male; Obesity - chemically induced; Obesity - genetics; Obesity - metabolism; Promoter Regions, Genetic - genetics; Rats; Rats, Wistar
• ISSN: 1138-7548; 1877-8755
• DOI: 10.1007/BF03165964

Leptin is an adipokine involved in body weight and food intake regulation whose promoter region presents CpG islands that could be subject to dynamic methylation. This methylation process could be affected by environmental (e.g. diet) or endogenous (e.g., adipocyte differentiation, inflammation, hypoxia) factors, and could influence adipocyte leptin gene expression. The aim of this article was to study whether a high-energy diet may affect leptin gene promoter methylation in rats. A group of eleven male Wistar rats were assigned into two dietary groups, one fed on a control diet for 11 weeks and the other on a high-fat cafeteria diet. Rats fed a high-energy diet become overweight and hyperleptin emic as compared to the controls. DNA isolated from retroperitoneal adipocytes was treated with bisulfite and a distal portion of leptin promoter (from −694 to −372 bp) including 13 CpG sites was amplified by PCR and sequenced. The studied promoter portion was slightly more methylated in the cafeteria-fed animals, which was statistically significant (p