Abstract
Obesity is increasing worldwide and closely associated with diabetes, abnormal lipid levels, hypertension and other diseases. Melanocortin 4 Receptor (Mc4R) deficiency is the most common monogenic form of obesity. It is estimated that 5% of extremely obese patients have loss‐of‐function mutations of Mc4R. The goal of this project was to determine how Mc4R affects energy homeostasis and diseases associated with obesity. It was hypothesized that a disruption of Mc4R signaling leads to obesity and its associated diseases. Metabolic parameters were compared between normal and Mc4R KO mice. Both genotypes were weaned on standard rodent chow. Food intake was weighed and body composition measured using Nuclear Magnetic Resonance, NMR. At 6 weeks, mice were euthanized and blood was harvested and centrifuged for serum chemistry analysis. Data were analyzed using t test or ANOVA. We found a significant increase in food intake and body weight, in Mc4R deficient mice. There was a mild difference in serum lipid levels suggesting that this model of obesity has a greater adverse impact on glucose homeostasis than lipid metabolism.
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