Nicotinamide adenine dinucleotide (NAD)+ precursors, such as nicotinamide, activate sirtuins and enhance energy metabolism. The aim of this study was to evaluate the metabolic effects of nicotinamide in ovariectomized (OVX) female rats to establish molecular targets against obesity, which support the safe therapeutic application of nicotinamide. The OVX animals were divided into groups: SHAM, SHAMn (15 days of 35 mg/kg nicotinamide, by gavage), OVX, and OVXn. The results indicated that nicotinamide favored lipolysis, as evidenced by an increase in free fatty acid and hepatic triglyceride levels, which were not fully normalized during the treatment period. The lipolysis appeared to be due to increased SIRT1 and mitochondrial oxidative phosphorylation in muscle and adipose tissue. There were decreases in muscle and fat NNMT (nicotinamide N-methyltransferase), which were associated with decreases in weight and triglyceride, LDL-c, and total cholesterol content. Nicotinamide appeared to be beneficial for the glycemic profile, with normal hepatic glycogen storage and a tendency towards insulin sensitivity in the OVXn. In the SHAMn, nicotinamide led to glucose intolerance, together with reduced muscle expressions of NAMPT (nicotinamide phosphoribosyltransferase) and SIRT3, suggesting that there were no short-term benefits. Supplementation with nicotinamide led to tissue-specific adaptive lipid and molecular changes in OVX rats.
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