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Effect of Naringin on Obesity

Obesity can be defined as increased energy intake compared with energy expenditure, which ultimately results in fat deposition and weight gain. According to the guidelines from the WHO, overweight in adults is defined as a BMI of 25.0–29.9 kg/m2, and obesity is defined as a BMI of ≥30.0 kg/m2 . High body fat also increases the risk of several diseases such as diabetes, hyperlipidemia, and hypertension, which leads to arteriosclerotic disease and metabolic syndrome . Body weight gain, fat accumulation, and the development of hyperlipidemia, hyperglycemia, and insulin resistance were significantly suppressed by lemon polyphenols in mice fed a high-fat diet . Lemon polyphenols suppressed diet-induced obesity by upregulation of mRNA levels of the enzymes involved in β-oxidation, such as peroxisome proliferator activated receptor (PPAR) α, acyl-CoA oxidase, FA synthase in liver, and white adipose tissue in mice . Naringenin supplementation (0.003%, 0.006%, and 0.012% of the diet for 6 wk) lowered adiposity and TG contents in parametrial adipose tissue in rats . Naringenin-fed animals had a significant increase in PPARα, carnitine palmitoyltransferase 1 (CPT-1), and uncoupling protein 2 (UCP-2) expression in the liver, which might be responsible for the reduction in adiposity in rats .

Adipocyte differentiation is a key regulatory step in fat deposition in adipose tissues. Naringenin promoted gene expression and adiponectin protein secretion from 3T3-L1 adipocytes . Naringenin may be useful for ameliorating the inflammatory changes in obese adipose tissue. It was suggested that adipose tissue–derived MCP-1, which exhibits chemotactic properties in inflammatory cells, is the key factor for inducing macrophage infiltration into adipose tissue . MCP-1 from hypertrophic adipocytes in obese adipose tissue can also trigger macrophage infiltration into adipose tissue and subsequently activates macrophages to release inflammatory mediators such as TNF-α . Naringenin inhibited the production of TNF-α, MCP-1, and nitric oxide  in a dose-dependent manner in RAW264 macrophages and coculture of 3T3-L1 adipocytes and RAW264 macrophages stimulated by LPS .

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