Obesity is associated with metabolic disorders, especially hyperlipidemia, nonalcoholic fatty liver disease (NAFLD), insulin resistance, and type 2 diabetes mellitus. It is at present considered a serious worldwide health risk factor, both for adults and children, and hence represents a serious burden on health care systems. The genesis of obesity is multifactorial, and dysregulated lipid and glucose metabolism in metabolic organs is thought to be a critical factor. An abundance of recent research has reported that energy expenditure (EE) is an important factor in metabolic control of the development of obesity, and that targeting brown adipose tissue (BAT) and skeletal muscle is a promising approach to protect against obesity and its complications in light of their role as thermogenic organs.

Most of the studies to date have indicated that certain flavonoids have beneficial effects on obesity and its related diseases such as dyslipidemia, NAFLD, and type 2 diabetes mellitus. Eriocitrin (EC, eriodictyol 7-O-β-rutinoside) is an abundant flavonoid in lemons, and its structure is very similar to hesperidin, which has activity against several types of cancer including liver cancer. Recent studies have demonstrated that EC also has antioxidant and antitumor activities, a lipid-lowering effect, and that it improves diet-induced hepatic steatosis. Hyperlipidemia and NAFLD are common in obese individuals, and thus we speculated that EC may also have anti-obesity activity. However, the effect of EC on obesity is yet to be elucidated, and the detailed mechanisms by which EC affects the anti-metabolic syndrome are still not understood.

Eriocitrin (EC) is an abundant flavonoid in lemons, which is known as a strong antioxidant agent. This study investigated the biological and molecular mechanisms underlying the anti-obesity effect of EC in high-fat diet (HFD)-fed obese mice. C57BL/6N mice were fed an HFD (40 kcal% fat) with or without 0.005% (w/w) EC for 16 weeks. Dietary EC improved adiposity by increasing adipocyte fatty acid (FA) oxidation, energy expenditure, and mRNA expression of thermogenesis-related genes in brown adipose tissue (BAT) and skeletal muscle, whereas it also decreased lipogenesis-related gene expression in white adipose tissue. In addition to adiposity, EC prevented hepatic steatosis by diminishing lipogenesis while enhancing FA oxidation in the liver and fecal lipid excretion, which was linked to attenuation of hyperlipidemia. Moreover, EC improved insulin sensitivity by decreasing hepatic gluconeogenesis and proinflammatory responses. These findings indicate that EC may protect against diet-induced adiposity and related metabolic disorders by controlling thermogenesis of BAT and skeletal muscle, FA oxidation, lipogenesis, fecal lipid excretion, glucose utilization, and gluconeogenesis.

Regards,

Jessica

Managing editor

Pancreatic disorder and therapy