Abstract
Various studies have shown that eicosapentaenoic acid (EPA) has beneficial effects on obesity and associated disorders. Apelin, the ligand of APJ receptor also exerts insulin-sensitizing effects especially by improving muscle metabolism. EPA has been shown to increase apelin production in adipose tissue but its effects in muscle have not been addressed. Thus, the effects of EPA supplementation (36 g/kg EPA) in high-fat diet (HFD) (45% fat, 20% protein, 35% carbohydrate) were studied in mice with focus on muscle lipid metabolism and apelin/APJ expression. Compared with HFD mice, HFD+EPA mice had significantly less weight gain, fat mass, lower blood glucose, insulinemia and hepatic steatosis after 10 weeks of diet. In addition, EPA prevented muscle metabolism alterations since intramuscular triglycerides were decreased and β-oxidation increased. In soleus muscles of HFD+EPA mice, apelin and APJ expression were significantly increased compared to HFD mice. However, plasma apelin concentrations in HFD and HFD+EPA mice were similar. EPA-induced apelin expression was confirmed in differentiated C2C12 myocytes but in this model, apelin secretion was also increased in response to EPA treatment. In conclusion, EPA supplementation in HFD prevents obesity and metabolic alterations in mice, especially in skeletal muscle. Since EPA increases apelin/APJ expression in muscle, apelin may act in a paracrine/autocrine manner to contribute to these benefical effects.
Highlights
Obesity and associated diseases such as type 2 diabetes or hypertension are a major public health problem
Since apelin regulation has been studied in adipose tissue, we focused on muscle metabolism and on expression of both apelin and APJ in skeletal muscle of mice fed with a high-fat diets (HFD) supplemented with Eicosapentaenoic acid (EPA)
In the present study we investigated in mice the effect of a HFD supplemented with EPA on metabolic disturbances usually associated with HFD feeding
Summary
Obesity and associated diseases such as type 2 diabetes or hypertension are a major public health problem. Since adipose tissue is considered as an endocrine organ, different studies have demonstrated the effect of EPA (alone or in combination with other n-3 PUFAs) on different adipokines expression and/or secretion. Increased adiponectin has been observed in adipose tissue of ob/ob mice receiving n-3 PUFA-enriched diet [9] or in adipose tissue of HFD fed mice [13] and in cultured human adipocytes in response to EPA [14]. Due to the more recent identification of apelin as an adipokine involved in glucose metabolism [15], EPA alone has been shown to increase apelin expression and secretion in 3T3-L1 adipocytes [16] and in adipose tissue of cafeteria diet-fed rats [17]
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