Department of Nutrition, Food Science, Physiology and Toxicology, University of Navarra, Pamplona, Spain.
Proc Nutr Soc. 2010 Aug;69(3):324-32. doi: 10.1017/S0029665110001801. Epub 2010 Jun 14.
Obesity leads to several chronic morbidities including type 2 diabetes, dyslipidaemia, atherosclerosis and hypertension, which are major components of the metabolic syndrome. White adipose tissue (WAT) metabolism and WAT-derived factors (fatty acids and adipokines) play an important role in the development of these metabolic disturbances. In fact, dysregulated adipokine secretion from the expanded WAT of obese individuals contributes to the development of systemic low-grade inflammation, insulin resistance and metabolic syndrome. The n-3 PUFA EPA and DHA have been widely reported to have protective effects in a range of chronic inflammatory conditions including obesity. In fact, n-3 PUFA have been shown to ameliorate low-grade inflammation in adipose tissue associated with obesity and up-regulate mitochondrial biogenesis and induce beta-oxidation in WAT in mice. Moreover, the ability of n-3 PUFA to regulate adipokine gene expression and secretion has been observed both in vitro and in vivo in rodents and human subjects. The present article reviews: (1) the physiological role of adiponectin, leptin and pre-B cell colony-enhancer factor/visfatin, three adipokines with immune-modulatory properties involved in the regulation of metabolism and insulin sensitivity and (2) the actions of n-3 PUFA on these adipokines focusing on the underlying mechanisms and the potential relationship with the beneficial effects of these fatty acids on obesity-associated metabolic disorders. It can be concluded that the ability of n-3 PUFA to improve obesity and insulin resistance conditions partially results from the modulation of WAT metabolism and the secretion of bioactive adipokines including leptin, adiponectin and visfatin.
肥胖会导致多种慢性疾病，包括 2 型糖尿病、血脂异常、动脉粥样硬化和高血压，这些都是代谢综合征的主要组成部分。白色脂肪组织（WAT）代谢和 WAT 衍生因子（脂肪酸和脂肪因子）在这些代谢紊乱的发展中起着重要作用。事实上，肥胖个体扩张的 WAT 中失调的脂肪因子分泌导致全身低度炎症、胰岛素抵抗和代谢综合征的发展。已经广泛报道 n-3PUFA EPA 和 DHA 在一系列慢性炎症性疾病中具有保护作用，包括肥胖症。事实上，n-3PUFA 已被证明可改善与肥胖相关的脂肪组织中的低度炎症，并上调 WAT 中的线粒体生物发生并诱导β氧化。此外，在啮齿动物和人类中已经观察到 n-3PUFA 调节脂肪因子基因表达和分泌的能力，无论是在体外还是体内。本文综述了：（1）三种具有免疫调节特性的脂肪因子脂联素、瘦素和前 B 细胞集落增强因子/内脂素的生理作用，它们参与调节代谢和胰岛素敏感性；（2）n-3PUFA 对这些脂肪因子的作用，重点关注潜在机制以及这些脂肪酸对肥胖相关代谢紊乱的有益影响与它们之间的潜在关系。可以得出结论，n-3PUFA 改善肥胖和胰岛素抵抗的能力部分归因于 WAT 代谢的调节和生物活性脂肪因子的分泌，包括瘦素、脂联素和内脂素。
