The University of Tennessee (UT) Obesity Research Center, Knoxville, TN 37996, USA.
Adv Nutr. 2011 Jul;2(4):304-16. doi: 10.3945/an.111.000505. Epub 2011 Jun 28.
Obesity is associated with the metabolic syndrome, a significant risk factor for developing type 2 diabetes and cardiovascular diseases. Chronic low-grade inflammation occurring in the adipose tissue of obese individuals is causally linked to the pathogenesis of insulin resistance and the metabolic syndrome. Although the exact trigger of this inflammatory process is unknown, adipose tissue hypoxia, endoplasmic reticular stress, and saturated fatty acid-mediated activation of innate immune processes have been identified as important processes in these disorders. Furthermore, macrophages and T lymphocytes have important roles in orchestrating this immune process. Although energy restriction leading to weight loss is the primary dietary intervention to reverse these obesity-associated metabolic disorders, other interventions targeted at alleviating adipose tissue inflammation have not been explored in detail. In this regard, (n-3) PUFA of marine origin both prevent and reverse high-fat-diet-induced adipose tissue inflammation and insulin resistance in rodents. We provide an update on the pathogenesis of adipose tissue inflammation and insulin resistance in obesity and discuss potential mechanisms by which (n-3) PUFA prevent and reverse these changes and the implications in human health.
肥胖与代谢综合征有关，代谢综合征是导致 2 型糖尿病和心血管疾病的重要危险因素。肥胖个体脂肪组织中发生的慢性低度炎症与胰岛素抵抗和代谢综合征的发病机制有因果关系。虽然这种炎症过程的确切触发因素尚不清楚，但脂肪组织缺氧、内质网应激以及饱和脂肪酸介导的固有免疫过程的激活已被确定为这些疾病中的重要过程。此外，巨噬细胞和 T 淋巴细胞在协调这种免疫过程中起着重要作用。虽然导致体重减轻的能量限制是逆转这些与肥胖相关的代谢紊乱的主要饮食干预措施，但其他旨在减轻脂肪组织炎症的干预措施尚未详细探讨。在这方面，海洋来源的(n-3)PUFA 既能预防又能逆转高脂肪饮食诱导的肥胖啮齿动物的脂肪组织炎症和胰岛素抵抗。我们提供了肥胖症中脂肪组织炎症和胰岛素抵抗的发病机制的最新信息，并讨论了(n-3)PUFA 预防和逆转这些变化的潜在机制及其对人类健康的影响。
