Townsend Logan K, Knuth Carly M, Wright David C
Department of Human Health and Nutritional Science, University of Guelph, Guelph, Canada.
Department of Human Health and Nutritional Science, University of Guelph, Guelph, Canada
Physiol Rep. 2017 Apr;5(7). doi: 10.14814/phy2.13247.
Adipose tissue is increasingly being recognized as a key regulator of whole body carbohydrate and lipid metabolism. In conditions of obesity and insulin resistance mitochondrial content in this tissue is reduced, while treatment with insulin sensitizing drugs such as thiazolidinediones (TZDs) increase mitochondrial content. It has been known for decades that exercise increases mitochondrial content in skeletal muscle and now several laboratories have shown similar effects in adipose tissue. To date the specific mechanisms mediating this effect have not been fully identified. In this review we highlight recent work suggesting that increases in lipolysis and subsequently fatty acid re-esterification trigger the activation of 5' AMP-activated protein kinase (AMP) activated protein kinase and ultimately the induction of mitochondrial biogenesis. It is our current view that this pathway could be a unifying mechanism linking numerous systemic factors (catecholamines, interleukin-6, meteorin-like) to induction of mitochondrial biogenesis following exercise.
脂肪组织日益被认为是全身碳水化合物和脂质代谢的关键调节因子。在肥胖和胰岛素抵抗的情况下，该组织中的线粒体含量会减少，而使用噻唑烷二酮类（TZDs）等胰岛素增敏药物进行治疗会增加线粒体含量。几十年来人们都知道运动能增加骨骼肌中的线粒体含量，现在有几个实验室也在脂肪组织中发现了类似的效果。迄今为止，介导这种效应的具体机制尚未完全明确。在这篇综述中，我们重点介绍了最近的研究工作，这些研究表明脂解作用的增强以及随后的脂肪酸再酯化会触发5' AMP活化蛋白激酶（AMPK）的激活，并最终诱导线粒体生物发生。我们目前的观点是，这条途径可能是一个统一的机制，将众多全身因素（儿茶酚胺、白细胞介素-6、类陨石素）与运动后线粒体生物发生的诱导联系起来。
