Grenier-Larouche T, Labbé S M, Noll C, Richard D, Carpentier A C
Department of Medicine, Division of Endocrinology, Centre Hospitalier Université de Sherbrooke , Sherbrooke, Québec, Canada.
Centre de recherche de l'Institut de cardiologie et de pneumologie de Québec, Université Laval Québec , Québec City, Québec, Canada.
Int J Obes Suppl. 2012 Dec;2(Suppl 2):S37-42. doi: 10.1038/ijosup.2012.21. Epub 2012 Dec 11.
Type 2 diabetes (T2D) is characterized by a general dysregulation of postprandial energy substrate partitioning. Although classically described in regard to glucose metabolism, it is now evident that metabolic inflexibility of plasma lipid fluxes is also present in T2D. The organ that is most importantly involved in the latter metabolic defect is the white adipose tissue (WAT). Both catecholamine-induced nonesterified fatty acid mobilization and insulin-stimulated storage of meal fatty acids are impaired in many WAT depots of insulin-resistant individuals. Novel molecular imaging techniques now demonstrate that these defects are linked to increased dietary fatty acid fluxes toward lean organs and myocardial dysfunction in humans. Recent findings also demonstrate functional abnormalities of brown adipose tissues in T2D, thus suggesting that a generalized adipose tissue dysregulation of energy storage and dissipation may be at play in the development of lean tissue energy overload and lipotoxicity.
2型糖尿病（T2D）的特征是餐后能量底物分配普遍失调。虽然传统上是从葡萄糖代谢方面进行描述，但现在很明显，T2D患者也存在血浆脂质通量的代谢灵活性受损。在这种代谢缺陷中最重要的器官是白色脂肪组织（WAT）。在胰岛素抵抗个体的许多WAT储存部位，儿茶酚胺诱导的非酯化脂肪酸动员和胰岛素刺激的膳食脂肪酸储存均受损。新型分子成像技术现在表明，这些缺陷与人类饮食中脂肪酸向瘦组织器官的通量增加以及心肌功能障碍有关。最近的研究结果还表明，T2D患者棕色脂肪组织存在功能异常，因此提示在瘦组织能量过载和脂毒性的发生过程中，可能存在能量储存和消耗的全身性脂肪组织失调。
