Olarescu Nicoleta Cristina, Bollerslev Jens
Section of Specialized Endocrinology, Department of Endocrinology, Oslo University Hospital, Rikshospitalet, Oslo, Norway; Faculty of Medicine, University of Oslo, Norway.
Section of Specialized Endocrinology, Department of Endocrinology, Oslo University Hospital, Rikshospitalet, Oslo, Norway; Faculty of Medicine, University of Oslo, Norway.
Trends Endocrinol Metab. 2016 Apr;27(4):226-237. doi: 10.1016/j.tem.2016.02.005. Epub 2016 Mar 2.
Adipose tissue (AT) is recognized as key contributor to the systemic insulin resistance and overt diabetes seen in metabolic syndrome. Acromegaly is a disease characterized by excessive secretion of growth hormone (GH) and insulin-like growth factor I (IGF-I). GH is known both for its action on AT and for its detrimental effect on glucose metabolism and insulin signaling. In active acromegaly, while body fat deports are diminished, insulin resistance is increased. Early studies have demonstrated defects in insulin action, both at the hepatic and extrahepatic (i.e., muscle and fat) levels, in active disease. This review discusses recent data suggesting that AT inflammation, altered AT distribution, and impaired adipogenesis are potential mechanisms contributing to systemic insulin resistance in acromegaly.
脂肪组织（AT）被认为是导致代谢综合征中出现全身性胰岛素抵抗和明显糖尿病的关键因素。肢端肥大症是一种以生长激素（GH）和胰岛素样生长因子I（IGF-I）分泌过多为特征的疾病。GH对脂肪组织有作用，且对葡萄糖代谢和胰岛素信号传导有不利影响。在活动性肢端肥大症中，虽然身体脂肪减少，但胰岛素抵抗增加。早期研究表明，在活动性疾病中，肝脏和肝外（即肌肉和脂肪）水平的胰岛素作用均存在缺陷。本综述讨论了近期数据，这些数据表明脂肪组织炎症、脂肪组织分布改变和成脂受损是导致肢端肥大症全身性胰岛素抵抗的潜在机制。
