Medical Department III - Endocrinology, Nephrology, Rheumatology, University of Leipzig, Leipzig, Germany and Helmholtz Institute for Metabolic, Obesity and Vascular Research, Helmholtz Zentrum München, University Hospital Leipzig, Leipzig, Germany.
Endocr Rev. 2020 May 1;41(3). doi: 10.1210/endrev/bnaa004.
Obesity contributes to reduced life expectancy, impaired quality of life, and disabilities, mainly in those individuals who develop cardiovascular diseases, type 2 diabetes, osteoarthritis, and cancer. However, there is a large variation in the individual risk to developing obesity-associated comorbid diseases that cannot simply be explained by the extent of adiposity. Observations that a proportion of individuals with obesity have a significantly lower risk for cardiometabolic abnormalities led to the concept of metabolically healthy obesity (MHO). Although there is no clear definition, normal glucose and lipid metabolism parameters-in addition to the absence of hypertension-usually serve as criteria to diagnose MHO. Biological mechanisms underlying MHO lower amounts of ectopic fat (visceral and liver), and higher leg fat deposition, expandability of subcutaneous adipose tissue, preserved insulin sensitivity, and beta-cell function as well as better cardiorespiratory fitness compared to unhealthy obesity. Whereas the absence of metabolic abnormalities may reduce the risk of type 2 diabetes and cardiovascular diseases in metabolically healthy individuals compared to unhealthy individuals with obesity, it is still higher in comparison with healthy lean individuals. In addition, MHO seems to be a transient phenotype further justifying therapeutic weight loss attempts-even in this subgroup-which might not benefit from reducing body weight to the same extent as patients with unhealthy obesity. Metabolically healthy obesity represents a model to study mechanisms linking obesity to cardiometabolic complications. Metabolically healthy obesity should not be considered a safe condition, which does not require obesity treatment, but may guide decision-making for a personalized and risk-stratified obesity treatment.
肥胖会导致预期寿命缩短、生活质量下降和残疾,主要发生在那些患有心血管疾病、2 型糖尿病、骨关节炎和癌症的人群中。然而,个体患肥胖相关合并症的风险存在很大差异,这不能简单地用肥胖程度来解释。有观察表明,一部分肥胖人群患代谢异常的风险明显较低,这导致了代谢健康型肥胖(MHO)的概念的产生。尽管目前还没有明确的定义,但通常将正常的葡萄糖和脂质代谢参数(除了没有高血压)以及不存在代谢异常作为诊断 MHO 的标准。MHO 的生物学机制是内脏和肝脏脂肪异位沉积减少,腿部脂肪沉积增加,皮下脂肪组织的扩展性增加,胰岛素敏感性和β细胞功能保持良好,以及与不健康肥胖相比,心肺功能更好。虽然与肥胖且代谢异常的个体相比,代谢健康的个体发生 2 型糖尿病和心血管疾病的风险可能会降低,但与健康的瘦个体相比,这种风险仍然更高。此外,MHO 似乎是一种短暂的表型,这进一步证明了即使在这个亚组中,治疗性减肥尝试也是合理的,即使不能像不健康肥胖患者那样通过减轻体重来获得同样的益处。代谢健康型肥胖代表了一种研究肥胖与代谢并发症之间联系的机制模型。代谢健康型肥胖不应被视为一种无需治疗的安全状态,但它可能有助于为个性化和风险分层的肥胖治疗做出决策。