Department of Medicine, University of Leipzig, Leipzig, Germany.
Curr Opin Lipidol. 2010 Feb;21(1):38-43. doi: 10.1097/MOL.0b013e3283346ccc.
The prevalence and severity of obesity are dramatically increasing throughout the world. Obesity causes a decline in life expectancy due to its associated metabolic and cardiovascular comorbid disorders. Therefore, it will become more important to distinguish obese individuals at high risk for obesity-related metabolic diseases from those who are metabolically 'healthy'. This review focuses on recent evidence suggesting that normal adipose tissue function contributes to the healthy obese phenotype.
The majority of individuals with obesity develop insulin resistance, type 2 diabetes, dyslipidemia, gout, hypertension and cardiovascular disease. However, approximately 10-25% of obese individuals are metabolically healthy most likely due to preserved insulin sensitivity. Recent studies suggest that inflammation of visceral adipose tissue, ectopic fat deposition and adipose tissue dysfunction mediate insulin resistance in human obesity independently of total body fat mass. This suggests that mechanisms beyond a positive caloric balance such as inflammation and adipokine release determine the pathological metabolic consequences in patients with obesity.
Recommendations for obesity treatment should distinguish the metabolically 'healthy' from 'unhealthy' obese phenotype to identify early the obese person who will benefit the most from losing weight. In addition, novel antiobesity treatment strategies targeting adipose tissue dysfunction are needed.
目的综述：肥胖在全球范围内的患病率和严重程度都在急剧上升。肥胖会导致预期寿命缩短，因为它会引起相关的代谢和心血管合并症。因此，区分肥胖相关代谢疾病高危人群和代谢健康的肥胖人群将变得更加重要。本文重点介绍了一些新的证据，表明正常的脂肪组织功能有助于肥胖者保持健康的表型。
最近发现：大多数肥胖患者会出现胰岛素抵抗、2 型糖尿病、血脂异常、痛风、高血压和心血管疾病。然而，大约 10-25%的肥胖患者在代谢上是健康的，这可能是由于胰岛素敏感性得到了保留。最近的研究表明，内脏脂肪组织的炎症、异位脂肪沉积和脂肪组织功能障碍在人类肥胖中独立于全身脂肪量介导胰岛素抵抗。这表明，决定肥胖患者发生病理性代谢后果的机制不仅仅是热量摄入的正平衡，还包括炎症和脂肪因子的释放。
总结：肥胖治疗的建议应该区分代谢健康的肥胖表型和代谢不健康的肥胖表型，以早期识别最受益于减肥的肥胖患者。此外，还需要针对脂肪组织功能障碍的新型抗肥胖治疗策略。
