JCI：新动物模型研究肥胖是不可逆转的

2012年10月29日--近日，科学家证实小鼠肥胖的时间越长，就越不可能修正自己的饮食习惯，长期活动使得体重正常化的成功的率也较低。
 
这项发表在10月24日的Journal of Clinical Investigation杂志上的研究揭示了肥胖是不可逆转的。

在新研究中利用了一个新的动物模型，随着时间的推移，尽管采取节食等措施，肥胖老鼠仍然超重。动物模型研究表明，肥胖是一个自我持续混乱的结果，部分研究结果进一步强调了儿童早期干预对预防肥胖的重要性，因为肥胖的效果可能会持续一。

新的动物模型将有助于查明为什么大多数成年人发现很难维持有意义的减肥节食和锻炼的原因。超过500万成年人和4300万年龄小于5岁的儿童受肥胖影响，超重的人患2型糖尿病、高血压和心血管疾病的风险要高得多。

与肥胖相关的拓展阅读：

• Diabetes Care：不符合手术标准的肥胖患者也能从减肥手术中获益
• Ann Surg：肥胖乳腺癌患者术前抗生素预防可降低手术部位感染发生率
• Lancet：利尿剂并不是对肥胖高血压患者合理的治疗方案
• Cell Metab：操纵Tyk2成功逆转小鼠肥胖
• Cell Metab：挑战常规，小鼠研究证实胰岛素导致肥胖
• Nat Medicine：开发出治疗肥胖的安全有效的激素结合疗法
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Obesity-programmed mice are rescued by early genetic intervention

Obesity is a chronic metabolic disorder affecting half a billion people worldwide. Major difficulties in managing obesity are the cessation of continued weight loss in patients after an initial period of responsiveness and rebound to pretreatment weight. It is conceivable that chronic weight gain unrelated to physiological needs induces an allostatic regulatory state that defends a supranormal adipose mass despite its maladaptive consequences. To challenge this hypothesis, we generated a reversible genetic mouse model of early-onset hyperphagia and severe obesity by selectively blocking the expression of the proopiomelanocortin gene (Pomc) in hypothalamic neurons. Eutopic reactivation of central POMC transmission at different stages of overweight progression normalized or greatly reduced food intake in these obesity-programmed mice. Hypothalamic Pomc rescue also attenuated comorbidities such as hyperglycemia, hyperinsulinemia, and hepatic steatosis and normalized locomotor activity. However, effectiveness of treatment to normalize body weight and adiposity declined progressively as the level of obesity at the time of Pomc induction increased. Thus, our study using a novel reversible monogenic obesity model reveals the critical importance of early intervention for the prevention of subsequent allostatic overload that auto-perpetuates obesity.