Neurobiology of Nutrition Laboratory, Pennington Biomedical Research Center, Louisiana State University System, Baton Rouge, LA 70808, USA.
Int J Obes (Lond). 2009 Jun;33 Suppl 2(Suppl 2):S8-13. doi: 10.1038/ijo.2009.65.
Powerful biological mechanisms evolved to defend adequate nutrient supply and optimal levels of body weight/adiposity. Low levels of leptin indicating food deprivation and depleted fat stores have been identified as the strongest signals to induce adaptive biological actions such as increased energy intake and reduced energy expenditure. In concert with other signals from the gut and metabolically active tissues, low leptin levels trigger powerful activation of multiple peripheral and brain systems to restore energy balance. It is not just neurons in the arcuate nucleus, but many other brain systems involved in finding potential food sources, smelling and tasting food, and learning to maximize rewarding effects of foods, that are affected by low leptin. Food restriction and fat depletion thus lead to a 'hungry' brain, preoccupied with food. By contrast, because of less (adaptive thrifty fuel efficiency) or lost (lack of predators) evolutionary pressure, the upper limits of body weight/adiposity are not as strongly defended by high levels of leptin and other signals. The modern environment is characterized by the increased availability of large amounts of energy-dense foods and increased presence of powerful food cues, together with minimal physical procurement costs and a sedentary lifestyle. Much of these environmental influences affect cortico-limbic brain areas concerned with learning and memory, reward, mood and emotion. Common obesity results when individual predisposition to deal with a restrictive environment, as engraved by genetics, epigenetics and/or early life experience, is confronted with an environment of plenty. Therefore, increased adiposity in prone individuals should be seen as a normal physiological response to a changed environment, not in the pathology of the regulatory system. The first line of defense should ideally lie in modifications to the environment and lifestyle. However, as such modifications will be slow and incomplete, it is equally important to gain better insight into how the brain deals with environmental stimuli and to develop behavioral strategies to better cope with them. Clearly, alternative therapeutic strategies such as drugs and bariatric surgery should also be considered to prevent or treat this debilitating disease. It will be crucial to understand the functional crosstalk between neural systems responding to metabolic and environmental stimuli, i.e. crosstalk between hypothalamic and cortico-limbic circuitry.
强大的生物学机制进化而来,以维持充足的营养供应和理想的体重/体脂肪水平。低水平的瘦素表明食物匮乏和脂肪储存耗尽,被认为是最强的信号,可引发适应性的生物学反应,如增加能量摄入和减少能量消耗。与来自肠道和代谢活跃组织的其他信号一起,低水平的瘦素触发了多个外周和大脑系统的强大激活,以恢复能量平衡。不仅是弓状核中的神经元,而且涉及寻找潜在食物来源、闻和品尝食物以及学习最大化食物奖励效果的许多其他大脑系统,都受到低水平瘦素的影响。因此,食物限制和脂肪消耗会导致大脑处于“饥饿”状态,全神贯注于食物。相比之下,由于较少的(适应性节俭的燃料效率)或失去的(缺乏捕食者)进化压力,高水平的瘦素和其他信号对体重/体脂肪的上限没有那么强烈的保护作用。现代环境的特点是大量高热量食物的供应增加,以及强有力的食物线索的大量存在,同时体力采购成本最小化和生活方式久坐不动。这些环境影响的大部分都会影响与学习和记忆、奖励、情绪和情感相关的皮质-边缘大脑区域。常见的肥胖是由于个体应对限制性环境的倾向,如遗传、表观遗传和/或早期生活经历所决定的,与丰富的环境相冲突而导致的。因此,易感个体的脂肪增加应该被视为对环境变化的正常生理反应,而不是调节系统的病理学。理想情况下,第一道防线应该在于环境和生活方式的改变。然而,由于这种改变将是缓慢和不完整的,同样重要的是更好地了解大脑如何应对环境刺激,并开发更好地应对这些刺激的行为策略。显然,还应该考虑替代治疗策略,如药物和减肥手术,以预防或治疗这种使人衰弱的疾病。了解代谢和环境刺激的神经系统之间的功能串扰至关重要,即下丘脑和皮质-边缘回路之间的串扰。