Obesity and its therapy: from genes to community action.
Obesity and its therapy: from genes to community action.
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肥胖及其治疗：从基因到社区行动。
DOI：
10.1016/j.pcl.2006.05.011
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发表时间：
2006
影响因子：
2.6
通讯作者：
Olivier,Michael
中科院分区：
文献类型：
--
作者：
Skelton,JosephA;DeMattia,Laure;Miller,Lawrence;Olivier,Michael
在过去的几十年里，超重儿童的数量增加对任何关心儿童或与儿童一起工作的人来说都是显而易见的。对于普通医生来说，这是一个特别令人沮丧的问题。几乎没有治疗方式存在，尽管有很大的知识的影响因素，很少可以完成在一个简短的办公室访问。此外，从1994年发现瘦素开始，基础科学研究取得了令人兴奋的进展[1]，但并没有产生用于日常临床实践的新工具。瘦素被证明是肥胖及其合并症的科学调查的冰山一角。迄今为止，超过600个基因，标记和染色体区域与肥胖有关[2]。这是否意味着我们离找到更好的治疗和预防肥胖的方法更近了还是更远了？传统上，肥胖作为一种疾病的生物心理社会模型被认为是合适的，因为模型的所有元素都是相关的（图1）。该模型显示了由组分重叠引起的疾病。在将这一模型应用于肥胖研究时，生物系统被孤立地看待，没有考虑到它们与环境和行为的相互作用，直到出现“疾病”。虽然在探索肥胖的病理生理学方面已经取得了长足的进步，但治疗和预防主要集中在其他两个方面：心理和社会。最好的干预措施是在饮食管理和行为改变领域[3-5]。药物治疗受到限制，特别是在儿童中[6-8]。基因检测只适用于少数肥胖症患者。探索肥胖背后的细胞和分子机制，同时从另一端进行临床治疗可能会导致进展缓慢。通过将基础科学与临床研究相结合，治疗和干预措施将更有针对性，并更快地转化为护理计划。为了促进这一点，已经发生了范式转变。
The increase in the number of overweight children over the last several decades is obvious to anyone who cares for or works with children. To the general practitioner, this is an especially frustrating problem. Few treatment modalities exist, and despite great knowledge of contributing factors, little can be accomplished in a brief office visit. Additionally, exciting advances in basic science research, beginning with the discovery of leptin in 1994 [1], have not led to novel tools for use in everyday clinical practice. Leptin turned out to be the tip of the iceberg in the scientific investigation of obesity and its comorbidities. To date, more than 600 genes, markers, and regions of chromosomes have been linked to obesity [2]. Does this mean we are closer or further away from finding better ways to treat and prevent obesity?Traditionally, the biopsychosocial model of obesity as a disease has been considered appropriate, as all elements of the model are relevant (Fig. 1). This model shows disease arising from the overlap of components. In applying this model to obesity research, biologic systems are viewed in isolation, not taking into account their interaction with the environment and behaviors until there is “disease” present. Although strides have been made exploring the pathophysiology of obesity, treatment and prevention have focused on the other two components: psychological and social. The best interventions have been in the fields of dietary management and behavioral change [3–5]. Drug therapy has been limited, especially in children [6–8]. Genetic testing is applicable to only a small number of those affected by obesity. Exploring the cellular and molecular mechanisms behind obesity while clinically treating from the other end of the spectrum can result in slow progress. By integrating basic science with clinical research, treatments and interventions will be better focused and more quickly translated into care plans. To facilitate this, a paradigm shift has taken place.