Hamilton B S, Paglia D, Kwan A Y, Deitel M
Institute of Medical Science, University of Toronto, Ontario, Canada.
Nat Med. 1995 Sep;1(9):953-6. doi: 10.1038/nm0995-953.
Obesity presents a significant challenge to the general health of affluent nations in terms of the number of people affected, the serious associated maladies and the lack of effective treatments. While common wisdom has held that obesity results from 'gluttony and sloth', a number of studies have indicated physiological causes of underlying the pathogenesis of obesity, with the degree of adiposity having a strong genetic component. Recently, the obese gene in the ob/ob mouse was cloned, along with its human homologue. The specific production of the obese protein by adipose tissue suggested that it may function in a feedback loop from fat tissue to the hypothalamus to control energy intake and/or energy expenditure, and that it may play a role in the pathogenesis of human obesity. In this study we report that obese mRNA expression is elevated in ex vivo omental adipocytes isolated from massively obese humans in the absence of an identifiable mutation. Therefore, we speculate that this increased expression may suggest that the massively obese are insensitive to the putative regulatory function(s) of the obese gene product.
肥胖在受影响的人数、严重的相关疾病以及缺乏有效治疗方法等方面，给富裕国家的公众健康带来了重大挑战。虽然人们普遍认为肥胖是由“暴饮暴食和懒惰”导致的，但一些研究表明肥胖发病机制存在生理原因，肥胖程度具有很强的遗传因素。最近，ob/ob小鼠的肥胖基因及其人类同源基因被克隆出来。脂肪组织特异性产生肥胖蛋白表明，它可能在从脂肪组织到下丘脑的反馈回路中发挥作用，以控制能量摄入和/或能量消耗，并且它可能在人类肥胖的发病机制中起作用。在本研究中，我们报告称，在没有可识别突变的情况下，从极度肥胖的人类分离出的离体网膜脂肪细胞中，肥胖mRNA表达升高。因此，我们推测这种表达增加可能表明极度肥胖者对肥胖基因产物的假定调节功能不敏感。
