坏脂肪转变:蛋白表达改变治肥胖

脂肪是人体重要的代谢器官,通常人们按照是否会导致肥胖这一原则把它分为“好脂肪”和“坏脂肪”两种类型。美国约翰·霍普金斯大学的研究人员近日成功地把老鼠身上的“坏脂肪”转化成了“好脂肪”,并预计该研究成果很快就可应用于人类。
脂肪对人体的能量平衡起着重要作用。所谓“坏脂肪”也叫白色脂肪组织,它在成年人的体内广泛分布,主要功能是将过剩的能量储存起来;“好脂肪”也叫棕色脂肪,它的功能是分解细胞内的热量,与白色脂肪的功能恰好相反,不过棕色脂肪在婴幼儿期所占比例较高,随着年龄的增长在人体内含量越来越少。
约翰·霍普金斯大学的科学家毕成(音译)介绍,当他们改变老鼠大脑中控制食欲区域的某些细胞的蛋白表达后,发现老鼠体内的部分白色脂肪转化成了棕色脂肪,结果那些天天吃高热量食物的老鼠也能保持苗条身材了。
毕成说,研究人员相信,利用类似原理,在人体皮肤下植入棕色脂肪的干细胞组织也可以使白色脂肪转化为棕色脂肪。一旦试验成功,这个办法将有效治疗肥胖,并降低与肥胖相关的高血压、糖尿病等顽疾的发病率。
不过英国伯明翰肥胖症研究中心的科学家提醒,人的身体是非常擅于保持平衡的,这就是为什么燃烧卡路里常常触发饥饿信号的原因,过多的棕色脂肪可能扰乱人体新陈代谢系统,易使人患上甲亢等病症。
原文阅读:
Prevents Hyperphagia and Obesity in Otsuka Long-Evans Tokushima Fatty Rats: Role of Hypothalamic Signaling
Sheng Bi, Karen A. Scott, Jayson Hyun, Ellen E. Ladenheim and Timothy H. Moran
Otsuka Long-Evans Tokushima fatty (OLETF) rats lacking cholecystokinin-A receptors are hyperphagic, obese, and diabetic. Although exercise attenuates OLETF rats’ obesity, the mechanisms underlying the effects of exercise are unclear. In this study, we determined the effects of running wheel activity on patterns of body weight gain, food intake, and hypothalamic gene expression. We demonstrate that voluntary running activity beginning at 8 wk of age normalized meal patterns, food intake, body weight, and plasma levels of glucose and leptin in OLETF rats. During the initial exercise period, corticotropin-releasing factor (CRF) mRNA expression was significantly elevated in the dorsomedial hypothalamus (DMH) but not in the paraventricular nucleus in both OLETF and control Long-Evans Tokushima rats. In response to long-term exercise, arcuate nucleus (Arc) neuropeptide Y (NPY), and proopiomelanocortin as well as DMH NPY and CRF mRNA expression were increased in Long-Evans Tokushima rats. In contrast, whereas exercising OLETF rats had increased Arc NPY and DMH CRF expression, Arc proopiomelanocortin and DMH NPY mRNA levels were not elevated. Finally, we demonstrate that the effects of exercise on body weight in OLETF rats were long lasting. Although food intake and body weight were increased in OLETF rats when running wheels were locked, weights did not return to those of sedentary OLETF rats. Together, these data suggest that the elevation of DMH CRF expression may mediate the short-term feeding inhibitory effects of exercise and that exercise limits the elevation of DMH NPY expression to account for the overall prevention of OLETF rats’ obesity.



