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体重及脂肪组织被认为受到能量稳态机制的严格调控,即脂肪细胞分泌的、显示机体脂肪含量的信号分子——瘦素通过下丘脑的信号通路对体重进行双向调控.近几十年来肥胖在全球暴发,肥胖个体中过量的瘦素并未抑制体重的增长,该现象被归因于“瘦素抵抗”.然而最近有证据显示,肥胖发生过程中瘦素功能没有改变,瘦素抵抗不存在.因此体重是否受稳态调控存有争议.而本研究组发现一种依赖R c a n 2基因且不受瘦素抑制的增加摄食及体重的机制,伴有高脂肪食物时可导致体重快速增加进而产生肥胖,该发现可为肥胖的流行提供新的解释.
Body weight and adipose tissue are thought to be tightly regulated by the steady-state mechanism of energy, the signal molecule secreted by fat cells that displays the body fat content - leptin regulates the body’s weight bidirectionally through the hypothalamus signaling pathway. Over recent decades, Excessive global leprosy in obese individuals does not inhibit the growth of body weight, which is attributed to “leptin resistance.” However, there is recent evidence that leptin function has not changed during obesity and that leptin resistance It is controversial whether the body weight is regulated by homeostasis.While the research team found a mechanism that increases food intake and body weight that relies on R can 2 gene and is not inhibited by leptin, Increased and thus obesity results in a new explanation for the prevalence of obesity.