Grunfeld C, Zhao C, Fuller J, Pollack A, Moser A, Friedman J, Feingold K R
Department of Medicine, University of California, San Francisco, USA.
J Clin Invest. 1996 May 1;97(9):2152-7. doi: 10.1172/JCI118653.
The expression of leptin, the ob gene product, is increased in adipose tissue in response to feeding and energy repletion, while leptin decreases food intake. Because adipose tissue gene expression is regulated by cytokines induced during infection and because infection is associated with anorexia, we tested whether induction of leptin might occur during the host response to infection. Administration of endotoxin (LPS), a model for gram negative infections, induces profound anorexia and weight loss in hamsters. In fasted adipose tissue to levels similar to fed control animals. There is a strong inverse correlation between mRNA levels of leptin and subsequent food intake. TNF and IL-1, mediators of the host response to LPS, also induced anorexia and increased levels of leptin in mRNA in adipose tissue. As assessed by immuknoprecipitation and Western blotting, circulating leptin protein is regulated by LPS and cytokines in parallel to regulation of adipose tissue leptin mRNA. Induction of leptin during the host response to infection may contribute to the anorexia of infection.
瘦素（ob基因产物）的表达在进食和能量充足时会在脂肪组织中增加，而瘦素会减少食物摄入量。由于脂肪组织基因表达受感染期间诱导的细胞因子调节，且感染与厌食症相关，我们测试了在宿主对感染的反应过程中是否会发生瘦素的诱导。给予内毒素（LPS）（革兰氏阴性感染的模型）会在仓鼠中引起严重的厌食症和体重减轻。在禁食的脂肪组织中，瘦素水平与进食的对照动物相似。瘦素的mRNA水平与随后的食物摄入量之间存在很强的负相关。肿瘤坏死因子（TNF）和白细胞介素-1（IL-1）是宿主对LPS反应的介质，它们也会诱导厌食症并增加脂肪组织中瘦素mRNA的水平。通过免疫沉淀和蛋白质印迹评估，循环中的瘦素蛋白受LPS和细胞因子的调节，与脂肪组织瘦素mRNA的调节平行。在宿主对感染的反应过程中瘦素的诱导可能导致感染性厌食症。
