SEVERELY IMPAIRED ADIPSIN EXPRESSION IN GENETIC AND ACQUIRED OBESITY
SEVERELY IMPAIRED ADIPSIN EXPRESSION IN GENETIC AND ACQUIRED OBESITY
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DOI：
10.1126/science.3299706
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发表时间：
1987-07-24
期刊：
影响因子：
56.9
通讯作者：
SPIEGELMAN, BM
中科院分区：
文献类型：
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作者：
FLIER, JS;COOK, KS;SPIEGELMAN, BM
脂肪酶是一种丝氨酸蛋白酶同系物，由脂肪细胞合成和分泌，存在于血液中。在啮齿动物代谢紊乱期间和几种肥胖实验模型中分析了脂蛋白信使RNA（mRNA）和蛋白质的表达。在正常大鼠和糖尿病大鼠中，由于链脲佐菌素诱导的胰岛素缺乏，在禁食期间脂肪组织中脂肪酶mRNA丰度增加。在连续输注葡萄糖期间，Adipsin mRNA丰度降低，这诱导伴随脂肪量增加的高血糖、高胰岛素血症状态;与其同类小鼠相比，在两种遗传性肥胖小鼠品系（db/db和ob/ob）中Adipsin mRNA丰度被抑制（>100倍），并且当通过向新生小鼠注射谷氨酸盐化学诱导肥胖时，Adipsin mRNA丰度也降低。在这些肥胖动物模型中，循环脂蛋白酶蛋白减少，如用脂蛋白酶抗血清免疫印迹所测定。在通过单纯过度喂养正常大鼠获得的肥胖模型（自助餐模型）中观察到脂蛋白酶表达的微小变化。这些数据表明，在上述代谢紊乱状态的可能作用，并提出的可能性，adipsin的表达可用于区分肥胖所产生的某些遗传或代谢缺陷，从那些纯粹的过度喂养。
Adipsin, a serine protease homolog, is synthesized and secreted by adipose cells and is found in the bloodstream. The expression of adipsin messenger RNA (mRNA) and protein was analyzed in rodents during metabolic perturbations and in several experimental models of obesity. Adipsin mRNA abundance is increased is adipose tissue during fasting in normal rats and in diabetes due to streptozotocin-induced insulin deficiency. Adipsin mRNA abundance decreased during the continuous infusion of glucose, which induces a hyperglycemic, hyperinsulinemic state that is accompanied by an increased adipose mass; it is suppressed (>100-fold) in two strains of genetically obese mice (db/db and ob/ob), compared to their congenic counterparts, and is also reduced when obesity is induced chemically by injection of monosodium glutamate into newborn mice. Circulating adipsin protein is decreased in these animal models of obesity, as determined by immunoblotting with antisera to adipsin. Little change in adipsin expression is observed in a model of obesity obtained by pure overfeeding of normal rats (cafeteria model). These data suggest a possible role for adipsin in the above-mentioned disordered metabolic states, and raise the possibility that adipsin expression may be used to distinguish obesities that arise from certain genetic or metabolic defects from those that result from pure overfeeding.