Harris R B, Martin R J
J Nutr. 1986 Oct;116(10):2013-27. doi: 10.1093/jn/116.10.2013.
When one member of a parabiosed pair of rats is made obese its partner experiences a specific loss of body fat. In this study we determined whether production of the "lipid-depleting" factor in obese rats was diet specific. One member in each of 30 pairs was tube fed 200% normal intake of high carbohydrate (CHO), high fat corn oil or high fat medium-chain triglyceride diet. Their partners and both members of five control pairs ate CHO diet ad libitum. After 27 d of 200% feeding, in vitro hepatic, adipose and hypothalamic metabolism were measured. Composition of the diet used to induce obesity did not change the response of partners. All non-tube-fed partners had normal food intakes, body protein, hepatic fatty acid synthesis (FAS) and esterification (FAE), palmitate, glucose and beta-hydroxybutyrate oxidation. Adipose FAS and FAE were depressed, body fat was halved. Hypothalamic metabolism was not changed. A lipid-depleting agent originating in obese rats specifically inhibits adipose lipogenesis in their partners. Production of this factor does not appear to be influenced by dietary energy source.
当联体大鼠中的一只变得肥胖时，其同伴会出现特定的体脂减少。在本研究中，我们确定肥胖大鼠中“脂质消耗”因子的产生是否具有饮食特异性。30对大鼠中的每对中的一只通过管饲给予正常摄入量200%的高碳水化合物（CHO）、高脂肪玉米油或高脂肪中链甘油三酯饮食。它们的同伴以及五对对照大鼠的两只均自由采食CHO饮食。在给予200%的食物27天后，测量肝脏、脂肪组织和下丘脑的体外代谢。用于诱导肥胖的饮食组成并未改变同伴的反应。所有非管饲的同伴食物摄入量正常，身体蛋白质、肝脏脂肪酸合成（FAS）和酯化（FAE）、棕榈酸、葡萄糖和β-羟基丁酸氧化均正常。脂肪组织的FAS和FAE降低，体脂减半。下丘脑代谢未改变。源自肥胖大鼠的脂质消耗剂特异性抑制其同伴脂肪组织的脂肪生成。该因子的产生似乎不受饮食能量来源的影响。
