Levin B E, Hogan S, Sullivan A C
Neurology Service, Veterans Administration Medical Center, East Orange 07019.
Am J Physiol. 1989 Mar;256(3 Pt 2):R766-71. doi: 10.1152/ajpregu.1989.256.3.R766.
A search was made for predisposing factors and sequelae of diet-induced obesity (DIO) or resistance to DIO (DR). During 3 mo on a high-energy (CM) diet, two-thirds of the male Sprague-Dawley rats ate 16% more calories over the first 30 days and developed DIO. The remaining one-third were DR, gaining the same amount of weight as chow-fed controls. Basal and norepinephrine (NE)-stimulated in vivo O2 consumption, performed before rats were placed on the CM diet, was the same in those rats that later became DR or DIO after 3 mo on the CM diet. DR rats were 4% lighter, whereas DIO rats were equal to chow-fed rats before their exposure to the CM diet. When CM-fed rats were switched to chow, DIO rats took 14 wk to reduce their body and retroperitoneal fat pad weights to those of chow-fed controls, whereas DR rats gained only 40% of the body weight, and fat pads were 34% lighter than controls. After 14 wk, DIO rats were neither hyperinsulinemic nor insulin resistant, whereas DR rats had 64% reduced areas under their insulin curves after intravenous glucose (1 g/kg) compared with controls. Unlike younger rats, animals here had inconsistent plasma NE responses to intravenous glucose. Therefore the CM diet produces DR and DIO states that tend to become self-perpetuating once established.
对饮食诱导肥胖（DIO）或对饮食诱导肥胖的抵抗（DR）的易感因素和后遗症进行了研究。在为期3个月的高能（CM）饮食期间，三分之二的雄性Sprague-Dawley大鼠在最初30天摄入的热量比正常多16%，并发展为饮食诱导肥胖。其余三分之一具有饮食诱导肥胖抵抗能力，体重增加量与正常饮食对照组相同。在大鼠开始食用CM饮食之前进行的基础和去甲肾上腺素（NE）刺激的体内耗氧量，在3个月后变为饮食诱导肥胖抵抗或饮食诱导肥胖的大鼠中是相同的。饮食诱导肥胖抵抗大鼠比正常饮食对照组轻4%，而饮食诱导肥胖大鼠在接触CM饮食前与正常饮食大鼠体重相当。当食用CM饮食的大鼠改为正常饮食时，饮食诱导肥胖大鼠需要14周才能将其体重和腹膜后脂肪垫重量降至正常饮食对照组水平，而饮食诱导肥胖抵抗大鼠体重仅增加了正常饮食对照组的40%，脂肪垫比对照组轻34%。14周后，饮食诱导肥胖大鼠既没有高胰岛素血症也没有胰岛素抵抗，而饮食诱导肥胖抵抗大鼠静脉注射葡萄糖（1 g/kg）后胰岛素曲线下面积比对照组减少了64%。与年轻大鼠不同，这里的动物对静脉注射葡萄糖的血浆去甲肾上腺素反应不一致。因此，CM饮食会产生饮食诱导肥胖抵抗和饮食诱导肥胖状态，一旦形成往往会自我延续。
