Triscari J, Nauss-Karol C, Levin B E, Sullivan A C
Metabolism. 1985 Jun;34(6):580-7. doi: 10.1016/0026-0495(85)90198-2.
Mature male Sprague-Dawley rats fed a powdered Purina Chow diet containing corn oil and condensed milk (CM) were compared to rats fed a Purina Chow diet (control). CM rats gained more weight and consumed more calories over a 73-day period than the control rats. The increased weight gain and body fat in CM rats was accompanied by increased cell number in retroperitoneal and inguinal but not epididymal fat pads while cell size was unchanged in all three pads. After obesity had developed there was an increase in insulin levels, lipolysis, hepatic fatty acid synthesis, and fatty acid oxidation. While CM rats demonstrated hyperinsulinemia and hyperglycerolemia, they maintained normal glucagon and glucose levels. They demonstrated higher rates of fatty acid synthesis in isolated hepatocytes but not in vivo, suggesting that a greater potential for fatty acid synthesis in CM rats was masked in vivo by the inhibitory action of dietary lipids. Beta-oxidation of (1-14C) palmitate in vivo and in vitro, and in vivo ketogenesis were greater in CM than in chow fed rats. These studies demonstrate that, after the development of obesity, CM rats, like genetically obese Zucker rats, are hyperinsulinemic and have elevated levels of fatty acid synthesis. However, unlike obese Zucker rats, CM rats displayed an increase in beta-oxidation. These studies suggest that increased insulin levels and hepatic fatty acid synthesis may contribute to dietary obesity (as they do to genetic obesity), whereas increased fatty acid oxidation in dietary obesity may be a compensatory response to maintain a lower body weight.
将喂食含玉米油和炼乳（CM）的普瑞纳干饲料粉末的成年雄性斯普拉格-道利大鼠与喂食普瑞纳干饲料（对照）的大鼠进行比较。在73天的时间里，CM组大鼠比对照组大鼠体重增加更多，摄入的热量更多。CM组大鼠体重增加和体脂增加伴随着腹膜后和腹股沟脂肪垫细胞数量增加，但附睾脂肪垫细胞数量未增加，而所有三个脂肪垫的细胞大小均未改变。肥胖发生后，胰岛素水平、脂肪分解、肝脏脂肪酸合成和脂肪酸氧化均增加。虽然CM组大鼠表现出高胰岛素血症和高甘油三酯血症，但它们的胰高血糖素和葡萄糖水平保持正常。它们在分离的肝细胞中表现出较高的脂肪酸合成速率，但在体内并非如此，这表明CM组大鼠中脂肪酸合成的更大潜力在体内被膳食脂质的抑制作用所掩盖。CM组大鼠体内和体外（1-14C）棕榈酸的β-氧化以及体内生酮作用均高于喂食普通饲料的大鼠。这些研究表明，肥胖发生后，CM组大鼠与遗传性肥胖的 Zucker 大鼠一样，具有高胰岛素血症且脂肪酸合成水平升高。然而，与肥胖的 Zucker 大鼠不同，CM组大鼠的β-氧化增加。这些研究表明，胰岛素水平升高和肝脏脂肪酸合成可能导致膳食性肥胖（就像它们导致遗传性肥胖一样），而膳食性肥胖中脂肪酸氧化增加可能是维持较低体重的一种代偿反应。
