Ji H, Friedman M I
Monell Chemical Senses Center, Philadelphia, PA 19104, USA.
Int J Obes (Lond). 2008 Aug;32(8):1331-4. doi: 10.1038/ijo.2008.71. Epub 2008 May 27.
Rats vary in their propensity to become obese when eating a high-fat diet, but the factors that make some rats susceptible and others resistant to diet-induced obesity are unclear. Recent studies show that rats predisposed to diet-induced obesity have a preexisting deficit in fat oxidation and suggest that this impairment is due in part to reduced fatty acid oxidation in liver. To determine directly whether rats susceptible to diet-induced obesity are less able to oxidize fatty acids in liver, we measured palmitate oxidation in hepatocytes isolated from outbred Sprague-Dawley rats that were identified while still eating a low-fat diet as obesity-prone or obesity-resistant by using a new screening procedure based on the change in plasma triglyceride concentration produced by an intragastric load of a fat and carbohydrate mixture. The results showed that hepatocytes from rats thus identified as obesity-prone oxidized 44% less palmitate in vitro than did those from obesity-resistant rats. This difference in hepatocyte fatty acid oxidation is consistent with and may explain at least in part the reduced capacity of obesity-prone rats to oxidize fat.
当食用高脂肪饮食时，大鼠在变得肥胖的倾向上存在差异，但导致一些大鼠易患饮食诱导性肥胖而另一些具有抗性的因素尚不清楚。最近的研究表明，易患饮食诱导性肥胖的大鼠在脂肪氧化方面预先存在缺陷，并表明这种损害部分归因于肝脏中脂肪酸氧化减少。为了直接确定易患饮食诱导性肥胖的大鼠肝脏氧化脂肪酸的能力是否较低，我们测量了从远交群斯普拉格-道利大鼠分离的肝细胞中的棕榈酸氧化，这些大鼠在仍食用低脂饮食时通过基于胃内负荷脂肪和碳水化合物混合物产生的血浆甘油三酯浓度变化的新筛选程序被鉴定为易肥胖或抗肥胖。结果表明，如此鉴定为易肥胖的大鼠的肝细胞在体外氧化棕榈酸的能力比抗肥胖大鼠的肝细胞低44%。肝细胞脂肪酸氧化的这种差异与易肥胖大鼠氧化脂肪能力降低相一致，并且至少可以部分解释该现象。
