Pérez-Echarri N, Pérez-Matute P, Martínez J A, Marti A, Moreno-Aliaga M J
Department of Physiology and Nutrition, University of Navarra, 31008 Pamplona, Spain.
J Physiol Biochem. 2005 Jun;61(2):333-42. doi: 10.1007/BF03167050.
The aim of the present study was to identify the role of leptin and adiponectin in the development of resistance or susceptibility to diet-induced obesity in rats. For this purpose, male Wistar rats were fed with standard laboratory diet (control group) or cafeteria diet. After 15 days, two groups of rats with different response respect to the cafeteria diet were identified, and were assigned as diet-induced obesity (DIO) and diet resistant (DR) rats. The high-fat diet induced a very significant increase in both body and fat mass weight in DIO group. However, DR rats, gained even less weight than control-fed animals. Food intake was increased in cafeteria-fed rats (both DIO and DR) in comparison to control group; but hyperphagia was higher in DIO rats. In addition, feed efficiency (the ratio of weight gained to calories consumed) was significantly decreased in DR as compared to DIO rats. Regarding leptin, a significant increase in both adipose tissue gene expression and serum levels was observed in DIO rats in comparison with other groups (control and DR). A significant increase in both adiponectin circulating levels and adipose tissue mRNA expression was also observed in DIO animals as compared with the other groups. These data suggest that the susceptibility to obesity of DIO rats might be secondary, at least in part, to an earlier development of leptin resistance, which could lead to alterations in food intake (hyperphagia) and energetic metabolism. However, neither changes in leptin or adiponectin seem to be involved in the adaptive mechanisms that confer resistance to high fat intake.
本研究的目的是确定瘦素和脂联素在大鼠饮食诱导肥胖的抗性或易感性发展中的作用。为此，给雄性Wistar大鼠喂食标准实验室饮食（对照组）或自助餐厅饮食。15天后，确定了两组对自助餐厅饮食有不同反应的大鼠，并将其分为饮食诱导肥胖（DIO）大鼠和饮食抗性（DR）大鼠。高脂饮食使DIO组的体重和脂肪量都显著增加。然而，DR大鼠的体重增加甚至比喂食对照饮食的动物还要少。与对照组相比，喂食自助餐厅饮食的大鼠（DIO和DR）的食物摄入量增加；但DIO大鼠的食欲亢进更高。此外，与DIO大鼠相比，DR大鼠的饲料效率（体重增加与消耗热量的比率）显著降低。关于瘦素，与其他组（对照组和DR组）相比，DIO大鼠的脂肪组织基因表达和血清水平均显著增加。与其他组相比，DIO动物的脂联素循环水平和脂肪组织mRNA表达也显著增加。这些数据表明，DIO大鼠对肥胖的易感性可能至少部分继发于早期的瘦素抵抗，这可能导致食物摄入量（食欲亢进）和能量代谢的改变。然而，瘦素或脂联素的变化似乎都不参与赋予对高脂肪摄入抗性的适应性机制。
