Kretschmer Beate D, Schelling Pierre, Beier Norbert, Liebscher Christiane, Treutel Sabine, Krüger Nicole, Scholz Hans-Peter, Haus Anke
Merck KGaA, Preclinical Research, Frankfurter Str. 250, 64293 Darmstadt, Germany.
Life Sci. 2005 Feb 18;76(14):1553-73. doi: 10.1016/j.lfs.2004.08.028. Epub 2004 Dec 22.
Energy intake and expenditure is a highly conserved and well-controlled system with a bias toward energy intake. In times of abundant food supply, individuals tend to overeat and in consequence to increase body weight, sometimes to the point of clinical obesity. Obesity is a disease that is not only characterized by enormous body weight but also by rising morbidity for diabetes type II and cardiovascular complications. To better understand the critical factors contributing to obesity we performed the present study in which the effects of energy expenditure and energy intake were examined with respect to body weight, localization of fat and insulin resistance in normal Wistar rats. It was found that a diet rich in fat and carbohydrates similar to "fast food" (cafeteria diet) has pronounced implication in the development of obesity, leading to significant body weight gain, fat deposition and also insulin resistance. Furthermore, an irregularly presented cafeteria diet (yoyo diet) has similar effects on body weight and fat deposition. However, these rats were not resistant to insulin, but showed an increased insulin secretion in response to glucose. When rats were fed with a specified high fat/carbohydrate diet (10% fat, 56.7% carbohydrate) ad lib or at the beginning of their activity phase they were able to detect the energy content of the food and compensate this by a lower intake. They, however, failed to compensate when food was given in the resting phase and gained more body weight as controls. Exercise, even of short duration, was able to keep rats on lower body weight and reduced fat deposition. Thus, inappropriate food intake with different levels of energy content is able to induce obesity in normal rats with additional metabolic changes that can be also observed in humans.
能量摄入与消耗是一个高度保守且受到良好调控的系统,且偏向于能量摄入。在食物供应充足的时期,个体往往会过度进食,进而导致体重增加,有时甚至达到临床肥胖的程度。肥胖是一种不仅以体重巨大为特征,还以II型糖尿病和心血管并发症发病率上升为特征的疾病。为了更好地理解导致肥胖的关键因素,我们开展了本研究,在正常Wistar大鼠中研究了能量消耗和能量摄入对体重、脂肪分布及胰岛素抵抗的影响。结果发现,富含脂肪和碳水化合物的类似“快餐”的饮食(自助餐饮食)对肥胖的发展有显著影响,导致体重显著增加、脂肪沉积以及胰岛素抵抗。此外,不定期提供的自助餐饮食(溜溜球饮食)对体重和脂肪沉积有类似影响。然而,这些大鼠对胰岛素并不抵抗,而是在对葡萄糖的反应中表现出胰岛素分泌增加。当大鼠自由采食或在活动期开始时喂食特定的高脂肪/碳水化合物饮食(10%脂肪,56.7%碳水化合物)时,它们能够检测食物的能量含量并通过减少摄入量来进行补偿。然而,当在休息期喂食时,它们无法进行补偿,体重比对照组增加得更多。运动,即使是短时间的运动,也能够使大鼠保持较低体重并减少脂肪沉积。因此,不同能量含量的不适当食物摄入能够在正常大鼠中诱发肥胖,并伴有在人类中也能观察到的额外代谢变化。