Naderali Ebrahim K, Estadella Debora, Rocha Milagros, Pickavance Lucy C, Fatani Sameer, Denis Raphael G P, Williams Gareth
Neuroendocrine and Obesity Biology Unit, Department of Medicine, University of Liverpool, Daulby Street, Liverpool L69 3GA, UK.
Clin Sci (Lond). 2003 Oct;105(4):403-8. doi: 10.1042/CS20030094.
Adiponectin levels are decreased in subjects with obesity, diabetes and coronary artery disease. In the present study, we have investigated whether the decrease in the levels and mRNA expression of adiponectin is due to obesity or to the diet itself. Wistar rats were either fed standard laboratory chow throughout (controls) or given a fat-enriched, glucose-enriched diet (diet-fed) for 2 days or 16 weeks. After 2 days of diet feeding, total body weight, fat pad masses and the plasma levels of glucose, insulin and leptin were all comparable between the two groups, while plasma NEFA (non-esterified fatty acid) and triacylglycerol levels were increased in the diet-fed animals (P<0.01 for both). There was a marked (P<0.01) decrease in plasma adiponectin levels. After 16 weeks of diet feeding, diet-fed rats had significantly higher body weight, fat pad mass and plasma levels of leptin, adiponectin, NEFA and triacylglycerol (P<0.001 for all) compared with chow-fed controls, whereas plasma levels of glucose and insulin were similar in the two groups. After 2 days of diet feeding, there were no significant changes in Ob mRNA levels in epididymal fat, whereas there was a marked decrease in adiponectin mRNA levels. After 16 weeks of diet feeding, rats had significantly increased levels of Ob mRNA, but decreased adiponectin mRNA levels, in epididymal fat compared with the chow-fed group (P<0.001 for both). These findings suggest that obesity per se is not a factor in the decreased adiponectin levels observed in obese subjects. We propose that the lipid profile of the plasma and/or the constituents of the diet consumed by rats may contribute to adiponectin levels more than obesity per se.
肥胖、糖尿病和冠状动脉疾病患者的脂联素水平会降低。在本研究中，我们调查了脂联素水平及其mRNA表达的降低是由于肥胖还是饮食本身所致。将Wistar大鼠分为两组，一组自始至终喂食标准实验室饲料（对照组），另一组给予富含脂肪和葡萄糖的饲料（饮食喂养组），持续2天或16周。饮食喂养2天后，两组大鼠的总体重、脂肪垫质量以及血浆葡萄糖、胰岛素和瘦素水平均无显著差异，而饮食喂养组大鼠的血浆非酯化脂肪酸（NEFA）和甘油三酯水平升高（两者均P<0.01）。血浆脂联素水平显著降低（P<0.01）。饮食喂养16周后，与喂食普通饲料的对照组相比，饮食喂养组大鼠的体重、脂肪垫质量以及血浆瘦素、脂联素、NEFA和甘油三酯水平显著更高（所有指标P<0.001），而两组大鼠的血浆葡萄糖和胰岛素水平相似。饮食喂养2天后，附睾脂肪中Ob mRNA水平无显著变化，而脂联素mRNA水平显著降低。饮食喂养16周后，与喂食普通饲料的组相比，大鼠附睾脂肪中Ob mRNA水平显著升高，但脂联素mRNA水平降低（两者均P<0.001）。这些发现表明，肥胖本身并非肥胖受试者脂联素水平降低的因素。我们认为，大鼠血浆中的脂质成分和/或所摄入饮食的成分对脂联素水平的影响可能大于肥胖本身。
