Veterinary Biomedical Sciences, Western College of Veterinary Medicine, University of Saskatchewan,52 Campus Drive,Saskatoon,SK,CanadaS7N 5B4.
College of Agriculture and Bioresources, University of Saskatchewan,51 Campus Drive,Saskatoon,SK,CanadaS7N 5A8.
Br J Nutr. 2014 Aug 28;112(4):647-56. doi: 10.1017/S0007114514001214. Epub 2014 May 30.
The time course of metabolic and cardiovascular changes with weight gain and subsequent weight loss has not been elucidated. The goal of the present study was to determine how weight gain, weight loss and altered body fat distribution affected metabolic and cardiovascular changes in an obese dog model. Testing was performed when the dogs were lean (scores 4-5 on a nine-point scale), after ad libitum feeding for 12 and 32 weeks to promote obesity (>5 score), and after weight loss. Measurements included serum glucose and insulin, plasma leptin, adiponectin and C-reactive protein, echocardiography, flow-mediated dilation and blood pressure. Body fat distribution was assessed by computed tomography. Fasting serum glucose concentrations increased significantly with obesity (P< 0·05). Heart rate increased by 22 (SE 5) bpm after 12 weeks of obesity (P= 0·003). Systolic left ventricular free wall thickness increased after 12 weeks of obesity (P= 0·002), but decreased after weight loss compared with that observed in the lean phase (P= 0·03). Ventricular free wall thickness was more strongly correlated with visceral fat (r 0·6, P= 0·001) than with total body fat (r 0·4, P= 0·03) and was not significantly correlated with subcutaneous body fat (r 0·3, P= 0·1). The present study provides evidence that metabolic and cardiovascular alterations occur within only 12 weeks of obesity in an obese dog model and are strongly predicted by visceral fat. These results emphasise the importance of obesity prevention, as weight loss did not result in the return of all metabolic indicators to their normal levels. Moreover, systolic cardiac muscle thickness was reduced after weight loss compared with the pre-obesity levels, suggesting possible acute adverse cardiovascular effects.
体重增加和随后的体重减轻过程中代谢和心血管变化的时间进程尚未阐明。本研究的目的是确定体重增加、体重减轻和改变的体脂分布如何影响肥胖犬模型中的代谢和心血管变化。在犬处于消瘦状态（九点量表评分为 4-5 分）时、在进行 12 和 32 周随意喂养以促进肥胖（>5 分）后以及在体重减轻后进行测试。测量指标包括血清葡萄糖和胰岛素、血浆瘦素、脂联素和 C 反应蛋白、超声心动图、血流介导的扩张和血压。通过计算机断层扫描评估体脂分布。肥胖时空腹血清葡萄糖浓度显著升高（P<0·05）。肥胖 12 周后心率增加 22（SE 5）bpm（P=0·003）。肥胖 12 周后左心室游离壁厚度增加（P=0·002），但与消瘦期相比，体重减轻后厚度降低（P=0·03）。心室游离壁厚度与内脏脂肪的相关性更强（r 0·6，P=0·001），与全身脂肪的相关性较弱（r 0·4，P=0·03），与皮下脂肪的相关性不显著（r 0·3，P=0·1）。本研究提供的证据表明，在肥胖犬模型中，仅在肥胖 12 周内就会发生代谢和心血管改变，并且与内脏脂肪密切相关。这些结果强调了肥胖预防的重要性，因为体重减轻并未使所有代谢指标恢复到正常水平。此外，与肥胖前水平相比，体重减轻后心肌厚度减少，表明可能存在急性不良心血管影响。
