Hoenig M, Thomaseth K, Waldron M, Ferguson D C
Department of Physiology and Pharmacology, University of Georgia College of Veterinary Medicine, Athens, GA 30602, USA.
Am J Physiol Regul Integr Comp Physiol. 2007 Jan;292(1):R227-34. doi: 10.1152/ajpregu.00313.2006. Epub 2006 Aug 10.
Obesity is a major health problem in cats and a risk factor for diabetes. It has been postulated that cats are always gluconeogenic and that the rise in obesity might be related to high dietary carbohydrates. We examined the effect of a high-carbohydrate/low-protein (HC) and a high-protein/low-carbohydrate (HP) diet on glucose and fat metabolism during euglycemic hyperinsulinemic clamp, adipocytokines, and fat distribution in 12 lean and 16 obese cats before and after weight loss. Feeding diet HP led to greater heat production in lean but not in obese cats. Regardless of diet, obese cats had markedly decreased glucose effectiveness and insulin resistance, but greater suppression of nonesterified fatty acids during the euglycemic hyperinsulinemic clamp was seen in obese cats on diet HC compared with lean cats on either diet or obese cats on diet HP. In contrast to humans, obese cats had abdominal fat equally distributed subcutaneously and intra-abdominally. Weight loss normalized insulin sensitivity; however, increased nonesterified fatty acid suppression was maintained and fat loss was less in cats on diet HC. Adiponectin was negatively and leptin positively correlated with fat mass. Lean cats and cats during weight loss, but not obese cats, adapted to the varying dietary carbohydrate/protein content with changes in substrate oxidation. We conclude that diet HP is beneficial through maintenance of normal insulin sensitivity of fat metabolism in obese cats, facilitating the loss of fat during weight loss, and increasing heat production in lean cats. These data also show that insulin sensitivity of glucose and fat metabolism can be differentially regulated in cats.
肥胖是猫的一个主要健康问题,也是糖尿病的一个风险因素。据推测,猫总是进行糖异生作用,肥胖率上升可能与高碳水化合物饮食有关。我们研究了高碳水化合物/低蛋白(HC)和高蛋白/低碳水化合物(HP)饮食对12只瘦猫和16只肥胖猫在体重减轻前后进行正常血糖高胰岛素钳夹期间的葡萄糖和脂肪代谢、脂肪细胞因子以及脂肪分布的影响。喂食HP饮食导致瘦猫的产热增加,但肥胖猫没有。无论饮食如何,肥胖猫的葡萄糖利用率和胰岛素抵抗均显著降低,但与喂食任何一种饮食的瘦猫或喂食HP饮食的肥胖猫相比,喂食HC饮食的肥胖猫在正常血糖高胰岛素钳夹期间对非酯化脂肪酸的抑制作用更强。与人类不同,肥胖猫的腹部脂肪在皮下和腹腔内分布均匀。体重减轻使胰岛素敏感性恢复正常;然而,喂食HC饮食的猫非酯化脂肪酸抑制作用增加的情况持续存在,且脂肪减少较少。脂联素与脂肪量呈负相关,瘦素与脂肪量呈正相关。瘦猫和体重减轻期间的猫,而不是肥胖猫,会随着底物氧化的变化适应不同的饮食碳水化合物/蛋白质含量。我们得出结论,HP饮食通过维持肥胖猫脂肪代谢的正常胰岛素敏感性、促进体重减轻期间的脂肪减少以及增加瘦猫的产热而有益。这些数据还表明,猫的葡萄糖和脂肪代谢的胰岛素敏感性可以受到不同的调节。