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In humans, obesity is closely associated with insulin resistance (IR) and dyslipidaemia. The purpose of this study was to explore the effect of age on metabolic disturbances related to obesity in dogs ( n = 25). Three age-groups of dogs (puppies, young adults and mature adults) were overfed to induce obesity, and body composition, insulin sensitivity index (IIS) (euglycaemic–hyperinsulinaemic glucose clamp) and plasma lipids were measured. Fat mass was similar in the three obese groups (30 ± 1% in puppies, 34 ± 1% in young adults and 39 ± 1% in mature adults). In mature adults, body weight (BW) increased (+45%, p < 0.001) and IIS decreased (−60%, p < 0.001) over 22 weeks. In young adults, BW gain was similar but slower (60 weeks) and IIS decreased to a lesser extent (−49%, p < 0.001). Overfed puppies weighed 30% more (p < 0.01) than normally-fed control puppies, but there was no change in IIS. Unlike young and mature adults, obese puppies did not exhibit significant changes in triglycerides (TG) and free fatty acid concentrations. In conclusion, as in humans, obese dogs develop IR that is associated with high TG levels; however, younger animals may be better able to balance energy needs with energy consumption. [ABSTRACT FROM AUTHOR]

Summary Many studies have shown that in humans insulin resistance (IR) is associated with obesity and hypertriglyceridaemia. The aim of our study was to develop slowly dietary-induced obesity in dogs through long-term overfeeding of a high-fat diet, and to characterize this IR, hypertriglyceridaemic and normotensive model. Insulin resistance was assessed by the euglycaemic hyperinsulinaemic clamp technique. The contribution of hepatic glucose production during the clamp was evaluated using a constant stable-isotope-labelled glucose infusion. Overfeeding a high-fat diet for 7 months was associated with a 43 ± 5% body weight increase. Insulin resistance was characterized by hyperinsulinaemia in the unfed state (10 ± 1 vs. 24 ± 1 μ U/ml, in healthy and obese dogs, respectively, p < 0.02) and by a reduction of the insulin-mediated glucose uptake (28 ± 3 vs. 16 ± 1 mg/kg/min, p < 0.02). Hepatic glucose production suppression under insulin infusion allowed to conclude that this reduced glucose uptake resulted from a decrease of insulin sensitivity in obese dogs. Furthermore, animals remained normotensive and exhibited a marked hypertriglyceridaemia (0.26 ± 0.04 vs. 0.76 ± 0.15 mmol/l, in healthy and obese dogs, respectively, p < 0.02). Because hypertriglyceridaemia is the most common lipid abnormality in insulin-resistant humans, this dog with slowly induced obesity may constitute a good model to study the consequences of IR in lipid metabolism independently of vascular changes. [ABSTRACT FROM AUTHOR]