Interactions between effects of adrenalectomy and diet on insulin secretion in fa/fa Zucker rats

Abstract

Our objective was to determine if a cafeteria-type diet with increased fat content would block the decrease in insulin secretion induced by adrenalectomy in obese rats. Five week old Zucker (fa/fa) rats were adrenalectomized. One week later, half of the adrenalectomized groups, and age-matched, sham-operated animals were given a diet of 16% fat and 44% carbohydrate. Control animals were maintained on standard rat chow (4.6% fat and 49% carbohydrate). After 4 weeks on the diets, in vivo measurements included caloric intake, weight gain, plasma corticosterone, triglyceride, free fatty acids, and oral glucose tolerance tests. In vitro measurements included glucose-stimulated insulin secretion, glucose phosphorylating activity, islet triglyceride content, and fatty acid oxidizing activity of cultured islets. Generally, the cafeteria diet did not block the effects of adrenalectomy on in vitro insulin secretion parameters, even though in sham-operated animals weight gain and insulin resistance was induced by the diet in vivo. Adrenalectomy and the diet exerted independent effects on glucose phosphorylation and fatty acid oxidation in islets. In conclusion, adrenalectomy decreased the elevated insulin secretion in fa/fa rats. The failure of a cafeteria diet enriched in fat to block the adrenalectomy-mediated changes in B-cell function indicates the importance of glucocorticoids and centrally-mediated effects on insulin secretion and other metabolic parameters.

Glucocorticoids contribute to metabolic and liver impairments induced by lactation overnutrition in male adult rats

“…ADX-induced reduction of body weight and plasma lipid profile in childhood obesity is following the reversal effect of ADX on metabolic parameters in other obesity models (Alarrayed et al, 1992;Mantha et al, 1999;Kibenge and Chan, 2001;Yilmaz et al, 2002). Additionally, the decrease of triglyceride content and FASN expression in the liver by ADX may be due to the well-established stimulatory effects of glucocorticoids on both the accumulation of lipids and TG in the liver (Suzuki and Mizugashira, 1979) and the expression of key enzymes of DNL in the liver, as FASN (Wang et al, 2004;Lee et al, 2011).…”