Abstract

It has been established that the liver, through the afferent pathway of the vagus nerve, can influence insulin secretion. The purpose of the present study was to determine if this influence can be altered by different nutritional status aimed at inducing metabolic changes in the liver. This was carried out by comparing the insulin response 30 min after sectioning of the hepatic vagus branch in five experimental conditions: a normal (NCD) and a medium-fat diet (MFD) for 3 weeks, both with and without an overnight fast, and after an overloading liver glycogen protocol (normal diet). All experiments were conducted using anesthetized, adrenodemedullated rats. Blood was collected before and after (30 min) the hepatic vagotomy (HV) or a sham operation (SHM). As expected, liver glycogen levels were significantly (< 0.01) lower in the fasted than in the fed condition, and were approximately 50% higher ( p < 0.01) in the overloaded than in the normally fed condition. Basal insulin concentrations were also lower ( p < 0.01) in the fasted compared to the fed groups, but were significantly ( p < 0.01) increased by the medium-fat diet. Plasma glucose levels were significantly ( p < 0.01) decreased by the overnight fast, but were not affected by the hepatic vagotomy. Plasma catecholamine concentrations were similar in all experimental conditions. Insulin concentrations were significantly ( p < 0.05) increased by the HV, compared to SHM rats, in all experimental conditions (from 50% to 75%). The extent of this response was altered by the diet manipulations as the HV-induced insulin increase was greater ( p < 0.01) in the MID than in the NCD groups, whether fed or fasted. Furthermore, and contrary to our expectations, high hepatic glycogen contents did not reduce the insulin response to an acute hepatic vagotomy. These results indicate that the insulin increase induced by an acute HV is influenced by the prevailing metabolic conditions, and suggest that the hepatic vagus nerve exerts a constant inhibition on insulin secretion, independently of the hepatic glycogen content.

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