ALTERED SYMPATHETIC CONTROL OF NUTRIENT MOBILIZATION DURING PHYSICAL EXERCISE AFTER LESIONS IN THE VMH

To study the impact of obesity on sympathetic nervous regulation of nutrient mobilization, obese rats and lean controls were subjected to physical exercise. Male Wistar rats, rendered obese by bilateral electrolytic lesions of the ventromedial hypothalamus (VMH) were subjected to 15 min swimming. Permanent cardiac catheters allowed frequent blood sampling. At rest, glucose, free fatty acids (FFA), and insulin concentrations were elevated in the obese animals, whereas catecholamine levels were similar in both groups. During exercise, glucose concentrations reached higher values in the lesioned rats, whereas these animals did not display the normal FFA increment. Plasma insulin concentrations were suppressed in both groups, and the rate of suppression was very similar when expressed as percentage change from resting levels. There was no difference in plasma epinephrine responses during swimming, but the increase in norepinephrine was diminished in the obese animals. The results suggest that obesity after VMH lesion leads to reduced stimulation of lipolysis by norepinephrine and a predominant mobilization of glucose during exercise, both favoring glucose utilization and the accumulation of fat

Immuno-virological and toxicity outcomes of HIV-infected patients after 48 months of ART in Phnom Penh, Cambodia

Mexico AIDS Conference 200

Overfeeding, Autonomic Regulation and Metabolic Consequences

The autonomic nervous system plays an important role in the regulation of body processes in health and disease. Overfeeding and obesity (a disproportional increase of the fat mass of the body) are often accompanied by alterations in both sympathetic and parasympathetic autonomic functions. The overfeeding-induced changes in autonomic outflow occur with typical symptoms such as adiposity and hyperinsulinemia. There might be a causal relationship between autonomic disturbances and the consequences of overfeeding and obesity. Therefore studies were designed to investigate autonomic functioning in experimentally and genetically hyperphagic rats. Special emphasis was given to the processes that are involved in the regulation of peripheral energy substrate homeostasis. The data revealed that overfeeding is accompanied by increased parasympathetic outflow. Typical indices of vagal activity (such as the cephalic insulin release during food ingestion) were increased in all our rat models for hyperphagia. Overfeeding was also accompanied by increased sympathetic tone, reflected by enhanced baseline plasma norepinephrine (NE) levels in both VMH-lesioned animals and rats rendered obese by hyperalimentation. Plasma levels of NE during exercise were, however, reduced in these two groups of animals. This diminished increase in the exercise-induced NE outflow could be normalized by prior food deprivation. It was concluded from these experiments that overfeeding is associated with increased parasympathetic and sympathetic tone. In models for hyperphagia that display a continuously elevated nutrient intake such as the VMH-lesioned and the overfed rat, this increased sympathetic tone was accompanied by a diminished NE response to exercise. This attenuated outflow of NE was directly related to the size of the fat reserves, indicating that the feedback mechanism from the periphery to the central nervous system is altered in the overfed state.