Studies on the regulation mechanism for sympathetic nervous system activity--using hypothalamic obese mice

Abstract

This study was designed to clarify the role of the ventromedial hypothalamus (VMH) in the regulation mechanism of sympathetic nervous system (SNS) activity. In obese mice with chemically destroyed VMH, norepinephrine (NE) turnover, which is a reliable indicator of SNS activity, was measured in the interscapular brown adipose tissue (IBAT) and heart using inhibition of NE biosynthesis with alpha-methyl-p-tyrosine; the core temperature was also measured. Two types of hypothalamic obese mice (monosodium glutamate (MSG)-treated mice and gold thioglucose (GTG)-treated mice) were used under two diverse conditions: overfeeding and acute cold exposure. The former was performed via sucrose addition, and the latter was carried out at 6 degrees C in two groups of obese mice and their controls. A comparison between the overfed mice and those fasted for 48 hours revealed that the fasted normal controls showed significantly lower core temperatures and significantly decreased NE turnover in the IBAT and heart as compared with the overfed normal controls, while no significant differences were observed between overfed and fasting obese mice in core temperature or NE turnover. Another comparison disclosed that the core temperatures were significantly lowered and NE turnover in both organs increased significantly after cold exposure in two obese groups and their normal controls, though there were no noticeable differences between the MSG- or GTG-treated mice and their controls. These results indicate that the VMH is a center of SNS for response to feeding but not for response to cold.