To clarify whether activity of the sympathetic nervous system is decreased in streptozotocin-induced diabetic rats, noradrenaline turnover, which is a reliable indicator of sympathetic nervous system activity, was measured in the interscapular brown adipose tissue, heart and pancreas of streptozotocin diabetic rats. Results from studies using inhibition of noradrenaline biosynthesis with alpha-methyl-p-tyrosine demonstrated significant reductions (p less than 0.05-0.001) in sympathetic nervous system activity in the interscapular brown adipose tissue, heart and pancreas of streptozotocin (65 mg/kg) diabetic rats, compared with measurements in streptozotocin (35 mg/kg) diabetic and saline-control rats. The daily injections of neutral protamine Hagedorn insulin to streptozotocin (65 mg/kg) diabetic rats prevented the decrease of noradrenaline turnover in the interscapular brown adipose tissue and heart significantly (p less than 0.02), but this was less marked in pancreas, compared with non-treated streptozotocin (65 mg/kg) diabetic rats. Furthermore reduced noradrenaline turnover was also observed in the control rats which showed comparable changes in body weight to the rats injected with streptozotocin (65 mg/kg). These results suggest that poorly controlled streptozotocin diabetic rats may have reduced sympathetic nervous function, and that insulin therapy might prevent this.
The disappearance of norepinephrine (NE) from brown adipose tissue, heart, and pancreas in vivo has been examined in rats with ventromedial hypothalamic (VMH) lesions and in appropriate control rats. Two weeks after the introduction of these lesions, the rate of NE turnover following blockade of NE synthesis with alpha-methyl-p-tyrosine was significantly greater in brown adipose tissue and heart of rats with VMH lesions than in sham-operated controls. This significant increase occurred whether the animals were fed ad libitum or pair-gained to the sham-operated controls. In the pancreas, on the other hand, no effects of hypothalamic lesions could be detected. When rats were fasted, NE turnover slowed in both sham-operated and VMH-lesioned rats, but the turnover slowed more in sham-operated than in VMH-lesioned rats. When exposed to the cold for 6 h during measurements of NE turnover, VMH-lesioned rats increased their rate of NE turnover as did sham-operated rats. Fasted animals exposed to the cold had significantly higher rates of NE turnover whether or not they also had VMH lesions. Animals with electrolytic or knife-cut VMH lesions showed comparable rates of NE turnover in the fasted state. Eight weeks after hypothalamic lesions, similar studies were conducted. By this time NE turnover was not significantly different between the VMH-lesioned and sham-operated rats fed ad libitum. However, fasting, which slowed NE turnover in sham-operated rats, had no effect in VMH-lesioned animals. These data are discussed in relation to the autonomic hypothesis.
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