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To examine whether insulin enhances norepinephrine (NE) turnover, an index of sympathetic nerve activity, the effects of excess insulin and streptozotocin (STZ) induced insulin deficiency were examined in Sprague-Dawley rats. Exogenous insulin caused hyperphagia and elevated (approximately 300%) urinary epinephrine excretion, but did not alter cardiac NE content or turnover. STZ-induced insulin deficiency caused hyperglycemia and hyperphagia, but also did not alter cardiac NE content or turnover. Insulin deficiency reduced hepatic NE content 18%, but did not affect NE turnover or content of kidney or spleen. These data do not support the hypothesis that insulin influences cardiac sympathetic nerve activity in rats. [ABSTRACT FROM AUTHOR]

The norepinephrine turnover in organs of glucose-fed and fat-fed rats were compared to those of starved rats. Rats fed only glucose had higher rates of norepinephrine turnover than starved rats in heart, pancreas, kidney, liver, and lung. The effect of glucose-feeding on norepinephrine turnover was most pronounced in heart (+ 197%) and pancreas (+ 120%), which were examined in the fat feeding study. Rats fed only fat showed the same suppression of insulin levels as fasting rats, and a greater reduction in plasma glucose levels. However, their norepinephrine turnover in heart (+ 182%) and pancreas (+ 173%) was similar to that of glucose-fed rats. Thus glucose and fat increase norepinephrine turnover in the absence of any other nutrients. If these nutrients increase norepinephrine turnover via the same intermediate signal, it cannot be insulin or increased glucose metabolism. [ABSTRACT FROM AUTHOR]