February 1, 1982
View Full PaperEffects of 2-Deoxy-D-Glucose on the Cardiac Sympathetic Nerves and the Adrenal Medulla in the Rat: Further Evidence for a Dissociation of Sympathetic Nervous System and Adrenal Medullary Responses*
Key Result
Chronic administration of 2-deoxy-D-glucose in rats suppressed cardiac sympathetic nerve activity and stimulated adrenal medullary epinephrine release, independent of adrenal catecholamine release.
Structured PICO
P
Population
Rats (including adrenalectomized rats)
I
Intervention
2-deoxy-D-glucose (2-DG) administration (ingestion and chronic subcutaneous injections)
O
Outcome
Cardiac sympathetic nerve activity (measured by cardiac [3H]norepinephrine turnover) and adrenal medullary stimulation (measured by urinary epinephrine excretion and adrenal epinephrine content)surrogate
Inhibition of intracellular glucose metabolism with 2-DG suppresses cardiac sympathetic activity while stimulating adrenal medullary release, suggesting that central nervous system glucose metabolism mediates diet-induced changes in sympathetic nervous system activity.
Abstract
In rats and mice, fasting suppresses and sucrose overfeeding stimulates sympathetic nervous system (SNS) activity. Fasting hypoglycemia in rats suppresses SNS activity while stimulating adrenal medullary catecholamine release. Administration of 2-deoxy-D-glucose (2-DG), an inhibitor of intracellular glucose metabolism, also stimulates the adrenal medulla. The studies reported here were undertaken to determine the SNS response to chronic 2-DG administration and to test the hypothesis that diet-induced changes in SNS activity are related to central nervous system glucose metabolism. Ingestion of 2-DG caused an increase in urinary epinephrine excretion and significant depletion of adrenal epinephrine content, both indices of adrenal medullary stimulation. Chronic sc injections of 2-DG in animals with normal or increased food consumption caused simultaneous suppression of cardiac sympathetic nerve activity, as evidenced by diminished cardiac 3Hnorepinephrine turnover, and stimulation of adrenal medullary epinephrine release. Parenteral 2-DG administration to adrenalectomized rats also caused suppression of cardiac sympathetic activity. Thus, this response to neuroglycopenia is independent of adrenal medullary catecholamine release. These results indicate that central nervous system glucose metabolism may mediate diet-induced changes in SNS activity.