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Impaired glucagon response to sympathetic nerve stimulation in the BB diabetic rat: effect of early sympathetic islet neuropathy

¹Division of Metabolism, Endocrinology and Nutrition, Veterans Affairs Puget Sound Health Care System, Seattle, 98108; and ²Division of Metabolism, Endocrinology and Nutrition, Department of Medicine, and ³Department of Psychiatry, University of Washington, Seattle, Washington 98195

Submitted 3 April 2003 ; accepted in final form 17 July 2003

We investigated the functional impact of a recently described islet-specific loss of sympathetic nerves that occurs soon after the autoimmune destruction of -cells in the BB diabetic rat (35). We found that the portal venous (PV) glucagon response to sympathetic nerve stimulation (SNS) was markedly impaired in newly diabetic BB rats (BB D). We next found a normal glucagon response to intravenous epinephrine in BB D, eliminating the possibility of a generalized secretory defect of the BB D -cell as the mediator of the impaired glucagon response to SNS. We then sought to determine whether the glucagon impairment to SNS in BB D was due solely to their loss of islet sympathetic nerve terminals or whether other effects of autoimmune diabetes contributed. We therefore reproduced, in nondiabetic Wistar rats, an islet nerve terminal loss similar to that in BB D with systemic administration of the sympathetic neurotoxin 6-hydroxydopamine. The impairment of the glucagon response to SNS in these chemically denervated, nondiabetic rats was similar to that in the spontaneously denervated BB D. We conclude that the early sympathetic islet neuropathy of BB D causes a functional defect of the sympathetic pathway to the -cell that can, by itself, account for the impaired glucagon response to postganglionic SNS.

norepinephrine; 6-hydroxydopamine; neuropathy

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