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1 Division of Metabolism, Endocrinology and Nutrition, VA Puget Sound Health Care System, Seattle, WA, USA; Department of Medicine, Division of Metabolism, Endocrinology and Nutrition, University of Washington, Seattle, WA, USA
2 Division of Metabolism, Endocrinology and Nutrition, VA Puget Sound Health Care System, Seattle, WA, USA; Department of Psychiatry, University of Washington, Seattle, WA, USA
3 Department of Medicine, Division of Metabolism, Endocrinology and Nutrition, University of Washington, Seattle, WA, USA
* To whom correspondence should be addressed. E-mail: mundin{at}u.washington.edu.
We investigated the functional impact of a recently described islet-specific loss of sympathetic nerves that occurs soon after the autoimmune destruction of beta cells in the BB diabetic rat (1). We found that the portal venous 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 alpha cell as the mediator of the impaired glucagon response to SNS. We then sought to determine if 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 non-diabetic Wistar rats, an islet nerve terminal loss similar to 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 (eSIN) of BB D causes a functional defect of the sympathetic pathway to the alpha cell that can, by itself, account for the impaired glucagon response to post-ganglionic SNS.
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