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

Research output: Contribution to journalArticle

Abstract

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 (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 alpha-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

Details

Authors
  • Thomas O Mundinger
  • Qi Mei
  • Dianne P Figlewicz
  • Åke Lernmark
  • Gerald J Jr Taborsky
External organisations
  • University of Washington, Seattle
Research areas and keywords

Subject classification (UKÄ) – MANDATORY

  • Physiology
Original languageEnglish
Pages (from-to)1047-1054
JournalAmerican Journal of Physiology: Endocrinology and Metabolism
Volume285
Issue number5
Publication statusPublished - 2003
Publication categoryResearch
Peer-reviewedYes
Externally publishedYes