Muscarinic stimulation and antagonism and glucoregulation in nondiabetic and obese hyperglycemic mice

S. Fukudo, S. Virnelli, C. M. Kuhn, C. Cochrane, M. N. Feinglos, R. S. Surwit

Research output: Contribution to journalArticlepeer-review

24 Citations (Scopus)

Abstract

Plasma glucose and insulin responses to a muscarinic agonist (bethanechol chloride) and a muscarinic antagonist (atropine) were evaluated in obese C57BL/6J ob/ob mice and in lean C57BL/6J +/? mice. In lean +/? mice, plasma glucose decreased in response to 1 and 2 μg/kg bethanechol chloride, whereas insulin increased significantly. In ob/ob mice, insulin increased remarkably in response to bethanechol administration (saline, 632 ± 80 μU/ml; 2 μg/kg bethanechol chloride, 1794 ± 97 μU/ml; n = 10), but surprisingly, plasma glucose also rose significantly (saline, 230 ± 14 mg/dl; 2 μg/g bethanechol chloride, 363 ± 18 mg/dl, n = 10). This exaggerated hyperglycemia in ob/ob mice was not associated with significant changes in plasma glucagon. Furthermore, administration of propranolol hydrochloride did not diminish bethanechol chloride-induced hyperglycemia in ob/ob mice. Administration of atropine (2.5, 5, and 10 mg/kg body wt) induced a significant decrease in plasma insulin without changes in plasma glucose in ob/ob mice, whereas neither plasma insulin nor plasma glucose changed in lean mice. Finally, conversion of [14C]alanine to glucose was increased in ob/ob mice after bethanechol chloride administration, indicating that muscarinic stimulation increases gluconeogenesis in an animal model of type II (non-insulin-dependent) diabetes.

Original languageEnglish
Pages (from-to)1433-1438
Number of pages6
JournalDiabetes
Volume38
Issue number11
DOIs
Publication statusPublished - 1989

ASJC Scopus subject areas

  • Internal Medicine
  • Endocrinology, Diabetes and Metabolism

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