Horm Metab Res 1980; 12(9): 421-425
DOI: 10.1055/s-2007-999165
© Georg Thieme Verlag, Stuttgart · New York

Pancreatic Alpha and Beta Cell Function in Familial Dysbetalipoproteinemia

M. H. Tan, R. J. Havel, J. E. Gerich, J. S. Soeldner, J. P. Kane
  • Cardiovascular Research Institute and Department of Medicine, University of California, San Francisco, California, and the Elliott P. Joslin Research Laboratory, Joslin Diabetes Foundation, Inc., Department of Medicine, Harvard Medical School, Boston, Massachusetts, U.S.A.
Further Information

Publication History

1979

1980

Publication Date:
24 April 2008 (online)

Summary

Resistance to both insulin and glucagon have been considered as possible causes of primary hypertriglyceridemia. In the present research, we have compared insulin and glucagon secretion in five hyperlipidemic patients with familial dysbetalipoproteinemia with five normolipidemic control subjects matched for age, sex and adiposity. Plasma insulin and glucagon concentrations measured during standard oral glucose tolerance and arginine infusion tests were similar in the two groups. Blood glucose fell transiently in the controls, but not in the patients, during the Himsworth test (100 g glucose orally plus 0.05 U insulin per kg body weight intravenously). There were no significant differences in plasma FFA concentrations and responses during all tests between the groups. The percentage reduction in plasma triglyceride concentration during infusion of arginine was similar in the two groups. These results suggest that the patients with familial dysbetalipoproteinemia were slightly less insulin sensitive than the controls. However, primary insensitivity to glucagon or insulin does not appear to be fundamental to the pathogenesis of hyperlipidemia in familial dysbetalipoproteinemia.