This Article Full Text (PDF) Submit a related Letter to the Editor Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Copyright Permission Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by MANDARINO, L. Articles by RIZZA, R. Search for Related Content PubMed PubMed Citation Articles by MANDARINO, L. Articles by RIZZA, R.

Mechanism of Hyperglycemia and Response to Treatment with an Inhibitor of Fatty Acid Oxidation in a Patient with Insulin Resistance due to Antiinsulin Receptor Antibodies^*

Endocrine Research Unit, Department of Medicine Mayo Medical School and Mayo Clinic, Rochester, Minnesota, 55905
Pediatrics Mayo Medical School and Mayo Clinic, Rochester, Minnesota, 55905
Pathology Mayo Medical School and Mayo Clinic, Rochester, Minnesota, 55905
Anesthesiology Mayo Medical School and Mayo Clinic, Rochester, Minnesota, 55905
McNeil Pharmaceutical Spring House, Pennsylvania, 19477

Address requests for reprints to: Robert A. Rizza, M.D., Mayo Clinic, Rochester, Minnesota 55905.

Severe hyperglycemia and insulin resistance due to antiinsulin receptor antibodies developed over a period of 3 months in a 50-yr-old insulin-requiring diabetic patient. The hyperglycemia resulted from overproduction of glucose due to excessive rates of glycogenolysis and gluconeogenesis rather than decreased glucose utilization. Treatment with methyl-2-tetradecylglycidate, an inhibitor of fatty acid oxidation, resulted in a decrease in plasma glucose concentration. This was associated with a decrease in the rate of glucose production due to decreases in both gluconeogenesis and glycogenolysis rates, as well as an increase in the respiratory quotient. Plasma glucose concentrations continued to respond to the drug for the next 2 months until the sudden development of terminal hypoglycemia. The hypoglycemic action of the drug is consistent with the existence of an insulin-independent effect of fatty acid oxidation on glucose metabolism in man.

^* This work was supported in part by USPHS Grants AM-29953 and AM-31082, grants from the Mayo Foundation and Mr. and Mrs. Bruce Rappaport, and the Rosalyn S. Yalow Research and Development Award (to L.M.) from the American Diabetes Association.

Received January 31, 1984.

This article has been cited by other articles:

				I. Duivenvoorden, B. Teusink, P. C. N. Rensen, F. Kuipers, J. A. Romijn, L. M. Havekes, and P. J. Voshol Acute inhibition of hepatic {beta}-oxidation in APOE*3Leiden mice does not affect hepatic VLDL secretion or insulin sensitivity J. Lipid Res., May 1, 2005; 46(5): 988 - 993. [Abstract] [Full Text] [PDF]

				R. O. Deems, R. C. Anderson, and J. E. Foley Hypoglycemic effects of a novel fatty acid oxidation inhibitor in rats and monkeys Am J Physiol Regulatory Integrative Comp Physiol, February 1, 1998; 274(2): R524 - R528. [Abstract] [Full Text] [PDF]

				M. Caruso and J. M. Miles Is There a Direct Relationship Between Lactic Acidosis and Epinephrine Administration?-Reply Arch Intern Med, April 1, 1988; 148(4): 981 - 981. [Abstract] [PDF]