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Research Article Free access | 10.1172/JCI107095

Resistance to Symptomatic Insulin Reactions after Fasting

Ernst J. Drenick, Lia C. Alvarez, Gabor C. Tamasi, and Arnold S. Brickman

Medical Service and Research, Veterans Administration Wadsworth Hospital Center, Los Angeles, California 90073

Department of Medicine, University of California at Los Angeles School of Medicine, Los Angeles, California 90024

Find articles by Drenick, E. in: PubMed | Google Scholar

Medical Service and Research, Veterans Administration Wadsworth Hospital Center, Los Angeles, California 90073

Department of Medicine, University of California at Los Angeles School of Medicine, Los Angeles, California 90024

Find articles by Alvarez, L. in: PubMed | Google Scholar

Medical Service and Research, Veterans Administration Wadsworth Hospital Center, Los Angeles, California 90073

Department of Medicine, University of California at Los Angeles School of Medicine, Los Angeles, California 90024

Find articles by Tamasi, G. in: PubMed | Google Scholar

Medical Service and Research, Veterans Administration Wadsworth Hospital Center, Los Angeles, California 90073

Department of Medicine, University of California at Los Angeles School of Medicine, Los Angeles, California 90024

Find articles by Brickman, A. in: PubMed | Google Scholar

Published October 1, 1972 - More info

Published in Volume 51, Issue 10 on October 1, 1972
J Clin Invest. 1972;51(10):2757–2762. https://doi.org/10.1172/JCI107095.
© 1972 The American Society for Clinical Investigation
Published October 1, 1972 - Version history
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Abstract

This study was carried out to determine if, in fasting, an adaptation to utilization of ketones could prevent cerebral dysfunction during periods of acute, insulin-induced glucopenia.

In the course of standard insulin tolerance tests (0.1-0.2 U/kg), nine obese subjects manifested frank hypoglycemic reactions resulting in an increase in urinary catecholamine excretion from 61 to 113 μg/24 hr (P < 0.01). After fasting 2 months, administration of weight-adjusted doses of insulin produced identical maximum insulin concentrations and disappearance curves. However, no insulin reactions nor significant rises in catecholamine excretion occurred despite equal extent and rate of glucose fall. Glucose concentrations as low as 0.5 mmoles/liter (9 mg/100 ml) failed to precipitate hypoglycemic reactions. During the postfast insulin tolerance tests, mean plasma 2-hydroxybutyrate (β-OHB) decreased from 8.02 to 6.69 mmoles/liter (P < 0.01). In another five fasting subjects tested, the A-V difference for β-OHB across brain increased progressively from 0.21 to 0.70 mmoles/liter whereas across the forearm no consistent uptake could be demonstrated. Simultaneously, the A-V difference across the brain for glucose decreased from 0.24 to 0.07 mmoles/liter of plasma.

In addition to insulin-induced suppression of hepatic ketogenesis, the augmented cerebral ketone uptake during insulin hypoglycemia contributes to the net fall in plasma β-OHB. Ketoacids, extracted by the fast-adapted brain, supplant glucose as a metabolic substrate preventing overt hypoglycemic reactions during acute glucopenia.

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