Drenick · The Journal of clinical investigation 1972 · Before-after physiological intervention study · n=14

Resistance to symptomatic insulin reactions after fasting.

Cited 102 times in the scientific literature.

Level 4 - case-series / case-control

Small non-randomized before-and-after physiological study

PubMed 5056667 · doi:10.1172/JCI107095 · record verified 2026-08-29

What was done

Nine obese participants underwent standard insulin tolerance tests (0.1-0.2 U/kg) before and after a 2-month fast to evaluate whether ketone utilization prevents cerebral dysfunction during acute glucopenia. Measures included symptomatic reactions, plasma glucose, insulin disappearance, urinary catecholamine excretion, and plasma beta-hydroxybutyrate. In an additional five fasting subjects, arteriovenous concentration differences for beta-hydroxybutyrate and glucose across the brain and forearm were measured during insulin-induced hypoglycemia.

What was found

Prior to fasting, insulin tolerance tests caused symptomatic hypoglycemic reactions and increased urinary catecholamines from 61 to 113 mug/24 hr (P < 0.01). Following 2 months of fasting, weight-adjusted insulin administration produced identical glucose declines (reaching as low as 0.5 mmoles/liter or 9 mg/100 ml) without triggering symptomatic hypoglycemic reactions or significant catecholamine increases. During postfast tests, mean plasma beta-hydroxybutyrate fell from 8.02 to 6.69 mmoles/liter (P < 0.01). In five tested subjects, the cerebral arteriovenous difference for beta-hydroxybutyrate increased from 0.21 to 0.70 mmoles/liter, while the cerebral arteriovenous difference for glucose decreased from 0.24 to 0.07 mmoles/liter of plasma; forearm uptake showed no consistent trend.

Why it matters

This study provides physiological evidence in humans that prolonged fasting enables the brain to extract and utilize ketoacids in place of glucose, protecting against symptomatic neuroglycopenia during profound hypoglycemia.

Limits

The study tested an extreme 2-month fast in a very small sample of obese individuals (n = 14 total), limiting applicability to shorter fasts, milder ketosis, or non-obese populations. Cerebral function was assessed via overt clinical symptoms and catecholamine response rather than formal neurocognitive testing.

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