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Abstract
Prolonged fasting (for days or weeks) decreases glucose production and oxidation.
The effects of short-term starvation (ie, < 24 hours) on glucose metabolism are not
known. To evaluate this issue, glucose oxidation and glucose turnover were measured
after 16-hour and subsequently after 22-hour fasting. Glucose oxidation was calculated
by indirect calorimetry in 12 healthy men (age 22 to 44 years); glucose turnover was
measured by primed, continuous infusion of 3-3H-glucose in eight of these 12 volunteers. After 16-hour fasting net glucose oxidation
was 0.59 ± 0.17 mg · kg−1 · min−1 and glucose tissue uptake 2.34 ± 0.12 mg · kg−1 · min−1. No correlation was found between net glucose oxidation and glucose tissue uptake.
Prolonging fasting with an addtional 6 hours resulted in decreases of respiratory
quotient (0.77 ± 0.01 v 0.72 ± 0.01) (P < .005), plasma glucose concentration (4.7 ± 0.1 v 4.6 ± 0.1 mmol/L) (P < .05), glucose tissue uptake (2.10 ± 0.12 mg · kg−1 · min−1)(P < .05), net glucose oxidation (0.09 ± 0.04 mg · kg−1 · min−1)(P < .005), and plasma insulin concentration (8 ± 1 v 6 ± 1 mU/L) (P < .005). Net glucose oxidation expressed as a percentage of glucose tissue uptake
decreased from 22% ± 8% to 2% ± 1% (P < .05). There was no net glucose oxidation in seven of 12 controls after 22-hour
fasting. Serum free fatty acid (FFA) concentration (364 ± 34 to 575 ± 48 μmol/L) (P < .005) and plasma ketone body concentration (104 ± 23 to 242 ± 38 μmol/L) (P < .005) increased between 16- and 22-hour fasting. After 16-hour fasting an inverse
correlation was found between ketone body concentration and net glucose oxidation
(P < .05) and between ketone body concentration and net glucose oxidation expressed
as a percentage of glucose tissue uptake (P = .07). No significant correlation could be demonstrated between FFA and ketone body
concentration and between FFA and net glucose oxidation. It is concluded that glucose
oxidation decreases rapidly even within 1 day of starvation. This may be explained
by physiological mechanisms like decreased insulin action and/or inhibition of glucose
oxidation by ketone bodies, even in relatively low concentrations.
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© 1990 Published by Elsevier Inc.
