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Laboratory of Experimental Medicine and Department of Endocrinology, Erasmus Hospital, University of Brussels, B-1070 Brussels, Belgium
The effects of
fasting on the pathways of insulin-stimulated glucose disposal were
explored in three groups of seven normal subjects.
Group
1 was submitted to a euglycemic
hyperinsulinemic clamp (~100 µU/ml) after both a 12-h and a 4-day
fast. The combined use of
[3-3H]- and
[U-14C]glucose allowed
us to demonstrate that fasting inhibits, by ~50%, glucose disposal,
glycolysis, glucose oxidation, and glycogen synthesis via the direct
pathway. In group
2, in which the clamp glucose disposal
during fasting was restored by hyperglycemia (155 ± 15 mg/dl),
fasting stimulated glycogen synthesis (+29 ± 2%) and inhibited
glycolysis (
32 ± 3%) but only in its oxidative component
(40 ± 3%). Results were similar in
group
3 in which the clamp glucose disposal
was restored by a pharmacological elevation of insulin (~2,800
µU/ml), but in this case, both glycogen synthesis and nonoxidative
glycolysis participated in the rise in nonoxidative glucose disposal.
In all groups, the reduction in total carbohydrate oxidation (indirect
calorimetry) induced by fasting markedly exceeded the reduction in
circulating glucose oxidation, suggesting that fasting also inhibits
intracellular glycogen oxidation. Thus prior fasting favors glycogen
retention by three mechanisms: 1)
stimulation of glycogen synthesis via the direct pathway;
2) preferential inhibition of
oxidative rather than nonoxidative glycolysis, thus allowing carbon
conservation for glycogen synthesis via the indirect pathway; and
3) suppression of intracellular
glycogen oxidation.
whole body glucose metabolism; glycolysis; glucose oxidation; glycogen synthesis; euglycemic hyperinsulinemic clamp
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