Elsevier

Metabolism

Volume 50, Issue 1, January 2001, Pages 47-52
Metabolism

Quantitative contributions of gluconeogenesis to glucose production during fasting in type 2 diabetes mellitus

https://doi.org/10.1053/meta.2001.19422Get rights and content

Abstract

Contributions of gluconeogenesis to glucose production were determined between 14 to 22 hours into a fast in type 2 diabetics (n = 9) and age-weight-matched controls (n = 7); ages, 60.4 ± 2.3 versus 55.6 ± 1.2 years and body mass indices (BMI) 28.6 ± 2.3 versus 26.6 ± 0.8 kg/m2. Production was measured using a primed-continuous [6,6-2H2]glucose infusion and gluconeogenesis from 2H enrichment at carbons 2 and 5 of blood glucose on 2H2O ingestion. Plasma glucose concentration declined from 9.6 ± 0.6 at 14 hours to 7.3 ± 0.6 at 22 hours in the diabetics (P = .001) and from 5.4 ± 0.1 to 5.0 ± 0.1 in the controls (P < .05). Production from the 17th to 22nd hour declined 27.1% ± 0.6% in the diabetics versus 18.5% ± 0.8% in the controls (P = .001); from 10.4 ± 0.3 to 7.6 ± 0.2 versus 10.0 ± 0.4 to 8.2 ± 0.4 μmol/kg/min. Percent contributions of gluconeogenesis to production measured at 112 to 2-hour intervals beginning the 15th hour were 6.8% ± 1.0% more in the diabetics than controls. The quantity of glucose contributed by gluconeogenesis declined 19.8% ± 3.8% (P < .001) in the diabetics and 6.9% ± 2.3% in the controls (P = .05); 7.21 ± 0.32 to 5.74 ± 0.26 versus 6.20 ± 0.28 to 5.75 ± 0.24 μmol/kg/min. The contribution of glycogenolysis to production, estimated from the difference between production and gluconeogenesis, declined to the same extent in diabetic and control subjects, 40.7% ± 6.6% and 37.7% ± 4.1%; from 3.23 ± 0.35 to 1.86 ± 0.26 versus 3.81 ± 0.22 to 2.42 ± 0.28 μmol/kg/min. Thus, gluconeogenesis contributed more to glucose production in the diabetic than control subjects. Production and the contribution of gluconeogenesis declined more in the diabetic subjects during the fast. The factors regulating these changes remain uncertain.

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Supported by Grant No. 72X-00034 from the Swedish Medical Research Council, Grant No. DK-14507 from the National Institutes of Health, and by the David S. Stein Foundation of the Jewish Federation of Cleveland.

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