Format

Send to

Choose Destination
See comment in PubMed Commons below
Metabolism. 1988 Jan;37(1):79-85.

The disposal of an oral glucose load in patients with non-insulin-dependent diabetes.

Author information

1
Department of Medicine, Yale University School of Medicine, New Haven, CT.

Abstract

Following glucose ingestion, tissue glucose uptake is enhanced and endogenous glucose production is inhibited, thus contributing to the maintenance of normal glucose tolerance. To examine whether these responses are disturbed in diabetes, glucose kinetics after oral glucose administration were studied in 12 non-insulin-dependent diabetic and 10 age- and weight-matched control subjects. A double tracer approach was used, whereby the endogenous glucose pool was labeled with 3-3H-glucose and the oral load with 1-14C-glucose. The two glucose tracers were separated in plasma by a two-step chromatographic procedure, and the two sets of isotopic data were analyzed according to a two-compartment model for the glucose system. Basally, glucose production was slightly higher in diabetics than in controls (2.51 +/- 0.24 v 2.28 +/- 0.11 mg/kg.min, NS) even though the former had higher plasma glucose (189 +/- 19 v 93 +/- 2 mg/dL, P less than .001) and insulin (23 +/- 4 v 12 +/- 1 microU/mL, P less than .05) concentrations. Following the ingestion of 1 g/kg of glucose, oral glucose appeared in the peripheral circulation in similar time-course and amount in the two groups (75 +/- 2% of the load over 3.5 hours in the diabetics v 76 +/- 3% in controls). Endogenous glucose production was promptly inhibited in diabetic and normal subjects alike, but the mean residual hepatic glucose production after glucose ingestion was significantly greater in the diabetic group (17 +/- 2 v 10 +/- 3 g/3.5 h, P less than .05).(ABSTRACT TRUNCATED AT 250 WORDS)

PMID:
3275860
[Indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science
    Loading ...
    Support Center