Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 1973 Dec;52(12):3033-45.
doi: 10.1172/JCI107502.

Glucose turnover and disposal in maturity-onset diabetes

Glucose turnover and disposal in maturity-onset diabetes

H F Bowen et al. J Clin Invest. 1973 Dec.

Abstract

The glucose turnover rate in maturity-onset diabetes in man has been variously reported as increased, normal, and decreased. The present experiments suggest that these discrepancies may have been due to methodology, and to nonrecognition of a circadian cycle in the glucose turnover rate that is present in health, and marked in diabetes. During the early morning hours the glucose turnover rate in maturity-onset diabetes is increased in proportion to the fasting blood glucose level. It may reach three to four times the rate found in health. During the evening hours the increments are about one-half as great. The glucose outflow rate constant, k, lower in diabetes than in health, is also lower in both groups in the evening than in the morning. An analysis of the relative contributions of glucose overproduction and underutilization to the development of hyperglycemia in maturity-onset diabetes indicates that overproduction is the greater factor. The relative role of underutilization appears to increase as the fasting blood glucose level increases. The circulating glucose oxidation rate in maturity-onset diabetes is only slightly lower than in health, but the fraction oxidized is markedly lower, and only a small fraction is excreted. The principal conclusion is that in maturity-onset diabetes there is a hypertrophied flux of endogenous glucose, most of which is neither oxidized nor excreted. The precursors and the qualitative and quantitative metabolic fates of this excess glucose are unknown.

PubMed Disclaimer

Similar articles

Cited by

References

    1. Diabetes. 1970 Jan;19(1):53-63 - PubMed
    1. Diabetologia. 1966 Sep;2(2):96-103 - PubMed
    1. Diabetes. 1959 May-Jun;8(3):167-73 - PubMed
    1. Science. 1970 May 1;168(3931):596-8 - PubMed
    1. J Physiol. 1971 Dec;219(2):267-80 - PubMed