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Krentz AJ, Singh BM, Hale PJ, et al. Basal intermediary metabolism in impaired glucose tolerance and morbid obesity. Diabetes Res. 1992;20(3):51-60
Krentz, A. J., Singh, B. M., Hale, P. J., Robertson, D. A., & Nattrass, M. (1992). Basal intermediary metabolism in impaired glucose tolerance and morbid obesity. Diabetes research (Edinburgh, Scotland), 20(3), 51-60.
Krentz, A J, et al. "Basal intermediary metabolism in impaired glucose tolerance and morbid obesity." Diabetes research (Edinburgh, Scotland) vol. 20,3 (1992): 51-60.
Krentz AJ, Singh BM, Hale PJ, Robertson DA, Nattrass M. Basal intermediary metabolism in impaired glucose tolerance and morbid obesity. Diabetes Res. 1992;20(3):51-60. PMID: 1345002.
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Diabetes Res. 1992;20(3):51-60.

Basal intermediary metabolism in impaired glucose tolerance and morbid obesity.

Diabetes research (Edinburgh, Scotland)

A J Krentz, B M Singh, P J Hale, D A Robertson, M Nattrass

Affiliations

  1. Diabetic Clinic, General Hospital, Birmingham, UK.

PMID: 1345002

Abstract

The effects of impaired glucose tolerance and obesity, in isolation and in combination, on basal (postabsorptive) intermediary metabolism were examined in four groups of subjects (n = 10 for each) matched for age and gender: Group 1: Non-obese healthy controls with normal glucose tolerance (75 g); Group 2: Non-obese subjects with impaired glucose tolerance; Group 3: Morbidly obese subjects with normal glucose tolerance; Group 4: Morbidly obese subjects with impaired glucose tolerance. While there was no significant difference in fasting blood glucose concentrations between the four groups plasma immuno-reactive insulin concentrations were elevated (p < 0.01 or less) in the obese subjects relative to the non-obese subjects within each category of glucose tolerance. Basal immunoreactive insulin concentrations in non-obese subjects with impaired glucose tolerance were also elevated (p < 0.01) relative to the non-obese healthy controls. Concentrations of glycerol (p < 0.01), non-esterified fatty acids (p < 0.01), and total ketone bodies (p < 0.001) were significantly higher in the obese/normal glucose tolerance and obese/impaired glucose tolerance groups relative to their matched non-obese counterparts. Compared with the subjects with normal glucose tolerance, only lactate (p < 0.05) and pyruvate (p < 0.05) concentrations were elevated in the non-obese/impaired glucose tolerance and obese/impaired glucose tolerance groups, respectively. In conclusion, in addition to fasting hyperinsulinaemia the regulation of lipolysis and ketone body metabolism is abnormal in the basal state in morbid obesity. By contrast, despite normal fasting blood glucose concentrations, impaired glucose tolerance is associated with disturbances of other aspects of basal carbohydrate metabolism.

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