Hyperinsulinemia of obesity is due to decreased clearance of insulin

The hyperinsulinemia of obesity could result from a decrease in the metabolic clearance rate of insulin (MCR-I), an increase in the secretory rate of insulin (SR-I), or a combination of both these processes. Because C-peptide and insulin are secreted in an equimolar ratio, the plasma concentrations...

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Bibliographic Details
Published inThe American journal of physiology Vol. 245; no. 2; pp. E155 - E159
Main Authors Meistas, M.T, Margolis, S, Kowarski, A.A
Format Journal Article
LanguageEnglish
Published United States 01.08.1983
Subjects
Adolescent
Adult
Aged
Blood Glucose - analysis
Body Height
Body Weight
C-Peptide - metabolism
diet-related diseases
Fasting
Female
human nutrition
Humans
Hyperinsulinism - etiology
Hyperinsulinism - metabolism
Insulin - metabolism
Male
Metabolic Clearance Rate
Middle Aged
Obesity - complications
Obesity - metabolism
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Summary:The hyperinsulinemia of obesity could result from a decrease in the metabolic clearance rate of insulin (MCR-I), an increase in the secretory rate of insulin (SR-I), or a combination of both these processes. Because C-peptide and insulin are secreted in an equimolar ratio, the plasma concentrations of C-peptide (C) and insulin (I) are inversely proportional to their rates of metabolic clearance (C/I = MCR-I/MCR-C). We obtained 24-h integrated concentrations (IC) of insulin (IC-I) and C-peptide (IC-C) in 23 obese and 45 nonobese subjects over a period of normal activity and food intake. The IC-I was 69% higher in the obese subjects (P less than 0.0001). A 13% increase in the IC-C (P = 0.04), with a constant rate of C-peptide clearance, indicates a proportionate increase in SR-I. A 33% decrease in the IC-C/IC-I in the obese group (P less than 0.005) reflects a decrease in MCR-I; hence, 75% of the hyperinsulinemia is due to a decrease in the clearance of insulin. Because peripheral MCR-I (pMCR-I) is similar in obese and nonobese subjects, the decrease in MCR-I may be due to a decrease in the hepatic clearance of insulin. This conclusion was supported by our comparison of 24-h IC-C/IC-I ratios in the obese and nonobese subjects. Whereas the 24-h IC-C/IC-I of the nonobese resembled the fasting state, the 24-h IC-C/IC-I of the obese resembled the postprandial state, when insulin removal by the liver is known to be suppressed. These data are consistent with a decreased 24-h hepatic MCR-I (hMCR-I) as the cause of the hyperinsulinemia of obesity.
ISSN:0002-9513
2163-5773
DOI:10.1152/ajpendo.1983.245.2.e155