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Cited by 252Adipokines, Inflammation, and Metabolic DiseasesDiabetes, Cardiovascular Risks, and LipoproteinsPancreatic function and diabetes

Insulin Binding to Monocytes and Insulin Action in Human Obesity, Starvation, and Refeeding

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Defronzo, Ralph A., Soman, Vijay, Sherwin, Robert S., Hendler, Rosa, Felig, Philip·1978·Journal of Clinical Investigation
DOI 10.1172/jci109108PMC PMC371755
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Abstract

Insulin binding to monocytes and insulin action in vivo was examined in 14 obese subjects during the postabsorptive state and after starvation and refeeding. Tissue sensitivity to insulin was evaluated with the euglycemic insulin clamp technique. The plasma insulin concentration is acutely raised and maintained 100 muU/ml above the fasting level, and plasma glucose is held constant by a variable glucose infusion. The amount of glucose infused is a measure of tissue sensitivity to insulin and averaged 285+/-15 mg/m(2) per min in controls compared to 136+/-13 mg/m(2) per min in obese subjects (P <0.001). (125)I-Insulin binding to monocytes averaged 8.3+/-0.4% in controls vs. 4.6+/-0.5% in obese subjects (P < 0.001). Insulin binding and insulin action were highly correlated in both control (r = 0.86, P < 0.001) and obese (r = 0.94, P < 0.001) groups. Studies employing tritiated glucose to measure glucose production indicated hepatic as well as extrahepatic resistance to insulin in obesity. After 3 and 14 days of starvation, insulin sensitivity in obese subjects decreased to 69+/-4 and 71+/-7 mg/m(2) per min, respectively, whereas (125)I-insulin binding increased to 8.8+/-0.7 and 9.0+/-0.4%. In contrast to the basal state, there was no correlation between insulin binding and insulin action. After refeeding, tissue sensitivity increased to 168+/-14 mg/m(2) per min (P < 0.001) whereas insulin binding fell to 5.0+/-0.3%. We conclude that (a) in the postabsorptive state insulin binding to monocytes provides an index of in vivo insulin action in nonobese and obese subjects and, (b) during starvation and refeeding, insulin binding and insulin action changes in opposite directions suggesting that postreceptor events determine in vivo insulin sensitivity.

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  • Our results are consistent with the diminished S of obese subjects elucidated by both qualitative and quantitative techniques.

    “Thus, our results are consistent with the diminished S of obese subjects elucidated by both qualitative (26) and quantitative techniques (25).”

    From Physiologic evaluation of factors controlling glucose tolerance in man: measurement of insulin sensitivity and beta-cell glucose sensitivity from the response to intravenous glucose (1981) · cites this paper as [25]

  • Using the euglycaemic hyperinsulinaemic clamp, lean and obese type 2 diabetic subjects show a greater than 50% decrease in whole-body glucose disposal during insulin infusion.

    “Using the gold standard euglycemic hyperinsulinemic clamp technique to quantify insulin-stimulated glucose uptake, they demonstrated that both lean and obese T2DM subjects have marked decrease (>50%) in whole body glucose disposal during the insulin clamp.”

    From Pathogenesis of insulin resistance in skeletal muscle (2010) · cites this paper as [28]

  • Both acute (4-hour) and chronic (4-day) physiological elevation of plasma free fatty acid concentration in insulin-sensitive individuals impairs insulin signalling and causes skeletal muscle insulin resistance.

    “Both acute (4 hours) and chronic (4 days) physiologic elevation of plasma FFA concentration in insulin sensitive individuals impairs insulin signaling and causes insulin resistance in skeletal muscle [28, 62–68].”

    From Pathogenesis of insulin resistance in skeletal muscle (2010) · cites this paper as [28]

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Cites

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Research works printed but not linked: 3

  1. Marinetti, G. V., L. Schlatz, and K. Reilly. 1972. Insulin Action I. Academic Press, Inc., New York. 224.
  2. Radziuk, J., K. H. Norwich, and M. Vranic. 1974. Meas- urement and validation of nonsteady state turnover rates with application to the insulin and glucose systems. Fed. Proc. 33: 1855-1864.
  3. Snedecor, G. W., and W. G. Cochran. 1967. Statistical Methods. 6th edition. Iowa State University Press, Ames, Iowa. 593 pp.

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Authors
Defronzo, R. A., Soman, V., Sherwin, R. S., Hendler, R., & Felig, P.
Affiliations
Yale University (US)
ORCID
Defronzo, Ralph A.
Venue
Journal of Clinical Investigation
Publisher
American Society for Clinical Investigation
Published
1978-07-01
Volume
62
Issue
1
Pages
204-213
ISSN
0021-9738 (ISSN-L)
DOI
10.1172/jci109108
PMC
PMC371755
OpenAlex
W1969572070
Cited by
252
References
41
Citations by year
2026: 1 · 2024: 4 · 2023: 3 · 2020: 1 · 2019: 2 · 2018: 3 · 2017: 3 · 2015: 2 · 2014: 4 · 2013: 3 · 2012: 5
FWCI
33.28
Type
journal article
Language
en
Status
Retracted
Open access
Locations
  • Journal of Clinical Investigation (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • American Diabetes Association
  • National Institutes of Health (RR-00125)
Topics
  • Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
  • Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
Keywords
insulin binding, monocytes, insulin resistance, obesity, starvation, refeeding, postabsorptive state, insulin action, hepatic insulin resistance, hyperinsulinemic-euglycemic clamp, glucose production
MeSH terms
Adolescent, Adult, Eating, Female, Glucose, Humans, Insulin, Liver, Male, Middle Aged, Monocytes, Obesity, Starvation

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