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Cited by 131Diabetes, Cardiovascular Risks, and LipoproteinsAdipokines, Inflammation, and Metabolic DiseasesAdipose Tissue and Metabolism

Relationship between obesity and maximal insulin-stimulated glucose uptake in vivo and in vitro in Pima Indians.

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Bogardus, C, Lillioja, S, Mott, D, Reaven, G R, Kashiwagi, A, Foley, J E·1984·Journal of Clinical Investigation
DOI 10.1172/jci111274PMC PMC425083
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Abstract

Previous studies have left unanswered whether human obesity, independent of glucose intolerance, is associated with a "postreceptor" defect in insulin action. We have studied the relationship between the degree of obesity (as estimated by underwater weighing) and the maximal insulin-stimulated glucose disposal rate (M) in vivo in 52 glucose-tolerant Pima Indian males. The relationship was examined independently of differences in age and maximal oxygen uptake (an estimate of "physical fitness"). The maximal insulin-stimulated glucose transport rate (MTR) was also measured in isolated abdominal adipocytes from the same subjects to determine whether differences in M could be explained by differences in glucose transport. The results showed that there was a large variance in M and MTR among these glucose-tolerant subjects. M was better correlated with glucose storage rates than with oxidation rates, as estimated by indirect calorimetry. The most obese subjects had only a 20% lower mean M and 30% lower MTR than the most lean subjects. The lower M in the obese subjects was due to both lower glucose oxidation and storage rates. There was no significant, independent correlation between age or degree of obesity and M or MTR. The maximal oxygen uptake (VO2 max) appeared to independently account for 20% of the variance observed in M. MTR was only weakly correlated with M (r = 0.36, P less than 0.02). We concluded that differences in M in these glucose-tolerant subjects must be explained by factor(s) other than maximal oxygen uptake, age, maximal insulin-stimulated glucose transport in vitro, or degree of adiposity per se.

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  • Skeletal muscle insulin resistance can develop without a family history of type 2 diabetes.

    “Insulin resistance in skeletal muscle also can develop independent of family history of T2DM.”

    From Pathogenesis of insulin resistance in skeletal muscle (2010) · cites this paper as [34]

  • The severity of skeletal muscle insulin resistance is related to an increase in body mass index.

    “and the severity of muscle insulin resistance is related to the increase in BMI [34].”

    From Pathogenesis of insulin resistance in skeletal muscle (2010) · cites this paper as [34]

  • Obese normal-glucose-tolerant subjects show marked skeletal muscle insulin resistance compared with lean age- and sex-matched individuals.

    “Obese NGT subjects display marked skeletal muscle insulin resistance compared to lean age and sex matched individuals [33, 34]”

    From Pathogenesis of insulin resistance in skeletal muscle (2010) · cites this paper as [34]

  • Obese normal-glucose-tolerant subjects without a family history of type 2 diabetes, individuals with essential hypertension, and individuals with ischaemic heart disease have a 35-50% decrease in whole-body insulin-mediated glucose disposal.

    “Thus, obese NGT subjects without a family history for T2DM [33, 34] and individuals with essential hypertension [35] and ischemic heart disease [36] also have a 35–50% decrease in whole body insulin-mediated glucose disposal (Figure 3).”

    From Pathogenesis of insulin resistance in skeletal muscle (2010) · cites this paper as [34]

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Research works printed but not linked: 1

  1. [12]12. Astrand, P.-O., and Radahl, K. 1970. Textbook of Work Physiology: Physiological Basis of Exercise. McGraw-Hill, Inc., New York. 447-477.

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Authors
Bogardus, C., Lillioja, S., Mott, D., Reaven, G. R., Kashiwagi, A., & Foley, J. E.
Affiliations
National Institutes of Health (US)
ORCID
Venue
Journal of Clinical Investigation
Publisher
American Society for Clinical Investigation
Published
1984-03-01
Volume
73
Issue
3
Pages
800-805
ISSN
0021-9738 (ISSN-L)
DOI
10.1172/jci111274
PMC
PMC425083
OpenAlex
W2049107834
Cited by
131
References
18
Citations by year
2023: 1 · 2022: 3 · 2021: 1 · 2020: 2 · 2019: 1 · 2018: 3 · 2017: 2 · 2016: 2 · 2014: 2 · 2013: 6 · 2012: 1
FWCI
6.36
Type
journal article
Language
en
Open access
Locations
  • Journal of Clinical Investigation (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
  • Research Online (University of Wollongong) (submittedVersion)
Topics
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
  • Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
  • Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
Keywords
obesity, insulin-stimulated glucose uptake, insulin resistance, glucose transport, adipocytes, glucose oxidation, glucose storage, VO2max, Pima Indians, adiposity
MeSH terms
Adipose Tissue, Glucose, Humans, Indians, North American, Insulin, Male, Obesity, In Vitro Techniques

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