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Relationship between obesity and maximal insulin-stimulated glucose uptake in vivo and in vitro in Pima Indians.
Open accessAbstract
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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“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]
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“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]
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“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]
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“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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Diversity of Insulin Resistance in Monkeys with Normal Glucose Tolerance
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Metabolic and Molecular Pathogenesis of Type 2 Diabetes Mellitus
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Glucose uptake saturation explains glucose kinetics profiles measured by different tests
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Metadata
- Authors
- Bogardus, C., Lillioja, S., Mott, D., Reaven, G. R., Kashiwagi, A., & Foley, J. E.
- Affiliations
- National Institutes of Health (US)
- Venue
- Journal of Clinical Investigation
- Published
- 1984-03-01
- Volume
- 73
- Issue
- 3
- Pages
- 800-805
- ISSN
- 0021-9738 (ISSN-L)
- 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
- green
- www.ncbi.nlm.nih.gov
- 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 › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Physiology (medical) › 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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