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Cited by 799Adipokines, Inflammation, and Metabolic DiseasesDiabetes, Cardiovascular Risks, and LipoproteinsAdipose Tissue and Metabolism

Enlarged subcutaneous abdominal adipocyte size, but not obesity itself, predicts Type II diabetes independent of insulin resistance

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Weyer, C., Foley, J. E., Bogardus, C., Tataranni, P. A., Pratley, R. E.·2000·Diabetologia
DOI 10.1007/s001250051560
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Abstract

Aims/hypothesis Cross-sectional studies indicate that enlarged subcutaneous abdominal adipocyte size is associated with hyperinsulinaemia, insulin resistance and glucose intolerance. To further explore the pathophysiological significance of these associations, we examined prospectively whether enlarged subcutaneous abdominal adipocyte size predicts Type II (non-insulin-dependent) diabetes mellitus.Methods Body composition (hydrodensitometry), mean subcutaneous abdominal adipocyte size (fat biopsy), insulin sensitivity (hyperinsulinaemic clamp) and the acute insulin secretory response (25-g i.v. GTT) were assessed in 280 Pima Indians with either normal (NGT), impaired (IGT) or diabetic glucose tolerance (75-g OGTT). Subjects with NGT were then followed prospectively.Results After adjusting for age, sex and per cent body fat, mean subcutaneous abdominal adipocyte size was 19% and 11% higher in subjects with diabetes and IGT, compared with those with NGT (p < 0.001). Insulin sensitivity was inversely correlated with mean subcutaneous abdominal adipocyte size (r = -0.53, p < 0.0001), even after adjusting for per cent body fat (r = -0.31, p < 0.001). In 108 NGT subjects followed over 9.3 +/- 4.1 years (33 of whom developed diabetes), enlarged mean subcutaneous abdominal adipocyte size but not high per cent body fat, was an independent predictor of diabetes, in addition to a low insulin sensitivity and acute insulin secretory response [relative hazard 10th vs 90th centile (95% CI): 5.8 (1.7-19.6), p < 0.005]. In 28 NGT subjects with a 9% weight gain over 2.7 +/- 1.3 years, changes in insulin sensitivity were inversely and independently related to changes in mean subcutaneous abdominal adipocyte size and per cent body fat.Conclusion/interpretation Although enlarged mean subcutaneous abdominal adipocyte size is associated with insulin resistance cross-sectionally, prospectively, both abnormalities are independent and additive predictors of Type II diabetes.

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  • Proinflammatory cytokine signalling activates IKKb and JNK1, which phosphorylate Ser307 of IRS-1, preventing insulin receptor tyrosine phosphorylation and downstream signalling.

    “Proinflammatory cytokine signalling usually activates the kinases IkB kinase b and C-jun N-terminal kinase 1, both of which in turn phosphorylate the Ser 307 residue of insulin receptor substrate (IRS)-1.This prevents the phosphorylation of tyrosine residues of IRS-1 by the insulin receptor and the downstream signalling cascade.”

    From Dietary factors and low-grade inflammation in relation to overweight and obesity (2011) · cites this paper as [128]

  • In vitro, hepatocytes, muscle cells, adipocytes and endothelial cells respond to TNF-a, IL-6 and/or IL-1b with impaired insulin signalling.

    “Experimental model systems in vitro have shown that hepatocytes as well as muscle cells, adipocytes and endothelial cells respond to exposure to the pro-inflammatory cytokines TNF-a, IL-6 and/or IL-1b with impaired insulin signalling (128) .”

    From Dietary factors and low-grade inflammation in relation to overweight and obesity (2011) · cites this paper as [128]

  • Paracrine concentrations of inflammatory mediators are sufficient to induce insulin resistance.

    “Paracrine concentrations of inflammatory mediators are sufficient to induce insulin resistance (128) .”

    From Dietary factors and low-grade inflammation in relation to overweight and obesity (2011) · cites this paper as [128]

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  1. [40]40. Weyer C, Salbe AD, Lindsay R, Bogardus C, Pratley RE, Tataranni PA (2001) Exaggerated pancreatic polypeptide secretion in Pima Indians: can increased parasympathetic drive to the pancreas contribute to hyperinsulinemia and diabetes in humans? Metabolism, in press.

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Authors
Weyer, C., Foley, J. E., Bogardus, C., Tataranni, P. A., & Pratley, R. E.
Affiliations
National Institutes of Health (US)
ORCID
Venue
Diabetologia
Publisher
Springer Science and Business Media LLC
Published
2000-11-30
Volume
43
Issue
12
Pages
1498-1506
ISSN
  • 0012-186X (ISSN-L)
  • 1432-0428
DOI
10.1007/s001250051560
OpenAlex
W2006433855
Semantic Scholar
7702640158cc73f615236e15d4c7daac13792dc9
Cited by
799
References
43
Citations by year
2026: 17 · 2025: 28 · 2024: 31 · 2023: 27 · 2022: 31 · 2021: 31 · 2020: 35 · 2019: 26 · 2018: 40 · 2017: 45 · 2016: 36 · 2015: 45 · 2014: 40 · 2013: 48 · 2012: 35
FWCI
8.02
Type
journal article
Language
en
Open access
Licence
www.springer.com/tdm (tdm)
Locations
  • Diabetologia (publishedVersion)
  • PubMed (publishedVersion)
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 › Physiology › Adipose Tissue and Metabolism
Keywords
type 2 diabetes, insulin resistance, impaired glucose tolerance, Pima Indians, insulin sensitivity, body fat percentage, weight gain, diabetes prediction, adipocyte hypertrophy
MeSH terms
Abdomen, Adipose Tissue, Adult, Blood Glucose, Body Composition, Cross-Sectional Studies, Diabetes Mellitus, Type 2, Fatty Acids, Nonesterified, Female, Follow-Up Studies, Glucose Tolerance Test, Humans, Hyperinsulinism, Insulin, Insulin Resistance, Lipolysis, Longitudinal Studies, Male, Obesity, Predictive Value of Tests, Prospective Studies, Regression Analysis, Glucose Clamp Technique, Adipocytes, Cell Size

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