Cited by 67Adipokines, Inflammation, and Metabolic DiseasesDiabetes, Cardiovascular Risks, and LipoproteinsAdipose Tissue and Metabolism

Insulin Sensitivity in African‐American and White Women: Association With Inflammation

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Hyatt, Tanya C., Phadke, Radhika P., Hunter, Gary R., Bush, Nikki C., Muñoz, A. Julian, Gower, Barbara A.·2009·Obesity

Abstract

Whether the contribution of inflammation to risk for chronic metabolic disease differs with ethnicity is not known. The objective of this study was to determine: (i) whether ethnic differences exist in markers of inflammation and (ii) whether lower insulin sensitivity among African Americans vs. whites is due to greater inflammatory status. Subjects were African-American (n = 108) and white (n = 105) women, BMI 27-30 kg/m(2). Insulin sensitivity was assessed with intravenous glucose tolerance test and minimal modeling; fat distribution with computed tomography; body composition with dual-energy X-ray absorptiometry; markers of inflammation (tumor necrosis factor (TNF)-alpha, soluble tumor necrosis factor receptor (sTNFR)-1, sTNFR-2, C-reactive protein (CRP), and interleukin (IL)-6) with enzyme-linked immunosorbent assay (ELISA). Whites had greater intra-abdominal adipose tissue (IAAT), insulin sensitivity, and concentrations of TNF-alpha, sTNFR-1, and sTNFR-2 than African Americans. Greater TNF-alpha in whites vs. African Americans was attributed to greater IAAT in whites. Among whites, but not African Americans, CRP was independently and inversely associated with insulin sensitivity, after adjusting for IAAT (r = -0.29 P < 0.05, and r = -0.13 P = 0.53, respectively). Insulin sensitivity remained lower in African Americans after adjusting for CRP (P < 0.001). In conclusion, greater IAAT among whites may be associated with greater inflammation. Insulin sensitivity was lower among African Americans, independent of obesity, fat distribution, and inflammation.

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Authors
Hyatt, T. C., Phadke, R. P., Hunter, G. R., Bush, N. C., Muñoz, A. J., & Gower, B. A.
Affiliations
University of Alabama at Birmingham (US)
Corresponding author
Gower, Barbara A.
Venue
Obesity
Publisher
Wiley
Published
2009-02
Volume
17
Issue
2
Pages
276-282
ISSN
  • 1930-7381 (ISSN-L)
  • 1930-739X
OpenAlex
W1977218988
Cited by
67
References
57
Citations by year
2025: 2 · 2024: 1 · 2023: 4 · 2022: 1 · 2021: 2 · 2020: 1 · 2019: 5 · 2018: 5 · 2017: 2 · 2016: 1 · 2015: 7 · 2014: 4 · 2013: 3 · 2012: 6
FWCI
5.69
Type
journal article
Language
en
Open access
Locations
  • Obesity (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • Institute of Advanced Aerospace Technology, Seoul National University
  • National Institute of Diabetes and Digestive and Kidney Diseases (R01DK49779, R01DK049779, R01 DK-51684, P30-DK56336, R01DK051684, P30DK056336)
  • National Center for Research Resources (M01RR00032, M01RR000032)
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
insulin sensitivity, inflammation, African American women, ethnic differences, C-reactive protein, TNF-α, soluble TNF receptors, interleukin-6, intra-abdominal adipose tissue, abdominal fat distribution, insulin resistance, metabolic disease risk
MeSH terms
Adult, Black or African American, Body Composition, C-Reactive Protein, Female, Glucose Tolerance Test, Humans, Inflammation, Insulin Resistance, Tumor Necrosis Factor-alpha, Biomarkers, Interleukin-6, Linear Models, White People, Receptors, Tumor Necrosis Factor, Type I, Receptors, Tumor Necrosis Factor, Type II, Intra-Abdominal Fat, Adiponectin

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