Adipose tissue oxygenation is associated with insulin sensitivity independently of adiposity in obese men and women

Gijs H. Goossens*, Max A. A. Vogel, Roel G. Vink, Edwin C. Mariman, Marleen A. van Baak, Ellen E. Blaak

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

Abstract

Adipose tissue (AT) dysfunction contributes to the pathophysiology of insulin resistance and type 2 diabetes. Previous studies have shown that altered AT oxygenation affects adipocyte functionality, but it remains to be elucidated whether altered AT oxygenation is more strongly related to obesity or insulin sensitivity. In the present study, we tested the hypothesis that AT oxygenation is associated with insulin sensitivity rather than adiposity in humans. Thirty-five lean and obese individuals (21 men and 14 women, aged 40-65 years) with either normal or impaired glucose metabolism participated in a cross-sectional single-centre study. We measured abdominal subcutaneous AT oxygenation, body composition and insulin sensitivity. AT oxygenation was higher in obese insulin resistant as compared to obese insulin sensitive (IS) individuals with similar age, body mass index and body fat percentage, both in men and women. No significant differences in AT oxygenation were found between obese IS and lean IS men. Moreover, AT oxygenation was positively associated with insulin resistance (r = 0.465; P = .005), even after adjustment for age, sex and body fat percentage (standardized = 0.479; P = .005). In conclusion, abdominal subcutaneous AT oxygenation is associated with insulin sensitivity both in men and women, independently of adiposity. AT oxygenation may therefore be a promising target to improve insulin sensitivity.

Original languageEnglish
Pages (from-to)2286-2290
Number of pages5
JournalDiabetes Obesity & Metabolism
Volume20
Issue number9
DOIs
Publication statusPublished - Sept 2018

Keywords

  • clinical physiology
  • glucose metabolism
  • insulin resistance
  • obesity therapy
  • TENSION
  • HYPOXIA
  • FAT
  • INFLAMMATION
  • PHENOTYPE
  • HUMANS

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