Abdominal subcutaneous and visceral adipocyte size, lipolysis and inflammation relate to insulin resistance in male obese humans

K. Verboven*, K. Wouters, K. Gaens, D. Hansen, M. Bijnen, S. Wetzels, C. D. Stehouwer, G. H. Goossens, C. G. Schalkwijk, E. E. Blaak, J. W. Jocken

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

92 Citations (Web of Science)

Abstract

Obesity is associated with a disturbed adipose tissue (AT) function characterized by adipocyte hypertrophy, an impaired lipolysis and pro-inflammatory phenotype, which contributes to insulin resistance (IR). We investigated whether AT phenotype in different AT depots of obese individuals with and without type 2 diabetes mellitus (T2DM) is associated with whole-body IR. Subcutaneous (SC) and visceral (V) AT biopsies from 18 lean, 17 obese and 8 obese T2DM men were collected. AT phenotype was characterized by ex vivo measurement of basal and stimulated lipolysis (mature adipocytes), adipocyte size distribution (AT tissue sections) and AT immune cells (flow cytometry). In VAT, mean adipocyte size, CD45(+) leukocytes and M1 macrophages were significantly increased in both obese groups compared to lean individuals. In SCAT, despite adipocyte hypertrophy, no significant differences in immune cell populations between groups were found. In SCAT, multiple linear regression analysis showed that none of the AT phenotype markers independently contributed to HOMA-IR while in VAT, mean adipocyte size was significantly related to HOMA-IR. In conclusion, beside adipocyte hypertrophy in VAT, M1 macrophage-or B-cell-mediated inflammation, may contribute to IR, while inflammation in hypertrophic SCAT does not seem to play a major role in IR.

Original languageEnglish
Article number4677
Number of pages8
JournalScientific Reports
Volume8
DOIs
Publication statusPublished - 16 Mar 2018

Keywords

  • ADIPOSE-TISSUE MACROPHAGES
  • ECTOPIC FAT DEPOSITION
  • METABOLIC DISEASE
  • OXYGEN-TENSION
  • CELL FUNCTION
  • PROMOTE
  • SENSITIVITY
  • MODULATION
  • PHENOTYPE
  • GLUCOSE

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