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

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 wi...

Descripción completa

Guardado en:
Detalles Bibliográficos
Autores principales: 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
Formato: article
Lenguaje:EN
Publicado: Nature Portfolio 2018
Materias:
R
Q
Acceso en línea:https://doaj.org/article/443cd9ffd09742e6ad0690ce44450891
Etiquetas: Agregar Etiqueta
Sin Etiquetas, Sea el primero en etiquetar este registro!
id oai:doaj.org-article:443cd9ffd09742e6ad0690ce44450891
record_format dspace
spelling oai:doaj.org-article:443cd9ffd09742e6ad0690ce444508912021-12-02T15:08:50ZAbdominal subcutaneous and visceral adipocyte size, lipolysis and inflammation relate to insulin resistance in male obese humans10.1038/s41598-018-22962-x2045-2322https://doaj.org/article/443cd9ffd09742e6ad0690ce444508912018-03-01T00:00:00Zhttps://doi.org/10.1038/s41598-018-22962-xhttps://doaj.org/toc/2045-2322Abstract 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.K. VerbovenK. WoutersK. GaensD. HansenM. BijnenS. WetzelsC. D. StehouwerG. H. GoossensC. G. SchalkwijkE. E. BlaakJ. W. JockenNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 8, Iss 1, Pp 1-8 (2018)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
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
Abdominal subcutaneous and visceral adipocyte size, lipolysis and inflammation relate to insulin resistance in male obese humans
description 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.
format article
author 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
author_facet 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
author_sort K. Verboven
title Abdominal subcutaneous and visceral adipocyte size, lipolysis and inflammation relate to insulin resistance in male obese humans
title_short Abdominal subcutaneous and visceral adipocyte size, lipolysis and inflammation relate to insulin resistance in male obese humans
title_full Abdominal subcutaneous and visceral adipocyte size, lipolysis and inflammation relate to insulin resistance in male obese humans
title_fullStr Abdominal subcutaneous and visceral adipocyte size, lipolysis and inflammation relate to insulin resistance in male obese humans
title_full_unstemmed Abdominal subcutaneous and visceral adipocyte size, lipolysis and inflammation relate to insulin resistance in male obese humans
title_sort abdominal subcutaneous and visceral adipocyte size, lipolysis and inflammation relate to insulin resistance in male obese humans
publisher Nature Portfolio
publishDate 2018
url https://doaj.org/article/443cd9ffd09742e6ad0690ce44450891
work_keys_str_mv AT kverboven abdominalsubcutaneousandvisceraladipocytesizelipolysisandinflammationrelatetoinsulinresistanceinmaleobesehumans
AT kwouters abdominalsubcutaneousandvisceraladipocytesizelipolysisandinflammationrelatetoinsulinresistanceinmaleobesehumans
AT kgaens abdominalsubcutaneousandvisceraladipocytesizelipolysisandinflammationrelatetoinsulinresistanceinmaleobesehumans
AT dhansen abdominalsubcutaneousandvisceraladipocytesizelipolysisandinflammationrelatetoinsulinresistanceinmaleobesehumans
AT mbijnen abdominalsubcutaneousandvisceraladipocytesizelipolysisandinflammationrelatetoinsulinresistanceinmaleobesehumans
AT swetzels abdominalsubcutaneousandvisceraladipocytesizelipolysisandinflammationrelatetoinsulinresistanceinmaleobesehumans
AT cdstehouwer abdominalsubcutaneousandvisceraladipocytesizelipolysisandinflammationrelatetoinsulinresistanceinmaleobesehumans
AT ghgoossens abdominalsubcutaneousandvisceraladipocytesizelipolysisandinflammationrelatetoinsulinresistanceinmaleobesehumans
AT cgschalkwijk abdominalsubcutaneousandvisceraladipocytesizelipolysisandinflammationrelatetoinsulinresistanceinmaleobesehumans
AT eeblaak abdominalsubcutaneousandvisceraladipocytesizelipolysisandinflammationrelatetoinsulinresistanceinmaleobesehumans
AT jwjocken abdominalsubcutaneousandvisceraladipocytesizelipolysisandinflammationrelatetoinsulinresistanceinmaleobesehumans
_version_ 1718387993918570496