Human visceral and subcutaneous adipose stem and progenitor cells retain depot-specific adipogenic properties during obesity
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Abdominal obesity associates with cardiometabolic disease and an accumulation of lipids in the visceral adipose depot, whereas lipid accumulation in the subcutaneous depot is more benign. We aimed to further investigate whether the adipogenic properties where cell-intrinsic, or dependent on a depot-specific or obesity-produced microenvironment. We obtained visceral and subcutaneous biopsies from non-obese women (n = 14) or women living with morbid obesity (n = 14) and isolated adipose stem and progenitor cells (ASPCs) from the stromal vascular fraction of non-obese (n = 13) and obese (n = 13). Following in vitro differentiation into mature adipocytes, we observed a contrasting pattern with a lower gene expression of adipogenic markers and a higher gene expression of immunogenic markers in the visceral compared to the subcutaneous adipocytes. We identified the immunogenic factor BST2 as a marker for visceral ASPCs. The effect of obesity and insulin resistance on adipogenic and immunogenic markers in the in vitro differentiated cells was minor. In contrast, differentiation with exogenous Tumor necrosis factor resulted in increased immunogenic signatures, including increased expression of BST2, and decreased adipogenic signatures in cells from both depots. Our data, from 26 women, underscore the intrinsic differences between human visceral and subcutaneous adipose stem and progenitor cells, suggest that dysregulation of adipocytes in obesity mainly occurs at a post-progenitor stage, and highlight an inflammatory microenvironment as a major constraint of human adipogenesis.
| Originalsprog | Engelsk |
|---|---|
| Artikelnummer | 983899 |
| Tidsskrift | Frontiers in Cell and Developmental Biology |
| Vol/bind | 10 |
| Antal sider | 12 |
| ISSN | 2296-634X |
| DOI | |
| Status | Udgivet - 2022 |
Bibliografisk note
Funding Information:
During the study period, the Center of Inflammation and Metabolism (CIM), Rigshospitalet, was supported by a grant from the Danish National Research Foundation (DNRF55). CIM/CFAS is a member of DD2, the Danish Center for Strategic Research in Type 2 Diabetes (the Danish Council for Strategic Research, grant nos. 09-067009 and 09-075724). The Centre for Physical Activity Research (CFAS) is supported by TrygFonden (grants ID 101390 and ID 20045). Novo Nordisk Foundation Center for Basic Metabolic Research is an independent Research Center, based at the University of Copenhagen, Denmark and partially funded by an unconditional donation from the Novo Nordisk Foundation www.cbmr.ku.dk (Grant number NNF18CC0034900.) This study was further supported by grants from the Danish Council for Independent research, Rigshospitalets Forskningsudvalg, P. Carl Petersens Fond, Illum Fondet, Direktør Jacob Madsen og hustru Olga Madsens fond, Direktør Emil Hertz og Hustru Inge Hertz’ Fond and the National Health and Medical Council of Australia (APP1098972).
Funding Information:
During the study period, the Center of Inflammation and Metabolism (CIM), Rigshospitalet, was supported by a grant from the Danish National Research Foundation (DNRF55). CIM/CFAS is a member of DD2, the Danish Center for Strategic Research in Type 2 Diabetes (the Danish Council for Strategic Research, grant nos. 09-067009 and 09-075724). The Centre for Physical Activity Research (CFAS) is supported by TrygFonden (grants ID 101390 and ID 20045). Novo Nordisk Foundation Center for Basic Metabolic Research is an independent Research Center, based at the University of Copenhagen, Denmark and partially funded by an unconditional donation from the Novo Nordisk Foundation www.cbmr.ku.dk (Grant number NNF18CC0034900.) This study was further supported by grants from the Danish Council for Independent research, Rigshospitalets Forskningsudvalg, P. Carl Petersens Fond, Illum Fondet, Direktør Jacob Madsen og hustru Olga Madsens fond, Direktør Emil Hertz og Hustru Inge Hertz’ Fond and the National Health and Medical Council of Australia (APP1098972).
Publisher Copyright:
Copyright © 2022 Mathur, Severinsen, Jensen, Naver, Schrölkamp, Laye, Watt, Nielsen, Krogh-Madsen, Pedersen and Scheele.
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