SUCNR1-mediated chemotaxis of macrophages aggravates obesity-induced inflammation and diabetes View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2017-07

AUTHORS

Janna A. van Diepen, Joris H. Robben, Guido J. Hooiveld, Claudia Carmone, Mohammad Alsady, Lily Boutens, Melissa Bekkenkamp-Grovenstein, Anneke Hijmans, Udo F. H. Engelke, Ron A. Wevers, Mihai G. Netea, Cees J. Tack, Rinke Stienstra, Peter M. T. Deen

ABSTRACT

AIMS/HYPOTHESIS: Obesity induces macrophages to drive inflammation in adipose tissue, a crucial step towards the development of type 2 diabetes. The tricarboxylic acid (TCA) cycle intermediate succinate is released from cells under metabolic stress and has recently emerged as a metabolic signal induced by proinflammatory stimuli. We therefore investigated whether succinate receptor 1 (SUCNR1) could play a role in the development of adipose tissue inflammation and type 2 diabetes. METHODS: Succinate levels were determined in human plasma samples from individuals with type 2 diabetes and non-diabetic participants. Succinate release from adipose tissue explants was studied. Sucnr1 -/- and wild-type (WT) littermate mice were fed a high-fat diet (HFD) or low-fat diet (LFD) for 16 weeks. Serum metabolic variables, adipose tissue inflammation, macrophage migration and glucose tolerance were determined. RESULTS: We show that hypoxia and hyperglycaemia independently drive the release of succinate from mouse adipose tissue (17-fold and up to 18-fold, respectively) and that plasma levels of succinate were higher in participants with type 2 diabetes compared with non-diabetic individuals (+53%; p < 0.01). Sucnr1 -/- mice had significantly reduced numbers of macrophages (0.56 ± 0.07 vs 0.92 ± 0.15 F4/80 cells/adipocytes, p < 0.05) and crown-like structures (0.06 ± 0.02 vs 0.14 ± 0.02, CLS/adipocytes p < 0.01) in adipose tissue and significantly improved glucose tolerance (p < 0.001) compared with WT mice fed an HFD, despite similarly increased body weights. Consistently, macrophages from Sucnr1 -/- mice showed reduced chemotaxis towards medium collected from apoptotic and hypoxic adipocytes (-59%; p < 0.05). CONCLUSIONS/INTERPRETATION: Our results reveal that activation of SUCNR1 in macrophages is important for both infiltration and inflammation of adipose tissue in obesity, and suggest that SUCNR1 is a promising therapeutic target in obesity-induced type 2 diabetes. DATA AVAILABILITY: The dataset generated and analysed during the current study is available in GEO with the accession number GSE64104, www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE64104 . More... »

PAGES

1304-1313

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s00125-017-4261-z

DOI

http://dx.doi.org/10.1007/s00125-017-4261-z

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1084517279

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/28382382


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