Staff Publications

Staff Publications

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    'Staff publications' is the digital repository of Wageningen University & Research

    'Staff publications' contains references to publications authored by Wageningen University staff from 1976 onward.

    Publications authored by the staff of the Research Institutes are available from 1995 onwards.

    Full text documents are added when available. The database is updated daily and currently holds about 240,000 items, of which 72,000 in open access.

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Record number 561601
Title HILPDA Uncouples Lipid Droplet Accumulation in Adipose Tissue Macrophages from Inflammation and Metabolic Dysregulation
Author(s) Dierendonck, Xanthe A.M.H. van; Rosa Rodriguez, Montserrat A. de la; Georgiadi, Anastasia; Mattijssen, Frits; Dijk, Wieneke; Weeghel, Michel van; Singh, Rajat; Borst, Jan Willem; Stienstra, Rinke; Kersten, Sander
Source Cell Reports 30 (2020)6. - ISSN 2211-1247 - p. 1811 - 1822.e6.
DOI https://doi.org/10.1016/j.celrep.2020.01.046
Department(s) Nutrition, Metabolism and Genomics
EPS
VLAG
Biochemistry
Publication type Refereed Article in a scientific journal
Publication year 2020
Keyword(s) ATGL - fatty acid metabolism - Hilpda - inflammation - lipid droplets - macrophages - obesity
Abstract

Obesity leads to a state of chronic, low-grade inflammation that features the accumulation of lipid-laden macrophages in adipose tissue. Here, we determined the role of macrophage lipid-droplet accumulation in the development of obesity-induced adipose-tissue inflammation, using mice with myeloid-specific deficiency of the lipid-inducible HILPDA protein. HILPDA deficiency markedly reduced intracellular lipid levels and accumulation of fluorescently labeled fatty acids. Decreased lipid storage in HILPDA-deficient macrophages can be rescued by inhibition of adipose triglyceride lipase (ATGL) and is associated with increased oxidative metabolism. In diet-induced obese mice, HILPDA deficiency does not alter inflammatory and metabolic parameters, despite markedly reducing lipid accumulation in macrophages. Overall, we find that HILPDA is a lipid-inducible, physiological inhibitor of ATGL-mediated lipolysis in macrophages and uncouples lipid storage in adipose tissue macrophages from inflammation and metabolic dysregulation. Our data question the contribution of lipid droplet accumulation in adipose tissue macrophages in obesity-induced inflammation and metabolic dysregulation.

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