MassIVE MSV000093409

Partial Public PXD047012

Loss of adipocyte-specific Olfactomedin-2 in obesity drives defective fat cell function, aggravating adipose tissue accretion

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Description

Olfactomedin-2 (OLFM2) participates in brain development and appears to be involved in energy handling. In adipose tissue, we here show expression of OLFM2 to be adipocyte-specific and opposed to obesity. OLFM2 levels are increased during adipogenesis, and impaired when differentiated fat cells are challenged with conditions emulating inflammation in the context of obesity. On the molecular level, examination of OLFM2 deficiency in human adipocytes indicated down-regulation of genes related to cell cycle. At the cellular level, the loss of OLFM2 compromised adipogenesis, while its over-production enhanced the adipogenic transformation of 3T3-L1 cells. Complementary loss and gain of function assays coupled to untargeted proteomics revealed the modulation of key protein pathways, including regulation of citrate cycle, fatty acid degradation, axon guidance and focal adhesion in mature adipocytes and precursor cells. Transferring these findings into animal models using a whole-body knockout and transcriptionally depleted adipose Olfm2 highlighted, respectively, a cluster of molecular changes connected with defective cell cycle (in both), fat mass accretion and impaired metabolism (in the latter). Our data underscores a key role for OLFM2 in fat cells, and suggests that the association between adipose OLFM2 and obesity is not only correlative but also causative. [doi:10.25345/C5MW28R3F] [dataset license: CC0 1.0 Universal (CC0 1.0)]

Keywords: Olfactomedin-2, adipocytes, adipose tissue, metabolism, obesity ; label-free, Orbitrap Eclipse, DIA

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Principal Investigators:
(in alphabetical order) 		Francisco J. Ortega, Ph.D., Institut d'Investigacio Biomedica de Girona (IDIBGI), Spain
Submitting User: Wszymanski
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