Dataset Information

MTCH2 modulates CPT1 activity to regulate lipid metabolism of adipocytes

ABSTRACT: MTCH2 is a protein localized in the outer membrane of mitochondria. It belongs to the solute carrier 25 family, but its substrates or transporter function remains unknown. Previous research links MTCH2 to apoptosis induction, and Alzheimer’s disease, mitochondrial metabolism and dynamics, and MTCH2 has been shown to function as a protein insertase and scramblase. Moreover, MTCH2 is a significant regulator of adipocyte differentiation and lipid homeostasis. Genome-wide association studies have identified MTCH2 variants to be associated with increased body mass index, obesity, and diabetes risk. Thus, MTCH2 emerges as a promising candidate for modulating adipocyte function and whole-body energy metabolism, but its specific metabolic role in mature adipose tissues remains unexplored. In this study, we show that MTCH2 regulates mitochondrial function and whole-body energy expenditure by regulating lipid utilization in adipose tissue.

INSTRUMENT(S): Orbitrap Fusion Lumos

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Cell Culture

SUBMITTER: Chunyan Wu

LAB HEAD: Christian Wolfrum

PROVIDER: PXD054881 | Pride | 2025-07-20

REPOSITORIES: pride

ACCESS DATA

Dataset's files

Source:

			Action	DRS
	20230131_C30582_002_S450014_mitoC2_Group_1.raw	Raw
	20230131_C30582_003_S450015_mitoC3_Group_1.raw	Raw
	20230131_C30582_004_S450019_mitoM3_Group_2.raw	Raw
	20230131_C30582_005_S450013_mitoC1_Group_1.raw	Raw
	20230131_C30582_007_S450017_mitoM1_Group_2.raw	Raw

Items per page:

1 - 5 of 17

Similar Datasets

Project description:Abstract Background In obesity, adipose tissue undergoes a remodeling process characterized by increased adipocyte size (hypertrophia) and number (hyperplasia). The individual ability to tip the balance toward the hyperplastic growth, with recruitment of new fat cells through adipogenesis, seems to be critical for a healthy adipose tissue expansion, as opposed to the development of inflammation and detrimental metabolic consequences. However, the molecular mechanisms underlying this fine-tuned regulation are far from being understood. Methods We analyzed by mass spectrometry-based proteomics visceral white adipose tissue (vWAT) samples collected from C57BL6 mice fed with a HFD for 8 weeks. A subset of these mice, called low responders (LowR HFD), showed a low susceptibility to the onset of adipose tissue inflammation, as opposed to their HFD counterpart. We identified the discriminants between LowR HFD and HFD vWAT samples and explored their function in Adipose Derived human Mesenchymal Stem Cells (AD-hMSCs) differentiated to adipocytes. Results We quantified 6051 proteins. Among the candidates that most differentiate LowR HFD from HFD vWAT, we found proteins involved in adipocyte function, including adiponectin and hormone sensitive lipase, suggesting that adipocyte differentiation is enhanced in LowR HFD, as compared to HFD. The chromatin modifier SET and MYND Domain Containing 3 (SMYD3), whose function in adipose tissue was totally unknown, was another top-scored hit. SMYD3 expression was significantly higher in LowR HFD vWAT, as confirmed by western blot analysis. In vitro, we found that SMYD3 mRNA and protein levels decrease rapidly along the differentiation process of AD-hMSCs. Moreover, SMYD3 knock-down at the beginning of adipocyte differentiation resulted in reduced cell proliferation and, at longer term, reduced lipid accumulation in adipocytes. Conclusions Our study describes for the first time the role of SMYD3 as a regulator of adipocyte proliferation during the early steps of adipogenesis.

Dataset Information

MTCH2 modulates CPT1 activity to regulate lipid metabolism of adipocytes

Dataset's files

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets