MTCH2 modulates CPT1 activity to regulate lipid metabolism of adipocytes

C Chunyan Wu (Zhejiang Key Laboratory of Excited-State Energy Conversion and Energy Storage, Department of Chemistry) T Tongtong Wang (School of Chemical Science and Engineering, Tongji University, 1239 Siping Rd, Shanghai, 200092, China) A Adhideb Ghosh F Fen Long A Anand Kumar Sharma T Tina Dahlby F Falko Noé I Ilenia Severi G Georgia Colleluori S Saverio Cinti A Antonio Giordano L Lianggong Ding R Radhika Khandelwal S Sarantos Kostidis (Center for Proteomics and Metabolomics, Leiden University Medical Center) M Martin Giera (Center for Proteomics and Metabolomics, Leiden University Medical Center) L Lucia Balazova V Vincent Gardeux L Laith Abu-Nawwas B Bart Deplancke S Sabita Chourasia S Sandra Kleiner B Bradford S. Hamilton J Juan Manuel Alcántara Alcántara J Jonatan R. Ruiz M Matthias Blüher A Anton Pekcec M Miroslav Balaz A Atan Gross H Heike Neubauer C Christian Wolfrum

Abstract

Abstract Metabolic disorders, including obesity and metabolic-associated steatohepatitis, arise from a chronic energy surplus. Thus, enhancing energy dissipation through increased respiration holds significant therapeutic potential for metabolic disorders. Through a comprehensive analysis of human and murine adipose tissues, along with a functional screen, we identify mitochondrial carrier homolog 2, a mitochondrial outer membrane protein, as a pivotal regulator of mitochondrial metabolism. Intriguingly, its expression in adipose tissue is a strong determinant of obesity in humans. Adipocyte-specific ablation of mitochondrial carrier homolog 2 improves mitochondrial function and whole-body energy expenditure, independent of uncoupling protein 1. Furthermore, mitochondrial carrier homolog 2 regulates mitochondrial influx of free fatty acids by modulating the sensitivity of carnitine palmitoyltransferase 1 to malonyl-CoA through direct physical interaction, leading to enhanced energy expenditure in adipocytes/adipose tissue. Here we show mitochondrial carrier homolog 2 functions as a negative regulator of energy metabolism in adipocytes and represents a potential target for treating obesity and related metabolic disorders.

Article Details

Volume / Issue Vol. 16, Issue 1
Published October 03, 2025
ISSN 2041-1723
Publisher Nature Portfolio

Journal Info

Nature Communications

Nature Portfolio

ISSN: 2041-1723 Open Access Life Sciences

Authors (30)

C

Chunyan Wu

Zhejiang Key Laboratory of Excited-State Energy Conversion and Energy Storage, Department of Chemistry

T

Tongtong Wang

School of Chemical Science and Engineering, Tongji University, 1239 Siping Rd, Shanghai, 200092, China

A

Adhideb Ghosh

F

Fen Long

A

Anand Kumar Sharma

T

Tina Dahlby

F

Falko Noé

I

Ilenia Severi

G

Georgia Colleluori

S

Saverio Cinti

A

Antonio Giordano

L

Lianggong Ding

R

Radhika Khandelwal

S

Sarantos Kostidis

Center for Proteomics and Metabolomics, Leiden University Medical Center

M

Martin Giera

Center for Proteomics and Metabolomics, Leiden University Medical Center

L

Lucia Balazova

V

Vincent Gardeux

L

Laith Abu-Nawwas

B

Bart Deplancke

S

Sabita Chourasia

S

Sandra Kleiner

B

Bradford S. Hamilton

J

Juan Manuel Alcántara Alcántara

J

Jonatan R. Ruiz

M

Matthias Blüher

A

Anton Pekcec

M

Miroslav Balaz

A

Atan Gross

H

Heike Neubauer

C

Christian Wolfrum