Scholarlink

<p>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.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

MTCH2 modulates CPT1 activity to regulate lipid metabolism of adipocytes

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年10月3日

查看全文
  • Chunyan Wu,
  • Tongtong Wang,
  • Adhideb Ghosh,
  • Fen Long,
  • Anand Kumar Sharma,
  • Tina Dahlby,
  • Falko Noé,
  • Ilenia Severi,
  • Georgia Colleluori,
  • Saverio Cinti,
  • Antonio Giordano,
  • Lianggong Ding,
  • Radhika Khandelwal,
  • Sarantos Kostidis,
  • Martin Giera,
  • Lucia Balazova,
  • Vincent Gardeux,
  • Laith Abu-Nawwas,
  • Bart Deplancke,
  • Sabita Chourasia,
  • Sandra Kleiner,
  • Bradford S. Hamilton,
  • Juan Manuel Alcántara Alcántara,
  • Jonatan R. Ruiz,
  • Matthias Blüher,
  • Anton Pekcec,
  • Miroslav Balaz,
  • Atan Gross,
  • Heike Neubauer,
  • Christian Wolfrum

摘要

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.