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RNF186 controls glucose metabolism in metabolic dysfunction-associated fatty liver disease.

Jiang Du1,2, Qizhang Du1,2, Yuxuan Zhang1,2

  • 1Henan Collaborative Innovation Center of Stem Cells and Biotherapy, School of Medical Engineering, Henan Medical University (Xinxiang Medical University), East of Jinsui Road #601, Xinxiang, 453003, Henan Province, China.

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Summary

RNF186 deficiency improves glucose metabolism and insulin signaling in metabolic dysfunction-associated fatty liver disease (MAFLD). This occurs by enhancing GLUT4 transcription and translocation in skeletal muscle, suggesting RNF186 as a therapeutic target.

Keywords:
GLUT4Glucose metabolismMetabolic dysfunction-associated fatty liver diseaseRNF186Skeletal muscle

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Area of Science:

  • Biochemistry
  • Metabolism
  • Molecular Biology

Background:

  • RNF186, an E3 ubiquitin ligase, is linked to lipid metabolism in MAFLD.
  • Its role in MAFLD-related glucose metabolism, especially in skeletal muscle, is not fully understood.

Purpose of the Study:

  • To investigate the function of RNF186 in glucose metabolism within the context of MAFLD.
  • To elucidate the molecular mechanisms underlying RNF186's influence on skeletal muscle glucose uptake and insulin signaling.

Main Methods:

  • In vitro studies using skeletal myocytes and hepatocytes exposed to high glucose.
  • In vivo MAFLD model induced by high-fat diet in mice.
  • Analysis of RNF186 expression, glucose metabolism, and insulin signaling via Western blotting, qPCR, and immunofluorescence.

Main Results:

  • RNF186 expression is modulated by glucose and insulin in skeletal muscle and hepatocytes.
  • RNF186 deficiency improved glucose metabolism and insulin signaling in MAFLD models across multiple tissues.
  • In skeletal muscle, RNF186 absence reduced ER stress, increased GLUT4 transcription via ATF6, and promoted GLUT4 translocation through the AKT/TBC1D4 pathway.

Conclusions:

  • RNF186 plays a critical role in regulating glucose metabolism in MAFLD, particularly in skeletal muscle.
  • RNF186 influences both GLUT4 transcription and translocation, impacting glucose uptake.
  • Targeting RNF186 presents a potential therapeutic avenue for MAFLD and associated metabolic disorders.