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Related Experiment Video

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FAM134B improves preadipocytes differentiation by enhancing mitophagy.

Min Cai1, Jing Zhao1, Qing Liu1

  • 1College of Animal Sciences, Zhejiang University, Key Laboratory of Animal Nutrition & Feed Sciences, Ministry of Agriculture, Zhejiang Provincial Laboratory of Feed and Animal Nutrition, No. 866 Yuhangtang Road, Hangzhou, Zhejiang 310058, PR China.

Biochimica Et Biophysica Acta. Molecular and Cell Biology of Lipids
|August 26, 2019
PubMed
Summary

Family with Sequence Similarity 134, Member B (FAM134B) protein promotes adipocyte differentiation by enhancing mitophagy. Overexpression leads to obesity and insulin resistance in mice, highlighting FAM134B's role in metabolic health.

Keywords:
AdipocyteAutophagyDifferentiationMitochondriaMitophagyfam134b

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Area of Science:

  • Cell Biology
  • Metabolic Research
  • Molecular Biology

Background:

  • Family with Sequence Similarity 134, Member B (FAM134B) is crucial for neuronal survival and involved in ER turnover, tumor inhibition, and lipid homeostasis.
  • FAM134B's specific role in adipocyte differentiation and metabolic regulation remains largely unexplored.

Purpose of the Study:

  • To elucidate the mechanistic links between FAM134B and adipocyte differentiation.
  • To investigate the impact of FAM134B on metabolic parameters, autophagy, and mitochondrial dynamics in adipocytes.

Main Methods:

  • Generation of adipocyte-specific FAM134B overexpression mice.
  • Analysis of metabolic parameters (obesity, glucose levels, insulin resistance) and white adipose tissue (WAT) mass.
  • In vitro studies using 3T3-L1 preadipocytes with FAM134B overexpression and autophagy inhibition (3-methyladenine).
  • Assessment of autophagy flux and mitochondrial content.

Main Results:

  • Adipocyte-specific FAM134B overexpression in mice resulted in obesity, increased WAT mass, hyperglycemia, and severe insulin resistance.
  • FAM134B overexpression in 3T3-L1 cells promoted adipocyte differentiation and autophagy, with reduced mitochondrial content.
  • Inhibition of autophagy attenuated the effects of FAM134B, indicating a critical role for autophagy in its function.
  • Increased autophagy flux and early reduction in mitochondria number were observed in FAM134B-overexpressing cells.

Conclusions:

  • FAM134B enhances adipocyte differentiation and promotes obesity and insulin resistance through the enhancement of mitophagy.
  • FAM134B plays a significant role in regulating adipocyte function and systemic metabolic homeostasis.
  • Targeting FAM134B could offer potential therapeutic strategies for metabolic disorders.