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Related Concept Videos

Role of ER in the Secretory Pathway01:17

Role of ER in the Secretory Pathway

Eukaryotic cells have a special pathway that enables communication between various intracellular membrane-bound compartments and also with the extracellular environment. This pathway is termed as the secretory pathway.
Components of the secretory pathway
About a third of proteins synthesized in the cell are sorted via the secretory route. They shuffle between different compartments in membrane-bound vesicles until they reach their final destination. The main intracellular compartments involved...

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A Murine Model of Hyperlipidemia&#45;Induced Heart Failure with Preserved Ejection Fraction
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Selenoprotein F Deficiency Drives Diet-Induced Metabolic Dysfunction in Female Mice by Aggravating Hypothalamic

Zimeng Li1, Pengyu Zhao2, Wanru Yang1

  • 1Hubei Key Laboratory of Bioinorganic Chemistry and Materia Medica, School of Chemistry and Chemical Engineering, Huazhong University of Science and Technology, Wuhan 430074, China.

Biology
|July 15, 2026
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Summary

Selenoprotein F deficiency worsens diet-induced obesity in female mice by increasing hypothalamic ER stress and impairing brown adipose tissue thermogenesis. This highlights SELENOF

Keywords:
endoplasmic reticulum stresshypothalamusleptin resistanceselenoprotein Fthermogenesis

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Area of Science:

  • Metabolic Regulation
  • Endocrinology
  • Obesity Research

Background:

  • Obesity shows sex-dependent differences, but central energy sensing and peripheral thermogenesis mechanisms are unclear.
  • Selenoprotein F (SELENOF), an ER-resident protein, has unknown roles in diet-induced obesity.
  • Investigating SELENOF's role in metabolic homeostasis is crucial.

Purpose of the Study:

  • To determine the role of SELENOF in systemic metabolic homeostasis.
  • To investigate SELENOF's involvement in diet-induced obesity, particularly its sex-dependent effects.
  • To elucidate the molecular mechanisms linking hypothalamic and peripheral responses.

Main Methods:

  • Wild-type and SELENOF-deficient mice were fed a high-fat diet (HFD) for 16 weeks.
  • Primary brown adipocyte experiments were conducted.
  • Analysis included body weight, adipose tissue, lipid profiles, leptin levels, hypothalamic ER stress markers, inflammatory pathways, thyroid hormone levels, and brown adipose tissue (BAT) gene expression.

Main Results:

  • SELENOF deficiency aggravated HFD-induced weight gain, adipose tissue expansion, dyslipidemia, and hyperleptinemia specifically in female mice.
  • Hypothalamic ER stress and leptin resistance were intensified in SELENOF-deficient females.
  • SELENOF deficiency reduced circulating FT3 levels and suppressed DIO2 and UCP1 expression in BAT, without affecting proximal β3-adrenergic signaling.

Conclusions:

  • SELENOF deficiency exacerbates metabolic dysfunction in a sex-dependent manner during HFD.
  • SELENOF links hypothalamic proteostasis to BAT thermogenic signaling, influencing metabolic adaptation.
  • These findings suggest SELENOF is a key player in sex-specific responses to metabolic stress.