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Targeting Progesterone Receptor Membrane Component 1 to Improve Muscle Development and Glucose Homeostasis.

Sang R Lee1,2,3, Moeka Mukae1, Globinna Kim4

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Journal of Cachexia, Sarcopenia and Muscle
|November 10, 2025
PubMed
Summary
This summary is machine-generated.

Inhibiting progesterone receptor membrane component 1 (PGRMC1) in skeletal muscle improves glucose metabolism and insulin sensitivity in type 2 diabetes (T2D). This suggests targeting PGRMC1 in muscle is a novel therapeutic strategy for T2D.

Keywords:
PGRMC1glucose homeostasisinsulin resistanceskeletal muscletype 2 diabetes

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Area of Science:

  • Endocrinology
  • Metabolic Diseases
  • Molecular Biology

Background:

  • Type 2 diabetes (T2D) involves insulin resistance and beta-cell dysfunction, necessitating new treatments.
  • Progesterone receptor membrane component 1 (PGRMC1) may influence metabolic function, but its role in T2D is unclear.

Purpose of the Study:

  • Investigate the role of skeletal muscle PGRMC1 in T2D pathogenesis.
  • Evaluate 11α-hydroxyprogesterone (11α-OHP) as a potential therapeutic agent targeting PGRMC1.

Main Methods:

  • Generated skeletal muscle-specific Pgrmc1 knockout (PKO) mice.
  • Induced T2D using high-fat diet/streptozotocin or db/db mice.
  • Assessed glucose metabolism via GTT, ITT, and HOMA-IR; analyzed cellular glycolysis using Seahorse analysis.

Main Results:

  • Skeletal muscle PKO improved glucose tolerance and insulin sensitivity, reduced insulin resistance, and promoted muscle development.
  • PGRMC1 loss enhanced myoblast proliferation, differentiation, and glycolysis via the RSK1/AKT pathway.
  • 11α-OHP treatment improved glucose metabolism and insulin sensitivity in wild-type mice, with effects abolished in PKO mice.

Conclusions:

  • Skeletal muscle PGRMC1 is a key regulator of glucose metabolism.
  • Inhibiting skeletal muscle PGRMC1 represents a promising therapeutic strategy for managing T2D.