ArticleJournal of cachexia, sarcopenia and muscle2025
Targeting Progesterone Receptor Membrane Component 1 to Improve Muscle Development and Glucose Homeostasis.
Article in Journal of cachexia, sarcopenia and muscle, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Targeting Progesterone Receptor Membrane Component 1 to Improve Muscle Development and Glucose Homeostasis.Journal of cachexia, sarcopenia and muscle · 2025Article
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Authors and funding
10 authors.
Funding
Abstract
backgroundType 2 diabetes mellitus (T2D) arises from the interplay between peripheral insulin resistance and pancreatic β-cell dysfunction, ultimately leading to impaired glucose utilization and chronic hyperglycemia. Despite therapeutic advances, the multifactorial nature of T2D continues to demand the development of novel treatment strategies. Progesterone receptor membrane component 1 (PGRMC1) has emerged as a potential modulator of metabolic function, though its role in T2D pathogenesis has not been fully elucidated.
methodsTo investigate the role of PGRMC1 in T2D, we generated skeletal muscle-specific Pgrmc1 knockout (PKO) mice (ACTA
resultsSkeletal muscle PKO improved glucose clearance in GTT (p < 0.0001) and insulin sensitivity in ITT (p < 0.0001). Skeletal muscle PKO mice under T2D suppressed insulin resistance according to reduced modified HOMA-IR (p < 0.05) and promoted muscle development (quadriceps femoris, gastrocnemius, tibialis anterior muscle and extensor digitorum longus; p < 0.05). Mechanistically, PGRMC1 interacted with PPP2R5D, a PP2A regulatory subunit, which dephosphorylates RSK1. PGRMC1 loss suppressed PP2A activity, increasing RSK1 phosphorylation and activating AKT signalling, thereby enhancing myoblast proliferation (p < 0.05), differentiation (p < 0.01) and glycolysis (p < 0.0001). 11α-OHP facilitated proteasomal degradation of PGRMC1, elevated pAKT levels and improved glucose clearance in GTT (p < 0.0001) and insulin sensitivity in ITT (p < 0.0001) in wild-type mice but not in PKO mice. Notably, 11α-OHP restored glucose clearance in GTT (p < 0.0001) and insulin sensitivity in ITT (p < 0.0001) and increased muscle mass in both HFD-STZ and db/db mice, but its effects were abolished in skeletal muscle PKO mice. Whole-body PKO mice still increased muscle development and metabolic activation, suggesting minimal interference by systemic PKO.
conclusionsThese findings identify skeletal muscle PGRMC1 as a pivotal regulator of glucose metabolism and highlight its inhibition as a promising muscle-targeted therapeutic approach for T2D management.
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