ArticleExperimental & molecular medicine2025
Inhibition of serotonin-Htr2b signaling in skeletal muscle mitigates obesity-induced insulin resistance.
Article in Experimental & molecular medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 3 papers.
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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
3 citing papers in PubMed.
- Serotonin Signaling and Vascular Reactivity in Cardiometabolic Disease and Cardiac Surgery.Cells · 2026Review
- Single-nuclei RNA-sequencing uncovers sexually divergent exercise signatures partially mimicked by TFEB overexpression in mouse skeletal muscle.bioRxiv : the preprint server for biology · 2026Article
- Neurotransmitter Alterations in Prediabetes and Type 2 Diabetes Mellitus: A Narrative Review.International journal of molecular sciences · 2025Review
Corrections and comments
- Erratum issued
Authors and funding
9 authors.
Funding
Abstract
Obesity-induced insulin resistance is a major cause of metabolic disorders, including type 2 diabetes mellitus. Although peripheral serotonin (5-hydroxytryptamine, 5-HT) has been implicated in energy balance and metabolism, its effect on skeletal muscle insulin sensitivity remains unclear. Here we identified the 5-HT receptor 2b (Htr2b) as a critical regulator of insulin sensitivity and energy metabolism in the skeletal muscle. Using genetic and pharmacological approaches, we showed that muscle-specific Tph1-knockout (Tph1 MKO) mice fed a high-fat diet exhibited reduced body weight, increased lean mass and improved glucose tolerance compared with wild-type mice. The pharmacological inhibition of Htr2b in myotubes reversed palmitate-induced insulin resistance and increased glycolytic activity. Moreover, muscle-specific HTR2b-knockout (HTR2b MKO) mice exhibited improved glucose uptake, insulin sensitivity and overall metabolic health under high-fat-diet-induced obesity. Mechanistically, both Tph1 MKO and Htr2b MKO mice showed increased phosphorylation of AKT and AMPK, indicating improved insulin sensitivity and energy metabolism in the skeletal muscle. These findings demonstrate that 5-HT-Htr2b signaling negatively regulates insulin sensitivity and energy metabolism in skeletal muscles, providing new insights into the role of peripheral serotonin in muscle metabolism and potential therapeutic targets for metabolic disorders.
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Registered trials
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