ArticleCurrent neuropharmacology2025
Olanzapine Induces Adipogenesis and Glucose Uptake by Activating Glycolysis and Synergizing with the PI3K-AKT Pathway.
Article in Current neuropharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Article
- Dual-target mechanisms of olanzapine in bipolar disorder: a network pharmacology and molecular docking study revealing phase-specific regulation of longevity and PI3K-Akt pathways.BMC psychiatry · 2025Article
- Supplementary Feeding Regulates Muscle Development of Oula Sheep (Tibetan Sheep,Animals : an open access journal from MDPI · 2025Article
- The relevance of resveratrol in ameliorating carotid atherosclerosis through glycolysis.BMC cardiovascular disorders · 2025Article
- Five differentially expressed proteins identified to serve as potential blood biomarkers for schizophrenia screening based on proteomics.Frontiers in psychiatry · 2025Article
Corrections and comments
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Authors and funding
13 authors.
Funding
Abstract
backgroundAdministration of olanzapine (OLA) is closely associated with obesity and glycolipid abnormalities in patients with schizophrenia (SCZ), although the exact molecular mechanisms remain elusive.
objectiveWe conducted comprehensive animal and molecular experiments to elucidate the mechanisms underlying OLA-induced weight gain.
methodsWe investigated the mechanisms of OLA-induced adipogenesis and lipid storage by employing a real-time ATP production rate assay, glucose uptake test, and reactive oxygen species (ROS) detection in 3T3-L1 cells and AMSCs. Rodent models were treated with OLA using various intervention durations, dietary patterns (normal diets/western diets), and drug doses. We assessed body weight, epididymal and liver fat levels, and metabolic markers in both male and female mice.
resultsOLA accelerates adipogenesis by directly activating glycolysis and its downstream PI3K signaling pathway in differentiated adipocytes. OLA promotes glucose uptake in differentiated 3T3-L1 preadipocytes. In mouse models with normal glycolipid metabolism, OLA administration failed to increase food intake and weight gain despite elevated GAPDH expression, a marker related to glycolysis and PI3K-AKT. This supports the notion that glycolysis plays a significant role in OLA-induced metabolic dysfunction.
conclusionOLA induces glycolysis and activates the downstream PI3K-AKT signaling pathway, thereby promoting adipogenesis.
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