ArticleDrug design, development and therapy2026
GLUT5-Mediated Disruption of the Gut-Testis Axis Deteriorates Olanzapine-Induced Testicular Fibrosis and is Ameliorated by Dapagliflozin.
Article in Drug design, development and therapy, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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10 authors.
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Abstract
Objective: Olanzapine (OLA)-induced male reproductive toxicity has attracted increasing attention; however, the underlying mechanism of OLA-induced testicular injury remains unclear. The present study aimed to uncover the particular mechanisms involved and to explore potential preventive and therapeutic strategies against OLA-induced testicular injury. Methods: This study explored the specific mechanism and potential prevention and treatment methods of OLA-induced testicular injury through transcriptomics, molecular biology, and pathological staining methods. Results: Transcriptomics analysis and molecular pharmacology approaches revealed that glucose transporter type 5 (GLUT5) mediated the disruption of intestinal tight-junction proteins via activation of the adenosine monophosphate-activated protein kinase (AMPK)/mammalian target of rapamycin (mTOR) signaling pathway (P<0.05 or P<0.01). This process promoted the impairment of the gut-testis axis and upregulated CD28, thereby activating the phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT)/mTOR pathway and facilitating OLA-induced testicular fibrosis (P<0.05 or P<0.01). In addition, dapagliflozin (DAP) could alleviate these pathological changes via downregulating GLUT5, thereby improving OLA-induced testicular fibrosis (P<0.05 or P<0.01). Conclusion: The current study demonstrated for the first time that OLA could induce testicular fibrosis through the activation of the GLUT5/AMPK/mTOR pathway, leading to gut-testis axis dysfunction and activation of the CD28/PI3K/AKT/mTOR pathway. However, DAP could reverse these adverse effects via downregulating GLUT5, thus supporting its potential as a therapeutic agent for OLA-induced testicular fibrosis. The above results could provide novel mechanistic insights and identify new molecular targets for the prevention and treatment of OLA-induced male reproductive toxicity.
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