Decoding the Association of Polycystic Ovary Syndrome With Metabolic-Associated Fatty Liver

Produkt bewerten

Anwar Seiwan

▪Sameeah Mejbel

▪Hebatallah Nahas

Verlag:

Eliva Press

Unsere-Artikel-Nr.: P35486735

EAN: 9789999342759

Erhältlich:

Nicht auf Lager

Zustellung: Di, 01.09.2026

Versand: Kostenlos

-9.4 %

CHF 90.–

CHF 81.50

Beschreibung

Polycystic ovary syndrome (PCOS) is a common endocrine-metabolic disorder often associated with insulin resistance and metabolic-associated fatty liver disease (MAFLD), both linked to impaired autophagy. This study evaluates the effects of metformin and levothyroxine on autophagy regulation in a PCOS-induced MAFLD rat model. Materials and methods: PCOS was induced in female Wistar rats by testosterone enanthate (7. 5 mg, E16-19). Post-weaning, rats were assigned to control, model, metformin (300 mg kg-1 per day), levothyroxine (50 μg kg-1 per day), or combination groups. Body/liver weight, serum markers (ALT, AST, TSH, lipid profile, testosterone, LH, estradiol), insulin sensitivity, autophagy-related proteins (LC3II, ATG7, p62, CK18), and histology were assessed. Network pharmacology, protein-protein interaction, KEGG enrichment, and molecular docking were performed. Results: combination therapy reduced body weight (10. 29%) and liver weight (37. 08%) and lowered ALT (26. 17%), AST (42. 69%), TSH (77. 9%), cholesterol (41. 32%), triglycerides (32. 37%), and LDL (43. 42%). Testosterone and LH declined (37. 25%, 14. 43%), while estradiol rose (37. 4%). HOMA-IR decreased by 51. 85%. Autophagy markers (CK18, LC3II, P62, ATG7) were suppressed, with improved hepatic and ovarian histology. Network analysis identified NOS2, KRT18, MAP1LC3B, ATG7, and SQSTM1 as key targets, with KEGG pathways implicated in autophagy, mitophagy, ferroptosis, and apelin signaling. Docking analysis showed stronger binding of levothyroxine to LC3II and ATG7, suggesting a direct modulatory role. Conclusion: metformin and levothyroxine synergistically improve PCOS-related MAFLD by restoring autophagy and metabolic-endocrine balance. System-level and docking analyses support autophagy regulation as a key therapeutic mechanism, highlighting the potential role of levothyroxine in modulating autophagy.

Spezifikationen

Sprache

Englisch

Autor

Anwar Seiwan
Sameeah Mejbel
Hebatallah Nahas

Erscheinungsjahr

2026

Format

Buch (Softcover)

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