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We report here the hormonal, metabolic and gonadal responses to the glucagon-like peptide-1 (GLP1)-based multi-agonists, GLP1/Estrogen (GLP1/E), GLP1/gastric inhibitory peptide (GLP1/GIP) and GLP1/GIP/Glucagon, in two mouse PCOS models, with variable penetrance of metabolic and reproductive traits, and their comparison with metformin

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Meanwhile, the ratio of GSR to GPX4 at the protein level was decreased in the A2ARi-treated group compared with the control group (Figure 3I), indicating that the GSSG accumulation upon A2ARi treatment is caused likely by an impaired capacity to recycle GSSG back to GSH