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Emerging evidence suggests that the underlying pathophysiology involves oxidative stress, impaired autophagy, ferroptosis, protein post-translational modifications, chronic low-grade inflammation, and gut microbiota dysbiosis affecting ovarian, hepatic, and pancreatic tissues

The insight that changed this view is that when glucagon receptor activation occurs alongside GLP-1 activity, the net effect is a shift toward increased energy expenditure and fat oxidation rather than hyperglycemia

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3d) bridges D270, D271 and E339 on SRCR3 AIM , and the carbonyl group of N106 on the J chain