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Their primary mechanisms of action include: Enhancing glucose-dependent insulin secretion from pancreatic beta cells Suppressing glucagon release , which reduces hepatic glucose production Slowing gastric emptying , leading to prolonged satiety Acting on appetite centres in the brain to reduce food intake These combined effects result in improved glycaemic control, reduced HbA1c levels, and significant weight loss in many patients
N-acetylcysteine (NAC), a GSH precursor that crosses the blood-brain barrier, has shown promise in preliminary studies and warrants further investigation as a preventive treatment [47, 48]
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