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The 2nd glutathione-interaction site appears to preferentially interact with the -glutamylcysteinyl moiety of GSH and is thought to facilitate the recruitment and activation of GSH as a preferred reducing agent 7,11,13,17,50

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This binding triggers several important physiological responses: enhanced insulin secretion from pancreatic beta cells in response to elevated blood glucose, suppression of glucagon release (which normally raises blood sugar), delayed gastric emptying (slowing food passage from stomach to intestine), and increased satiety through effects on appetite centres in the brain

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