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John Buse, Director of the Diabetes Care Center at the University of North Carolina and a principal investigator in GLP-1 outcomes trials, has noted in published commentary that "the antioxidant milieu in type 2 diabetes is genuinely impaired, but whether exogenous supplementation corrects the underlying defect or simply raises circulating levels without tissue impact remains unresolved." [9] That distinction shapes the practical advice: correcting a documented deficiency (measured low whole-blood glutathione in a patient with poorly controlled diabetes) is a different clinical decision from empirically adding glutathione to a well-controlled patient already benefiting from dulaglutide's own oxidative-stress effects

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doi: 10.1046/j.1440-1746.2001.02611.x 101 Al-AlimiAAAliSAAl-HassanFMIdrisFMTeowSYMohd YusoffN

Semaglutide and testosterone work through different biological pathways and do not have significant pharmacokinetic interactions