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Accordingly, despite the loss of highly glycosylated proIGF-1Ea after the 2-DG treatment, the condition media of these cells fully activated the IGF-1R of human breast cancer cell line MCF-7 (Fig
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It inhibits NNMT (nicotinamide N-methyltransferase), an enzyme regulating metabolism, fat storage, and NAD+ consumption.[4][27][6] NNMT methylates nicotinamide, a NAD+ breakdown product, diverting it from recycling and reducing available NAD+
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