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Therefore, particular interest lies in elucidating the molecular and functional changes occurring in -cells and other islet endocrine cells in T2D, as these cellular adaptations and dysfunctions constitute the foundation of disease pathogenesis and provide a rationale for the development of targeted therapeutic strategies

Despite the high conservation of GDH1 and GDH3 , Gdh1p exhibits higher utilization rates of -ketoglutarate under glucose conditions compared to Gdh3p [15, 16]

Metabolic approaches: GLP-1 Incretins (semaglutide): appetite suppression | GLP-1/GIP incretins (tirzepatide): dual hormonal agonism | 5-Amino-1MQ: NNMT enzyme inhibition a non-hormonal mechanism, directly targeting lipid and NAD+ metabolism

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