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A deeper understanding of how distinct metabolic subtypes function under stress and influence the tumor microenvironment will inform the development of more selective and subtype-specific metabolic interventions

Additionally, obesity and IR both contribute to -cell dysfunction and apoptosis, mechanistically explained by glucotoxicity and increased immunogenicity (the accelerator hypothesis) or by -cell exhaustion due to increased metabolic demand (the overload hypothesis) [23]

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doi:10.1016/j.eururo.2009.09.035