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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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Werner syndrome (WS), which is distinguished by severe metabolic dysfunction, dyslipidemia, early atherosclerosis, and insulin resistance diabetes, is thought to most closely mimic normal aging

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