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The pathophysiologic mechanisms for sepsis-associated hypoglycemia (SAH) are multifactorial and include depletion of glycogen stores due to increased metabolic demands, impaired hepatic gluconeogenesis caused by inflammatory cytokines, excess lactate, and liver failure in the setting of multiple organ failure [32], sepsis- associated acute kidney injury resulting in impaired insulin catabolism and decreased tubular glucose absorption, and relative adrenal insufficiency is another possible underlying pathogenetic mechanism of SAH

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