From a physiological standpoint, hyperglycemia during illness is an adaptive mechanism. The liver’s increased glucose output fuels leukocytes and supports the acute phase response. Cytokines such as IL‑6 and TNF‑α further impair insulin signaling in muscle and fat, ensuring glucose remains available. While beneficial short‑term, chronic activation contributes to insulin resistance and may unmask prediabetes. Clinicians therefore view stress‑induced hyperglycemia as a marker of physiological strain rather than a standalone disease.