The development of hyperglycemia arising from disruption of immune metabolic homeostasis in COVID-19. High glucose levels induced by psychological stress, lingering inflammation, and β-cell dysfunction can lead to activation of the NLRP3 inflammasome in pancreatic β cells. As a result, pro–IL-1β is processed to the biologically active IL-1β. IL-1β released from β cells causes the recruitment and activation of macrophages, which prompts the release of more IL-1β. High local concentrations of IL-1β in the β-cell microenvironment may inhibit insulin secretion and trigger β-cell dysfunction and apoptosis. This leads to further increases in levels of glucose, thereby causing IL-1β autostimulation and establishing a vicious cycle. Exercise induces the release of circulating factors that mediate the anti-inflammatory response, support brain homeostasis, and increase insulin sensitivity. The net effect is the lowering of glucose levels and could be envisioned as a remission-induction therapy to counter the sequelae of COVID-19 (graphics program: Biorender). IL-1β, Interleukin-1β; NLRP3, NOD-, LRR-, and pyrin domain-containing protein 3