Chronic pulmonary diseases such as chronic obstructive pulmonary disease, obstructive sleep apnea and obesity hypoventilation syndrome are common conditions which share decreased pulmonary ventilation and CO2 retention. CO2 is an end-product of metabolism of all body cells. When CO2 accumulates, it is recommended to consider measures to reduce its endogenous production. One such measure relates to the sources of energy ingested as nutrition. It is recommended to increase the intake of dietary lipids and reduce carbohydrates, as the former produces less endogenous CO2 when metabolized. Our hypothesis focuses on a different mechanism for reducing the availability of carbohydrates, especially glucose, as a fuel for body cells metabolism. Sodium-glucose cotransporter-2 inhibitors (SGLT2i) are a new class of oral anti-hyperglycemic agents. Physiologically, glucose filtered through kidney glomeruli is reabsorbed in the proximal convoluted tubule; SGLT2i inhibit this mechanism. Therefore, glucose is secreted in the urine (glucosuria) and as a result glucose serum level is reduced. If glucose serum level is reduced, less glucose is available for metabolism, less CO2 is endogenously produced, and less CO2 must be expelled from the diseased lungs. It is hypothesized that these agents may be beneficial for patients with diabetes and concomitant pulmonary disease who retain CO2.
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