CHIẾN LƯỢC DINH DƯỠNG ĐƯỜNG TIÊU HOÁ NHẰM TỐI ƯU HOÁ CÂN BẰNG KIỀM-TOAN TRONG ĐIỀU TRỊ ĐÁI THÁO ĐƯỜNG TÝP 2

Abstract

This narrative review clarifies the role of dietary acid–base status in the management of type 2 diabetes (T2D), emphasizing two practical indices: PRAL (Potential Renal Acid Load) and NEAP (Net Endogenous Acid Production). Mild chronic metabolic acidosis arising from acidogenic eating patterns may attenuate insulin signaling, amplify low-grade inflammation, promote muscle proteolysis, and adversely affect bone and kidney health. Cohort data indicate that higher dietary acid load confers a moderate increase in incident T2D risk (HR/OR ≈ 1.2–1.6). Intermediate phenotypes are likewise unfavorable: higher HOMA-IR, lower ISI-Matsuda, and higher 120-minute OGTT glucose. In chronic kidney disease, trials show that increasing fruit–vegetable intake or adding bicarbonate raises serum HCO₃⁻, reduces albuminuria, and slows eGFR decline, supporting an alkali-leaning dietary strategy. Guided by ADA 2024, DNSG/EASD 2023, and KDIGO 2024, we propose an internal target of PRAL around −5 to 0 mEq/day where appropriate; adopt a plant-forward, low-GI, high-fiber pattern; prioritize plant or fish protein; and limit red/processed meats, refined grains, and sodium. For patients receiving enteral nutrition, diabetes-specific formulas provide better glycemic control than standard formulas. Alkaline bicarbonate mineral waters may be considered as selective adjuncts, but are not recommended for routine glycemic management.