ESC Congress 2026 Abstract · Oct 26, 2026

D-allulose attenuates D-galactose-induced cardiac aging rats by preserving mitochondrial function, mitochondrial dynamics, and cardiac apoptosis

By Lu D, Maneechote C, Tokuda M et al.

Background: Cardiac aging is characterized by progressive deterioration of cardiac function, mitochondrial dysfunction, cardiomyocyte apoptosis, and cellular senescence. D-galactose-induced aging is a well-established experimental model that recapitulates these alterations. Although D-allulose, a rare sugar with metabolic benefits, and Inulin, a natural soluble prebiotic fiber, have demonstrated beneficial health effects via antioxidant and metabolic regulatory mechanisms, their cardioprotective effects in D-galactose-induced aging remain incompletely understood. Purpose: This study investigated whether D-allulose exerts anti-cardiac aging effects through modulation of mitochondrial function, dynamics, and apoptosis in an aging rat model. Methods: Twenty male Wistar rats (~4 months old) were assigned to either a control group (CON, n=5) or a D-galactose group (D-gal, 150 mg/kg/day, s.c., n=15) for 8 weeks to induce a cardiac aging phenotype. D-galactose-treated rats were subsequently randomized to receive vehicle (VEH, n=5), oral inulin (positive control, INU, 2.0 g/kg/day, n=5), or D-allulose (DAL, 1.9 g/kg/day, n=5) for 12 weeks. Cardiac function was assessed by echocardiography. Mitochondrial function, dynamics, apoptosis, and senescence-related markers were evaluated in cardiac tissue. Results: D-galactose (VEH group) administration induced a cardiac aging phenotype characterized by impaired cardiac function, mitochondrial depolarization, altered mitochondrial dynamics, increased cellular senescence, and apoptosis. Specifically, these aging rats had reduced fractional shortening (%), increased senescence-associated β-galactosidase (SA-β-gal) activity, decreased the red-to-green fluorescence ratio, increased phosphorylation of dynamin-related protein 1 at serine 616 (p-Drp1Ser616), decreased mitofusin-2 (MFN2), and increased the number of TUNEL-positive cells (Figure 1A-F). Notably, D-allulose treatment markedly attenuated these adverse alterations, with effects comparable to those observed with Inulin (Figure 1A-F). Conclusions: D-allulose and Inulin attenuated D-galactose-induced cardiac aging by preserving mitochondrial function, maintaining mitochondrial dynamics, and reducing apoptosis. These findings support D-allulose as a promising nutritional intervention for age-related cardiac dysfunction.Figure 1

doi.org/10.1093/eurheartj/ehag785.3571Open accessInterventions