The Buckwheat Iminosugar d‐Fagomine Attenuates Sucrose‐Induced Steatosis and Hypertension in Rats

Scope This study examines the long‐term functional effects of d‐fagomine on sucrose‐induced factors of metabolic dysfunctions and explores possible molecular mechanisms behind its action. Methods and results Wistar Kyoto rats are fed a 35% sucrose solution with d‐fagomine (or not, for comparison) or mineral water (controls) for 24 weeks. The following are recorded: body weight; energy intake; glucose tolerance; plasma leptin concentration and lipid profile; populations of Bacteroidetes, Firmicutes, bacteroidales, clostridiales, enterobacteriales, and Escherichia coli in feces; blood pressure; urine uric acid and F2t isoprostanes (F2‐IsoPs); perigonadal fat deposition; and hepatic histology and diacylglycerols (DAGs) in liver and adipose tissue. d‐Fagomine reduces sucrose‐induced hypertension, urine uric acid and F2‐IsoPs (markers of oxidative stress), steatosis, and liver DAGs, without significantly affecting perigonadal fat deposition, and impaired glucose tolerance. It also promotes excretion of enterobacteriales generated by the dietary intervention. Conclusion d‐fagomine counteracts sucrose‐induced steatosis and hypertension, presumably by reducing the postprandial levels of fructose in the liver. The buckwheat iminosugar d‐fagomine reduces high‐sucrose‐induced hypertension, urine uric acid, and F2‐isoprostanes (markers of oxidative stress), steatosis, and liver diacylglicerols, without affecting perigonadal fat deposition. It is suggested that d‐fagomine counteracts sucrose‐induced steatosis and hypertension by reducing the postprandial levels of fructose in the liver.