Ramos-Romero, SaraHereu, MercèAtienza, LidiaCasas, JosefinaTaltavull, NúriaRomeu, MartaAmézqueta, SusanaDasilva, GabrielMedina, IsabelTorres, Josep L2023-01-252023-01-252018-08-01http://hdl.handle.net/10668/12686The goals of this work are to test if d-fagomine, an iminosugar that reduces body weight gain, can delay the appearance of a fat-induced prediabetic state in a rat model and to explore possible mechanisms behind its functional action. Wistar Kyoto rats were fed a high-fat diet supplemented with d-fagomine (or not, for comparison) or a standard diet (controls) for 24 weeks. The variables measured were fasting blood glucose and insulin levels; glucose tolerance; diacylglycerols as intracellular mediators of insulin resistance in adipose tissue (AT), liver, and muscle; inflammation markers (plasma IL-6 and leptin, and liver and AT histology markers); eicosanoids from arachidonic acid as lipid mediators of inflammation; and the populations of Bacteroidetes, Firmicutes, Enterobacteriales, and Bifidobacteriales in feces. It was found that d-fagomine reduces fat-induced impaired glucose tolerance, inflammation markers, and mediators (hepatic microgranulomas and lobular inflammation, plasma IL-6, prostaglandin E2 , and leukotriene B4 ) while attenuating the changes in the populations of Enterobacteriales and Bifidobacteriales. d-Fagomine delays the development of a fat-induced prediabetic state in rats by reducing low-grade inflammation. We suggest that the anti-inflammatory effect of d-fagomine may be linked to a reduction in fat-induced overpopulation of minor gut bacteria.endiabetesiminocyclitoliminosugarsinflammationmicrobiotaobesityAdipose TissueAnimalsBlood GlucoseBody WeightDiet, High-FatFagopyrumGastrointestinal MicrobiomeImino PyranosesInflammationInsulinLipidsMalePrediabetic StateRatsRats, Inbred WKYresearch article29979820open access10.1002/mnfr.2018003731613-4133https://digital.csic.es/bitstream/10261/193348/1/Functional_effects_buckwheat_2018.pdf