000100650 001__ 100650
000100650 005__ 20240118091947.0
000100650 0247_ $$2doi$$a10.1155/2020/7315253
000100650 0248_ $$2sideral$$a118792
000100650 037__ $$aART-2020-118792
000100650 041__ $$aeng
000100650 100__ $$aMartínez Soriano, B.$$uUniversidad de Zaragoza
000100650 245__ $$aEffect of Melatonin as an Antioxidant Drug to Reverse Hepatic Steatosis: Experimental Model
000100650 260__ $$c2020
000100650 5060_ $$aAccess copy available to the general public$$fUnrestricted
000100650 5203_ $$aIntroduction. The hepatic steatosis of the nonalcoholic origin or NAFLD is increasing at present, particularly in Western countries, parallel to the increase in obesity, constituting one of the most prevalent hepatic processes in the Western society. Melatonin has been successfully tested in experimental models in mice as a drug capable of reversing steatosis. The effect of melatonin on fat metabolism can be summarized as a decrease in lipid peroxidation and a decrease in oxidative stress, biochemical phenomena intimately related to fat deposition in the hepatocyte. There are hardly any studies in large animals. Objective. In this study, we investigate the effects of melatonin administered orally at a dose of 10 mg/kg/day to reverse established hepatic steatosis induced by a special diet in a porcine animal model. Materials and Methods. We analyze the parameters of oxidative stress: malondialdehyde (MDA), 4-hydroxyalkenals (4-HDA), and carbonyls, degree of fat infiltration (analyzed by direct vision by a pathologist and by means of a computer program of image treatment), and serological parameters of lipid metabolism and hepatic damage. These parameters were analyzed in animals to which hepatic steatosis was induced by means of dietary modifications. Results. We have not been able to demonstrate globally a beneficial effect of melatonin in the improvement or reversal of liver steatosis once established, induced by diet in a porcine animal model. However, we have found several signs of improvement at the histological level, at the level of lipid metabolism, and at the level of oxidative stress parameters. We have verified in our study that, in the histological analysis of the liver sample by means of the program image treatment (free of subjectivity) of the animals that continue with the diet, those that consume melatonin do not increase steatosis as much as those that do not consume it significantly (p=0.002). Regarding the parameters of oxidative stress, MDA modifies in a significant manner within the group of animals that continue with the diet and take melatonin (p=0.004). As for lipid metabolism, animals that maintain the steatotic diet and take melatonin lower total and LDL cholesterol levels and increase HDL levels, although these results do not acquire statistical significance. Conclusions. In this study, it has not been possible to demonstrate a beneficial effect of melatonin in the improvement or reversal of liver steatosis once established and induced by diet in the porcine model. It is true that signs of improvement have been found at the histological level, at the level of lipid metabolism, and at the level of oxidative stress phenomena, when comparing animals with established steatosis that are treated with melatonin with those who do not take it. This work is the first study conducted in a large animal model in which the effect of melatonin is studied as a treatment in the reversal of established hepatic steatosis.
000100650 540__ $$9info:eu-repo/semantics/openAccess$$aby$$uhttp://creativecommons.org/licenses/by/3.0/es/
000100650 590__ $$a3.522$$b2020
000100650 591__ $$aGASTROENTEROLOGY & HEPATOLOGY$$b57 / 92 = 0.62$$c2020$$dQ3$$eT2
000100650 592__ $$a0.921$$b2020
000100650 593__ $$aGastroenterology$$c2020$$dQ2
000100650 593__ $$aMedicine (miscellaneous)$$c2020$$dQ2
000100650 593__ $$aHepatology$$c2020$$dQ2
000100650 655_4 $$ainfo:eu-repo/semantics/article$$vinfo:eu-repo/semantics/publishedVersion
000100650 700__ $$0(orcid)0000-0002-4437-2581$$aGüemes, A.$$uUniversidad de Zaragoza
000100650 700__ $$aPola, G.$$uUniversidad de Zaragoza
000100650 700__ $$0(orcid)0000-0003-3065-8893$$aGonzalo, A.$$uUniversidad de Zaragoza
000100650 700__ $$0(orcid)0000-0002-9031-3961$$aPalacios Gasós, P.$$uUniversidad de Zaragoza
000100650 700__ $$0(orcid)0000-0002-0460-5256$$aNavarro, A.C.$$uUniversidad de Zaragoza
000100650 700__ $$0(orcid)0000-0002-8100-5596$$aMartínez-Beamonte, R.$$uUniversidad de Zaragoza
000100650 700__ $$0(orcid)0000-0002-8251-8457$$aOsada, J.$$uUniversidad de Zaragoza
000100650 700__ $$0(orcid)0000-0001-9507-6478$$aGarcía, J.J.$$uUniversidad de Zaragoza
000100650 7102_ $$12008$$2640$$aUniversidad de Zaragoza$$bDpto. Produc.Animal Cienc.Ali.$$cÁrea Nutrición Bromatología
000100650 7102_ $$11012$$2410$$aUniversidad de Zaragoza$$bDpto. Farmac.Fisiol.y Med.L.F.$$cÁrea Fisiología
000100650 7102_ $$11013$$2090$$aUniversidad de Zaragoza$$bDpto. Cirugía$$cÁrea Cirugía
000100650 7102_ $$11002$$2060$$aUniversidad de Zaragoza$$bDpto. Bioq.Biolog.Mol. Celular$$cÁrea Bioquímica y Biolog.Mole.
000100650 773__ $$g2020 (2020), 7315253 [12 pp]$$pCan. J. Gastroenterol. Hepatol.$$tCanadian Journal of Gastroenterology and Hepatology$$x2291-2789
000100650 8564_ $$s1591545$$uhttps://zaguan.unizar.es/record/100650/files/texto_completo.pdf$$yVersión publicada
000100650 8564_ $$s2389112$$uhttps://zaguan.unizar.es/record/100650/files/texto_completo.jpg?subformat=icon$$xicon$$yVersión publicada
000100650 909CO $$ooai:zaguan.unizar.es:100650$$particulos$$pdriver
000100650 951__ $$a2024-01-18-09:11:17
000100650 980__ $$aARTICLE