Browsing by Subject "Western Diet"
Now showing 1 - 1 of 1
Results Per Page
Sort Options
- PublicationOpen AccessEarly effects of high-fat diet, extra-virgin olive oil and vitamin D in a sedentary rat model of non-alcoholic fatty liver disease(Universidad de Murcia. Departamento de Biología Celular e Histología, 2018) Trovato, Francesca Maria; Castrogiovanni, Paola; Szychlinska, Marta Anna; Purrello, Francesco; Musumeci, GiuseppeBackground and Aim. Western high-fat diet is related to metabolic syndrome and non-alcoholic fatty liver disease (NAFLD). Decreased levels of Vitamin D (VitD) and IGF-1 and their mutual relationship were also reported. We aimed to evaluate whether different dietary profiles, containing or not VitD, may exert different effects on liver tissue. Methods. Twenty-eight male rats were fed for 10 weeks by different dietary regimens: R, regular diet; RDS and R-DR, regular diet with respectively VitD supplementation (DS) and restriction (DR); HFB-DS and HFB-DR (41% energy from fat), high fat (butter) diet; HFEVO-DS and HFEVO-DR (41% energy from fat), high fat (Extra-virgin olive oil-EVO) diet. Severity of NAFLD was assessed by NAFLD Activity Score. Collagen type I, IL-1beta, VitD-receptor, DKK-1 and IGF1 expressions were evaluated by immunohistochemistry. Results. All samples showed a NAS between 0 and 2 considered not diagnostic of steatohepatitis. Collagen I, although weakly expressed, was statistically greater in HFB-DS and HFB-DR groups. IL-1 was mostly expressed in rats fed with HFBs and HFEVOs and RDR, and almost absent in R and R-DS diets. IGF-1 and DKK-1 were reduced in HFBs and HFEVOs diets and in particular in DR groups. Conclusions. A short-term high-fat diet could damage liver tissue in terms of inflammation and collagen I deposition, setting the basis for the subsequent steatohepatitis, still not identifiable anatomopathologically. Vitamin D restriction increases inflammation and reduces the expression of IGF-1 in the liver, worsening the fat-induced changing. EVOO seems be protective against the collagen I production.