Publication: Early effects of high-fat diet, extra-virgin olive oil and vitamin D in a sedentary rat model of non-alcoholic fatty liver disease
Authors
Trovato, Francesca Maria ; Castrogiovanni, Paola ; Szychlinska, Marta Anna ; Purrello, Francesco ; Musumeci, Giuseppe
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Publisher
Universidad de Murcia. Departamento de BiologĂa Celular e HistologĂa
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DOI
DOI: 10.14670/HH-18-008
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info:eu-repo/semantics/article
Description
Abstract
Background 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.
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Citation
Histology and Histopathology, Vol.33, nÂş11, (2018)
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