VITAMIN D DEFICIENCY DID NOT AUGMENT THE PROGRESSION OF HIGH-FRUCTOSE-INDUCED NONALCOHOLIC FATTY LIVER DISEASE IN RATS

Objective: Vitamin D has antioxidant, anti-inflammatory and antiglycation activities, and hepatoprotective potential. There is a relationship between vitamin D deficiency (VDD) and the severity of liver disorders. VDD has been proposed to contribute to the progression of nonalcoholic fatty liver dis...

Full description

Saved in:
Bibliographic Details
Main Authors: İlknur Bingül, Canan Küçükgergin, Abdurrahman Fatih Aydın, Asiye Işın Doğan Ekici, Semra Doğru Abbasoğlu, Mehmet Müjdat Uysal
Format: Article
Language:English
Published: Istanbul University Press 2021-07-01
Series:İstanbul Tıp Fakültesi Dergisi
Subjects:
Online Access:https://cdn.istanbul.edu.tr/file/JTA6CLJ8T5/F055F7C0382D44D6BC94CA5DB57CB2EB
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1850190355975110656
author İlknur Bingül
Canan Küçükgergin
Abdurrahman Fatih Aydın
Asiye Işın Doğan Ekici
Semra Doğru Abbasoğlu
Mehmet Müjdat Uysal
author_facet İlknur Bingül
Canan Küçükgergin
Abdurrahman Fatih Aydın
Asiye Işın Doğan Ekici
Semra Doğru Abbasoğlu
Mehmet Müjdat Uysal
author_sort İlknur Bingül
collection DOAJ
description Objective: Vitamin D has antioxidant, anti-inflammatory and antiglycation activities, and hepatoprotective potential. There is a relationship between vitamin D deficiency (VDD) and the severity of liver disorders. VDD has been proposed to contribute to the progression of nonalcoholic fatty liver disease (NAFLD). However, experimental results are not clear. Therefore, in this study, the effects of a VDD diet on high fructose (HFr) drinking-induced NAFLD was evaluated. Material and Method: Male Wistar rats were divided into four groups as control, HFr, VDD+HFr, and VDD. Control and HFr groups were fed a control diet, and other groups with a VDD-diet for 12 weeks. HFr (30%; w/v; in drinking water) was given in the last 8 weeks. Insulin resistance (IR), serum lipids, hepatic triglyceride, lipid peroxide, protein carbonyl, advanced glycation end products (AGEs) and inflammation (TNF-α and myeloperoxidase) parameters, and histopathological changes were investigated. Results: Increases in serum transaminases, hypertriglyceridemia, and IR were observed in HFr and VDD+HFr groups. Increased liver triglyceride, lipid and protein oxidation products, protein glycation and inflammation markers as well as microvesicular hepatic steatosis and hepatocyte ballooning were observed in both groups. Although IR and hepatic inflammation markers were higher in the VDD+HFr group, serum transaminases, hepatic triglyceride, lipid and protein oxidation products, and glycation indicators in the liver did not alter between the two groups. However, Nrf2 mRNA expression and superoxide dismutase andglutathione peroxidase mRNA expression and activities were significantly higher in the VDD+HFr group. Conclusion: Our results show that VDD did not augmented HFr-induced hepatotoxicity and glycooxidative stress in the liver of rats.
format Article
id doaj-art-d7b91ca2338745f6b65250e2ab1a010a
institution OA Journals
issn 1305-6441
language English
publishDate 2021-07-01
publisher Istanbul University Press
record_format Article
series İstanbul Tıp Fakültesi Dergisi
spelling doaj-art-d7b91ca2338745f6b65250e2ab1a010a2025-08-20T02:15:19ZengIstanbul University Pressİstanbul Tıp Fakültesi Dergisi1305-64412021-07-0184336036810.26650/IUITFD.2021.849531123456VITAMIN D DEFICIENCY DID NOT AUGMENT THE PROGRESSION OF HIGH-FRUCTOSE-INDUCED NONALCOHOLIC FATTY LIVER DISEASE IN RATSİlknur Bingül0https://orcid.org/0000-0002-6432-3541Canan Küçükgergin1https://orcid.org/0000-0002-1797-5889Abdurrahman Fatih Aydın2https://orcid.org/0000-0002-2595-0833Asiye Işın Doğan Ekici3https://orcid.org/0000-0003-4062-9519Semra Doğru Abbasoğlu4https://orcid.org/0000-0003-3467-9763Mehmet Müjdat Uysal5https://orcid.org/0000-0002-8802-8766İstanbul Üniversitesi, İstanbul, Türkiyeİstanbul Üniversitesi, İstanbul, Türkiyeİstanbul Üniversitesi, İstanbul, TürkiyeAcıbadem Mehmet Ali Aydınlar Üniversitesi, Istanbul, Turkiyeİstanbul Üniversitesi, İstanbul, Türkiyeİstanbul Üniversitesi, İstanbul, TürkiyeObjective: Vitamin D has antioxidant, anti-inflammatory and antiglycation activities, and hepatoprotective potential. There is a relationship between vitamin D deficiency (VDD) and the severity of liver disorders. VDD has been proposed to contribute to the progression of nonalcoholic fatty liver disease (NAFLD). However, experimental results are not clear. Therefore, in this study, the effects of a VDD diet on high fructose (HFr) drinking-induced NAFLD was evaluated. Material and Method: Male Wistar rats were divided into four groups as control, HFr, VDD+HFr, and VDD. Control and HFr groups were fed a control diet, and other groups with a VDD-diet for 12 weeks. HFr (30%; w/v; in drinking water) was given in the last 8 weeks. Insulin resistance (IR), serum lipids, hepatic triglyceride, lipid peroxide, protein carbonyl, advanced glycation end products (AGEs) and inflammation (TNF-α and myeloperoxidase) parameters, and histopathological changes were investigated. Results: Increases in serum transaminases, hypertriglyceridemia, and IR were observed in HFr and VDD+HFr groups. Increased liver triglyceride, lipid and protein oxidation products, protein glycation and inflammation markers as well as microvesicular hepatic steatosis and hepatocyte ballooning were observed in both groups. Although IR and hepatic inflammation markers were higher in the VDD+HFr group, serum transaminases, hepatic triglyceride, lipid and protein oxidation products, and glycation indicators in the liver did not alter between the two groups. However, Nrf2 mRNA expression and superoxide dismutase andglutathione peroxidase mRNA expression and activities were significantly higher in the VDD+HFr group. Conclusion: Our results show that VDD did not augmented HFr-induced hepatotoxicity and glycooxidative stress in the liver of rats.https://cdn.istanbul.edu.tr/file/JTA6CLJ8T5/F055F7C0382D44D6BC94CA5DB57CB2EBvitamin d deficiencyhigh fructose dietnonalcoholic liver diseaseglycooxidative stressantioxidantinflammation
spellingShingle İlknur Bingül
Canan Küçükgergin
Abdurrahman Fatih Aydın
Asiye Işın Doğan Ekici
Semra Doğru Abbasoğlu
Mehmet Müjdat Uysal
VITAMIN D DEFICIENCY DID NOT AUGMENT THE PROGRESSION OF HIGH-FRUCTOSE-INDUCED NONALCOHOLIC FATTY LIVER DISEASE IN RATS
İstanbul Tıp Fakültesi Dergisi
vitamin d deficiency
high fructose diet
nonalcoholic liver disease
glycooxidative stress
antioxidant
inflammation
title VITAMIN D DEFICIENCY DID NOT AUGMENT THE PROGRESSION OF HIGH-FRUCTOSE-INDUCED NONALCOHOLIC FATTY LIVER DISEASE IN RATS
title_full VITAMIN D DEFICIENCY DID NOT AUGMENT THE PROGRESSION OF HIGH-FRUCTOSE-INDUCED NONALCOHOLIC FATTY LIVER DISEASE IN RATS
title_fullStr VITAMIN D DEFICIENCY DID NOT AUGMENT THE PROGRESSION OF HIGH-FRUCTOSE-INDUCED NONALCOHOLIC FATTY LIVER DISEASE IN RATS
title_full_unstemmed VITAMIN D DEFICIENCY DID NOT AUGMENT THE PROGRESSION OF HIGH-FRUCTOSE-INDUCED NONALCOHOLIC FATTY LIVER DISEASE IN RATS
title_short VITAMIN D DEFICIENCY DID NOT AUGMENT THE PROGRESSION OF HIGH-FRUCTOSE-INDUCED NONALCOHOLIC FATTY LIVER DISEASE IN RATS
title_sort vitamin d deficiency did not augment the progression of high fructose induced nonalcoholic fatty liver disease in rats
topic vitamin d deficiency
high fructose diet
nonalcoholic liver disease
glycooxidative stress
antioxidant
inflammation
url https://cdn.istanbul.edu.tr/file/JTA6CLJ8T5/F055F7C0382D44D6BC94CA5DB57CB2EB
work_keys_str_mv AT ilknurbingul vitaminddeficiencydidnotaugmenttheprogressionofhighfructoseinducednonalcoholicfattyliverdiseaseinrats
AT canankucukgergin vitaminddeficiencydidnotaugmenttheprogressionofhighfructoseinducednonalcoholicfattyliverdiseaseinrats
AT abdurrahmanfatihaydın vitaminddeficiencydidnotaugmenttheprogressionofhighfructoseinducednonalcoholicfattyliverdiseaseinrats
AT asiyeisındoganekici vitaminddeficiencydidnotaugmenttheprogressionofhighfructoseinducednonalcoholicfattyliverdiseaseinrats
AT semradogruabbasoglu vitaminddeficiencydidnotaugmenttheprogressionofhighfructoseinducednonalcoholicfattyliverdiseaseinrats
AT mehmetmujdatuysal vitaminddeficiencydidnotaugmenttheprogressionofhighfructoseinducednonalcoholicfattyliverdiseaseinrats