Cholecalciferol (vitamin D 3) improves cognitive dysfunction and reduces inflammation in a rat fatty liver model of metabolic syndrome

被引:43
作者
Erbas, Oytun [1 ]
Solmaz, Volkan [2 ]
Aksoy, Durdane [2 ]
Yavasoglu, Altug [3 ]
Sagcan, Mustafa [4 ]
Taskiran, Dilek [5 ]
机构
[1] Gaziosmanpasa Univ, Fac Med, Dept Physiol, Tokat, Turkey
[2] Gaziosmanpasa Univ, Fac Med, Dept Neurol, Tokat, Turkey
[3] Ege Univ, Sch Med, Dept Histol & Embryol, Izmir, Turkey
[4] Kilis State Hosp, Dept Internal Med, Kilis, Turkey
[5] Ege Univ, Sch Med, Dept Physiol, Izmir, Turkey
关键词
Fatty liver; Memory functions; Inflammation; Cholecalciferol; ALZHEIMERS-DISEASE; INTRANASAL INSULIN; TAU-PROTEIN; EXPRESSION; MODULATION; PHOSPHORYLATION; ASSOCIATION; RECEPTOR; DECLINE; PATHWAY;
D O I
10.1016/j.lfs.2014.03.035
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Aim: The aim of this study was to examine the effects of cholecalciferol on systemic inflammation and memory in the setting of fatty liver disease in rats. Materials and methods: To induce the development of fatty liver disease, the rats were fed a 35% fructose solution over 8 weeks. Group I (n = 6) was designated as the control group and fed with standard rat chow. Group II (n = 6) was provided with, standard rat chow, and 03 mu g/kg/day of oral cholecalciferol over a duration of 2 weeks. In addition to standard rat chow, group III (n = 6) and group IV (n = 6) were given 4 mL of the 35% fructose solution per day via oral gavage for 8 weeks. However, group IV was also given 03 mu g/kg/day of oral cholecalciferol over 2 weeks. After the treatment period, passive avoidance tasks were performed by all groups. The liver and brain were harvested for subsequent biochemical and histopathologic analyses. Key findings: The development of fatty liver extends the memory latency period of passively avoiding tasks after I trial. Moreover, there were increases in brain TNF-alpha and plasma MDA levels according to two-way analysis of variance. Cholecalciferol supplementation decreased the latency period of passively avoiding tasks in rats with hepatosteatosis, and also significantly reduced brain TNF-alpha and plasma MDA levels. Significance: Fatty liver may contribute to the development of systemic inflammation, which affects cognition and causes deficits in memory; however, the anti-inflammatory and antioxidant properties of vitamin D may improve the cognitive function of rats with hepatosteatosis. (C) 2014 Elsevier Inc. All rights reserved.
引用
收藏
页码:68 / 72
页数:5
相关论文
共 34 条
[1]   Meta-Analysis of Memory and Executive Dysfunctions in Relation to Vitamin D [J].
Annweiler, Cedric ;
Montero-Odasso, Manuel ;
Llewellyn, David J. ;
Richard-Devantoy, Stephane ;
Duque, Gustavo ;
Beauchet, Olivier .
JOURNAL OF ALZHEIMERS DISEASE, 2013, 37 (01) :147-171
[2]   Alzheimer's disease - input of vitamin D with mEmantine assay (AD-IDEA trial): study protocol for a randomized controlled trial [J].
Annweiler, Cedric ;
Fantino, Bruno ;
Parot-Schinkel, Elsa ;
Thiery, Samuel ;
Gautier, Jennifer ;
Beauchet, Olivier .
TRIALS, 2011, 12
[3]   Vitamin D mitigates age-related cognitive decline through the modulation of pro-inflammatory state and decrease in amyloid burden [J].
Briones, Teresita L. ;
Darwish, Hala .
JOURNAL OF NEUROINFLAMMATION, 2012, 9
[4]   Cyclooxygenase-2 Promotes Hepatocellular Apoptosis by Interacting with TNF-α and IL-6 in the Pathogenesis of Nonalcoholic Steatohepatitis in Rats [J].
Cheng, Qi ;
Li, Ning ;
Chen, Mingquan ;
Zheng, Jianming ;
Qian, Zhiping ;
Wang, Xinyu ;
Huang, Chong ;
Xu, Shuchang ;
Shi, Guangfeng .
DIGESTIVE DISEASES AND SCIENCES, 2013, 58 (10) :2895-2902
[5]   Importance of iron location in iron-induced hydroxyl radical production by brain slices [J].
Demougeot, C ;
Marie, C ;
Beley, A .
LIFE SCIENCES, 2000, 67 (04) :399-410
[6]   Regulation of relB in dendritic cells by means of modulated association of vitamin D receptor and histone deacetylase 3 with the promoter [J].
Dong, XY ;
Lutz, W ;
Schroeder, TM ;
Bachman, LA ;
Westendorf, JJ ;
Kumar, R ;
Griffin, MD .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2005, 102 (44) :16007-16012
[7]   Hyperinsulinemia provokes synchronous increases in central inflammation and β-amyloid in normal adults [J].
Fishel, MA ;
Watson, S ;
Montine, TJ ;
Wang, Q ;
Green, PS ;
Kulstad, JJ ;
Cook, DG ;
Peskind, ER ;
Baker, LD ;
Goldgaber, D ;
Nie, W ;
Asthana, S ;
Plymate, SR ;
Schwartz, MW ;
Craft, S .
ARCHIVES OF NEUROLOGY, 2005, 62 (10) :1539-1544
[8]   EXPRESSION OF AMYLOID PRECURSOR PROTEIN MESSENGER-RNAS IN ENDOTHELIAL, NEURONAL AND GLIAL-CELLS - MODULATION BY INTERLEUKIN-1 [J].
FORLONI, G ;
DEMICHELI, F ;
GIORGI, S ;
BENDOTTI, C ;
ANGERETTI, N .
MOLECULAR BRAIN RESEARCH, 1992, 16 (1-2) :128-134
[9]   ETHANOL-INDUCED HEPATIC-FIBROSIS IN THE RAT - ROLE OF THE AMOUNT OF DIETARY-FAT [J].
FRENCH, SW ;
MIYAMOTO, K ;
TSUKAMOTO, H .
ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH, 1986, 10 (06) :S13-S19
[10]   New clues about vitamin D functions in the nervous system [J].
Garcion, E ;
Wion-Barbot, N ;
Montero-Menei, CN ;
Berger, F ;
Wion, D .
TRENDS IN ENDOCRINOLOGY AND METABOLISM, 2002, 13 (03) :100-105