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Nutritional Status and Diet Style Affect Cognitive Function in Alcoholic Liver Disease.

ABSTRACT: Malnutrition and cognitive dysfunction are typical features of alcoholic liver disease (ALD) and are correlated with the development of complications. The aim of this study is to explore the effect of nutritional state and diet on cognitive function in ALD. A total of 43 patients with compensated alcoholic cirrhosis were enrolled, and a neuropsychological test was assessed according to body mass index (BMI, <22 and ≥22). In the ALD animal study, mice were divided into five groups (n = 9/group; normal liquid, 5% EtOH + regular liquid, 5% EtOH + high-carbohydrate liquid, 5% EtOH + high-fat liquid, and 5% EtOH + high-protein liquid diet) and fed the same calories for eight weeks. To assess cognitive function, we performed T-maze studies weekly before/after alcohol binging. In cognitive function (BMI < 22/≥22), language score of Korea mini-mental state (7.4 ± 1.4/7.9 ± 0.4), Boston naming (11.7 ± 2.7/13.0 ± 1.8), forward digit span (6.7 ± 1.8/7.5 ± 1.6), Korean color word stroop (24.2 ± 26.5/43.6 ± 32.4), and interference score (33.9 ± 31.9/52.3 ± 33.9) revealed significant differences. In the T-maze test, alcohol significantly delayed the time to reach food, and binge drinking provided a temporary recovery in cognition. The alcohol-induced delay was significantly reduced in the high-carbohydrate and high-fat diet groups. Synaptic function exhibited no changes in all groups. Cognitive dysfunction is affected by nutritional status and diet in ALD.

SUBMITTER: Choi YR

PROVIDER: S-EPMC7826807 | biostudies-literature | 2021 Jan

REPOSITORIES: biostudies-literature

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Nutritional Status and Diet Style Affect Cognitive Function in Alcoholic Liver Disease.

Choi Ye Rin YR Kim Hyeong Seop HS Yoon Sang Jun SJ Lee Na Young NY Gupta Haripriya H Raja Ganesan G Gebru Yoseph Asmelash YA Youn Gi Soo GS Kim Dong Joon DJ Ham Young Lim YL Suk Ki Tae KT

Nutrients 20210109 1

Malnutrition and cognitive dysfunction are typical features of alcoholic liver disease (ALD) and are correlated with the development of complications. The aim of this study is to explore the effect of nutritional state and diet on cognitive function in ALD. A total of 43 patients with compensated alcoholic cirrhosis were enrolled, and a neuropsychological test was assessed according to body mass index (BMI, <22 and ≥22). In the ALD animal study, mice were divided into five groups (<i>n</i> = 9/g ...[more]

PMID: 33435328

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Project description:BackgroundThe mechanisms underlying muscle alteration associated to alcoholic liver disease (ALD) are not fully understood and the physiopathologic mediators of the liver-muscle interplay remains elusive. We investigated the role of circulating extracellular vesicles (EVs) in ALD as potential mediators of muscle atrophy.MethodsWe established a mouse model of sarcopenia associated to ALD, by feeding mice with an alcoholic diet for 8 weeks. We investigated the effects of hepatic and circulating EVs isolated from these mice (EtOH mice; n = 7 females) on muscle cell cultures, comparing them with EVs from mice fed with a standard diet (CD mice; n = 6 females). Additionally, we examined the impact of circulating EVs from patients with alcohol-related cirrhosis (7 males and 2 females, mean age 55.4 years) on primary human muscle cells, comparing them with EVs from age-matched healthy subjects (6 males and 3 females). We analysed the miRNA profile of the EVs to identify potential mediators of ALD-associated sarcopenia.ResultsWe demonstrated that circulating EVs were internalized by muscle cells and that EVs from ALD mice and cirrhotic patients caused alteration in the myogenic program. Molecular analysis revealed that serum EVs from ALD mice reduced protein synthesis in C2C12 cells, decreasing levels of p-AKT/AKT (-54.6%; p < 0.05), p-mTOR/mTOR (-54.5%; p < 0.05) and p-GSK3(Ser9)/GSK3 (-30.63%). Similarly, hepatic EVs induced defects in muscle differentiation, with reduced levels of p-AKT/AKT (-39.1%; p < 0.05), p-mTOR/mTOR (-30.1%; p < 0.05) and p-GSK3(Ser9)/GSK3 (-40%). C2C12 cells treated with either serum or hepatic EtOH-EVs exhibited upregulated expression of muscle-specific atrophy markers Atrogin-1 (+61.2% and +189.5%, respectively; p < 0.05) and MuRF1 (+260.4% and +112.5%, respectively; p < 0.05), along with an increased LC3-II/-I ratio (+131.5% and +40.2%, respectively; p < 0.05), indicating enhanced autophagy. MiRNA analysis revealed that both circulating and hepatic EVs from ALD mice showed elevated expression of miR-21, miR-155, miR-223 and miR-122 (+230% and +292%, respectively; p < 0.01) suggesting their potential role in sarcopenia. Human muscle cells exposed to EVs from cirrhotic patients exhibited reduced protein synthesis and upregulated Atrogin-1 (+113%; p < 0.05) and MuRF1 (+86.3%; p < 0.05), indicating proteasome activation. Circulating EVs of alcoholic patients showed upregulation of the same miRNAs observed in EtOH mice, including the liver-specific miR-122 (+260%; p < 0.05) suggesting, also in human liver disease, a hepatic origin of circulating EVs.ConclusionsOur study highlights the critical role of ALD-derived circulating EVs in affecting muscle homeostasis and myogenic program, suggesting potential therapeutic targets for mitigating muscle loss in ALD.

Project description:BackgroundA Mediterranean diet (MedDiet) is recommended as a therapy for non-alcoholic fatty liver disease (NAFLD) because there is no specific pharmacological treatment for this disease.ObjectiveTo assess the relationship between the adherence to the Mediterranean diet and the intrahepatic fat content (IFC), levels of oxidative stress, and inflammation biomarkers after a 6-month lifestyle intervention in NAFLD patients.MethodsPatients diagnosed with NAFLD (n = 60 adults; 40-60 years old) living in the Balearic Islands, Spain, were classified into two groups, according to the adherence to the MedDiet after 6 months of lifestyle intervention. Anthropometry, blood pressure, IFC, maximal oxygen uptake, and pro/antioxidant and inflammatory biomarkers were measured in plasma and in PBMCs before and after the intervention.ResultsReductions in weight, body mass index, IFC, blood pressure levels, circulating glucose, glycosylated hemoglobin, and markers of liver damage-aspartate aminotransferase (AST), alanine aminotransferase (ALT), gamma-glutamyl transferase (GGT), and cytokeratin 18 (CK-18)-were observed after the intervention. The highest reductions were observed in the group with the best adherence to the MedDiet. A significant improvement in cardiorespiratory fitness was also observed in the group with a higher adherence. The activities of catalase in plasma and catalase and superoxide dismutase in blood mononuclear cells increased only in the group with a higher adherence, as well as the catalase gene expression in the blood mononuclear cells. The plasma levels of malondialdehyde and myeloperoxidase decreased, and resolvin-D1 increased in both groups after the intervention, whereas interleukin-6 levels decreased only in the group with a higher adherence to the MedDiet.ConclusionsA greater adherence to the MedDiet is related to greater improvements in IFC, cardiorespiratory fitness, and pro-oxidative and proinflammatory status in NAFLD patients after a 6-month nutritional intervention based on the MedDiet.

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Nutritional Status and Diet Style Affect Cognitive Function in Alcoholic Liver Disease.

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Nutritional Status and Diet Style Affect Cognitive Function in Alcoholic Liver Disease.

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