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A special issue of Nutrients (ISSN 2072-6643). This special issue belongs to the section "Clinical Nutrition".

Deadline for manuscript submissions: closed (1 July 2020) | Viewed by 59130

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Special Issue Editor

Prof. Dr. Takashi Himoto

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Guest Editor

Department of Medical Technology, Kagawa Prefectural University of Health Sciences, Takamatsu, Japan
Interests: hepatocellular carcinoma; diagnosis; treatment; precision medicine
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

We are pleased to announce this special issue on “Diet and Nutrition for Hepatitis”. The liver is one of the main organs that maintain nutritional status. The impairment of liver function results in varieties of malnutrition. Therefore, the assessment of nutritional disorders is absolutely essential for the management of liver disease. The nutritional support can restore an impaired nutritional balance and improve the unfavorable prognosis in such patients. Recent advances in molecular biological techniques prompted us to elucidate the correlations between nutritional status and genomics, epigenetics, microRNAs, microbiota or immunologic disorders.

The special issue welcomes original articles based on experimental or clinical studies that mainly focused on the relationship between the nutritional status and its genetic and immunologic background in liver disease. The special issue also welcomes reviews on current trends in the nutritional management of liver disease. We expect many interesting and relevant articles to be submitted.

Prof. Dr. Takashi Himoto
Guest Editor

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Keywords

Diet treatment
Nutritional assessment
Liver disease
Viral hepatitis
Steatohepatitis
Alcoholic hepatitis
Macronutrients
Micronutrients

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Published Papers (10 papers)

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Editorial

Jump to: Research, Review

3 pages, 160 KiB

Open AccessEditorial

Diet and Nutrition for Hepatitis

by Takashi Himoto

Nutrients 2021, 13(4), 1210; https://doi.org/10.3390/nu13041210 - 7 Apr 2021

Cited by 3 | Viewed by 4215

Abstract

The impairment of liver function frequently causes various type of malnutrition, as the liver is one of the most important organs involved in maintaining nutritional homeostasis [...] Full article

(This article belongs to the Special Issue Diet and Nutrition for Hepatitis)

Research

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15 pages, 3366 KiB

Open AccessArticle

Dietary Iron Overload Differentially Modulates Chemically-Induced Liver Injury in Rats

by Mutsuki Mori, Takeshi Izawa, Yohei Inai, Sho Fujiwara, Ryo Aikawa, Mitsuru Kuwamura and Jyoji Yamate

Nutrients 2020, 12(9), 2784; https://doi.org/10.3390/nu12092784 - 11 Sep 2020

Cited by 15 | Viewed by 3401

Abstract

Hepatic iron overload is well known as an important risk factor for progression of liver diseases; however, it is unknown whether it can alter the susceptibility to drug-induced hepatotoxicity. Here we investigate the pathological roles of iron overload in two single-dose models of chemically-induced liver injury. Rats were fed a high-iron (Fe) or standard diet (Cont) for four weeks and were then administered with allyl alcohol (AA) or carbon tetrachloride (CCl₄). Twenty-four hours after administration mild mononuclear cell infiltration was seen in the periportal/portal area (Zone 1) in Cont-AA group, whereas extensive hepatocellular necrosis was seen in Fe-AA group. Centrilobular (Zone 3) hepatocellular necrosis was prominent in Cont-CCl₄ group, which was attenuated in Fe-CCl₄ group. Hepatic lipid peroxidation and hepatocellular DNA damage increased in Fe-AA group compared with Cont-AA group. Hepatic caspase-3 cleavage increased in Cont-CCl₄ group, which was suppressed in Fe-CCl₄ group. Our results showed that dietary iron overload exacerbates AA-induced Zone-1 liver injury via enhanced oxidative stress while it attenuates CCl₄-induced Zone-3 liver injury, partly via the suppression of apoptosis pathway. This study suggested that susceptibility to drugs or chemical compounds can be differentially altered in iron-overloaded livers. Full article

(This article belongs to the Special Issue Diet and Nutrition for Hepatitis)

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14 pages, 485 KiB

Open AccessArticle

Serum Mac-2 Binding Protein Levels Associate with Metabolic Parameters and Predict Liver Fibrosis Progression in Subjects with Fatty Liver Disease: A 7-Year Longitudinal Study

by Yoshihiro Kamada, Koichi Morishita, Masahiro Koseki, Mayu Nishida, Tatsuya Asuka, Yukiko Naito, Makoto Yamada, Shinji Takamatsu, Yasushi Sakata, Tetsuo Takehara and Eiji Miyoshi

Nutrients 2020, 12(6), 1770; https://doi.org/10.3390/nu12061770 - 12 Jun 2020

Cited by 10 | Viewed by 3646

Abstract

Background: Mac-2 binding protein (M2BP) is a highly glycosylated secreted glycoprotein that is involved in immune defense and regulation. Our cross-sectional studies indicated that serum M2BP was a useful liver fibrosis biomarker for nonalcoholic fatty liver disease (NAFLD). In this study, we conducted a 7-year longitudinal study to investigate the significance of serum M2BP levels (baseline and at 7-year follow-up) and their relationships with other metabolic parameters of fatty liver disease. Methods: We enrolled 715 study subjects (521 male and 194 female) during health examinations. Study subjects received blood sampling tests and abdominal ultrasound tests at baseline and follow-up. Results: Univariate analyses demonstrated that serum M2BP levels were significantly correlated with various parameters related to metabolic risk (body mass index (BMI), systolic blood pressure, triglyceride, high density lipoprotein (HDL)-cholesterol) and metabolic syndrome diseases (obesity, hypertension, dyslipidemia, diabetes mellitus, fatty liver (FL)). Multiple logistic regression analyses demonstrated that BMI and FL were independent determinants for serum M2BP levels. Baseline serum M2BP levels were significant independent determinants for changes in platelet count, Fibrosis-4 (FIB4) index, and NAFLD fibrosis score. Higher serum M2BP levels (>1.80 μg/mL) strongly correlated with changes in the FIB4-index. Conclusions: The results of this study suggest that changes in serum M2BP levels reflect changes in specific metabolic disease-related parameters, and baseline serum M2BP levels could predict changes in liver fibrosis. Full article

(This article belongs to the Special Issue Diet and Nutrition for Hepatitis)

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16 pages, 2799 KiB

Open AccessArticle

Increase of Akkermansia muciniphila by a Diet Containing Japanese Traditional Medicine Bofutsushosan in a Mouse Model of Non-Alcoholic Fatty Liver Disease

by Mitsue Nishiyama, Nobuhiro Ohtake, Atsushi Kaneko, Naoko Tsuchiya, Sachiko Imamura, Seiichi Iizuka, Shiori Ishizawa, Akinori Nishi, Masahiro Yamamoto, Akinobu Taketomi and Toru Kono

Nutrients 2020, 12(3), 839; https://doi.org/10.3390/nu12030839 - 20 Mar 2020

Cited by 22 | Viewed by 5716

Abstract

Non-alcoholic fatty liver disease (NAFLD) is considered a worldwide healthcare problem that mirrors the increased prevalence of obesity. Gut microbiota plays a crucial role in the progression and treatment of NAFLD. Bofutsushosan (BTS), a pharmaceutical-grade Japanese traditional medicine, has long been prescribed in Japan for obesity and obesity-related syndrome. Although BTS has been reported to exert an anti-obesity effect in obese patients as well as various obesity-model animals, its effect on gut microbiota is unknown. Here, the effects of BTS on obesity, liver damage, and the gut microbiome in genetically obese mice, ob/ob, were studied. Seven-week-old ob/ob mice were fed a standard diet with (BTS group) or without (CONT group) 5% BTS for 4 weeks. By comparison to the CONT group, the BTS group showed reduced body weight gain and hyperlipidemia as well as improved liver function. Moreover, gut microbiota in the CONT and BTS group formed a significantly different cluster. Specifically, the genera Akkermansia, Bacteroides and an unknown genus of the family Enterobacteriaceae expanded dramatically in the BTS group. Noteworthy, the population of Akkermansia muciniphila, which is reported to elicit an anti-obesity effect and improve various metabolic abnormalities, was markedly increased (93-fold) compared with the CONT group. These results imply that BTS may be a promising agent for treating NAFLD. Full article

(This article belongs to the Special Issue Diet and Nutrition for Hepatitis)

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16 pages, 7297 KiB

Open AccessArticle

Probiotic Bacillus Spores Protect Against Acetaminophen Induced Acute Liver Injury in Rats

by Maria Adriana Neag, Adrian Catinean, Dana Maria Muntean, Maria Raluca Pop, Corina Ioana Bocsan, Emil Claudiu Botan and Anca Dana Buzoianu

Nutrients 2020, 12(3), 632; https://doi.org/10.3390/nu12030632 - 27 Feb 2020

Cited by 58 | Viewed by 6281

Abstract

Acetaminophen (APAP) is one of the most used analgesics and antipyretic agents in the world. Intoxication with APAP is the main cause of acute liver toxicity in both the US and Europe. Spore-forming probiotic bacteria have the ability to resist harsh gastric and intestinal conditions. The aim of this study was to investigate the possible protective effect of Bacillus (B) species (sp) spores (B. licheniformis, B. indicus, B. subtilis, B. clausii, B. coagulans) against hepatotoxicity induced by APAP in rats. A total of 35 rats were randomly divided into seven groups: group I served as control; group II received silymarin; group III received MegaSporeBiotic^TM (MSB); group IV received APAP and served as the model of hepatotoxicity; group V received APAP and silymarin; group VI received APAP and MSB; group VII received APAP, silymarin and MSB. The livers for histopathological examination and blood samples were collected on the last day of the experiment. We determined aspartate aminotransferase (AST), alanine aminotransferase (ALT) and total antioxidant capacity (TAC) levels and zonula occludens (ZO-1), tumor necrosis factor α (TNF-α) and interleukin 1β (IL-1β) expression. APAP overdose increased AST and ALT. It slowly decreased TAC compared to the control group, but pretreatment with silymarin and MSB increased TAC levels. Elevated plasma concentrations were identified for ZO-1 in groups treated with APAP overdose compared with those without APAP or receiving APAP in combination with silymarin, MSB or both. The changes were positively correlated with the levels of other proinflammatory cytokines (TNF-α, IL-1β). In addition, histopathological hepatic injury was improved by preadministration of MSB or silymarin versus the disease model group. Bacillus sp spores had a protective effect on acute hepatic injury induced by APAP. Pretreatment with MSB resulted in a significant reduction in serum AST, ALT, TNF-α, IL-1β, ZO-1, TAC and also hepatocyte necrosis, similar to the well-known hepatoprotective agent—silymarin. Full article

(This article belongs to the Special Issue Diet and Nutrition for Hepatitis)

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17 pages, 4384 KiB

Open AccessArticle

A Diterpenoid, 14-Deoxy-11, 12-Didehydroandrographolide, in Andrographis paniculata Reduces Steatohepatitis and Liver Injury in Mice Fed a High-Fat and High-Cholesterol Diet

by Yun-Ta Liu, Haw-Wen Chen, Chong-Kuei Lii, Jia-Hua Jhuang, Chin-Shiu Huang, Mei-Ling Li and Hsien-Tsung Yao

Nutrients 2020, 12(2), 523; https://doi.org/10.3390/nu12020523 - 18 Feb 2020

Cited by 46 | Viewed by 5851

Abstract

14-Deoxy-11,12-didehydroandrographolide (deAND), a diterpenoid in Andrographis paniculata (Burm. f.) Nees, acts as a bioactive phytonutrient that can treat many diseases. To investigate the protective effects of deAND on reducing fatty liver disease, male mice were fed a high-fat and high-cholesterol (HFHC) diet without or with 0.05% and 0.1% deAND supplementation. Cholesterol accumulation, antioxidant, and anti-inflammatory activities in liver and liver injury were evaluated after deAND treatment. The results show that deAND treatment for seven weeks reduced plasma alanine aminotransferase activity and lowered hepatic cholesterol accumulation, tumor nuclear factor-α, and histological lesions. The 0.1% deAND treatment reduced HFHC diet-induced apoptosis by lowering the caspase 3/pro-caspase 3 ratio. After 11 weeks of deAND treatment, increased NOD-like receptor protein 3 (NLRP3), capase-1, and interleukin-1β protein levels in liver were suppressed by deAND treatment. In addition, nuclear factor erythroid 2-related factor 2 (Nrf2) mRNA expression, heme oxygenase-1 protein expression, and the activities of glutathione peroxidase and glutathione reductase were increased in mice fed the HFHC diet. However, those activities of antioxidant enzymes or proteins were also upregulated by 0.1% deAND treatment. Furthermore, deAND treatment tended to lower hepatic lipid peroxides. Finally, deAND treatment reversed the depletion of hepatic glutamate level induced by the HFHC diet. These results indicate that deAND may ameliorate HFHC diet-induced steatohepatitis and liver injury by increasing antioxidant and anti-inflammatory activities. Full article

(This article belongs to the Special Issue Diet and Nutrition for Hepatitis)

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Review

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12 pages, 1052 KiB

Open AccessReview

Involvement of the Autophagy-ER Stress Axis in High Fat/Carbohydrate Diet-Induced Nonalcoholic Fatty Liver Disease

by Xiu Zhou, Sherouk Fouda, Dongli Li, Kun Zhang and Ji-Ming Ye

Nutrients 2020, 12(9), 2626; https://doi.org/10.3390/nu12092626 - 28 Aug 2020

Cited by 18 | Viewed by 4344

Abstract

Nonalcoholic fatty liver disease (NAFLD) is the most common chronic liver disease that can progress from simple hepatic steatosis to nonalcoholic steatohepatitis (NASH), and even further to liver cirrhosis or liver cancer. Overconsumption of high fat and/or carbohydrate are among the most common lifestyle factors that drive the development and progression of NAFLD. This review evaluates recent reports on the involvement of autophagy and endoplasmic reticulum (ER) stress in the pathogenesis of NAFLD. Here, we reveal a mechanism of an intrinsically linked axis of impaired autophagy and unresolved ER stress that mediates the development and progression of NAFLD resulting from the overconsumption of high fat and/or carbohydrate. Full article

(This article belongs to the Special Issue Diet and Nutrition for Hepatitis)

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17 pages, 2444 KiB

Open AccessReview

The Importance of the Fatty Acid Transporter L-Carnitine in Non-Alcoholic Fatty Liver Disease (NAFLD)

by Dragana Savic, Leanne Hodson, Stefan Neubauer and Michael Pavlides

Nutrients 2020, 12(8), 2178; https://doi.org/10.3390/nu12082178 - 22 Jul 2020

Cited by 50 | Viewed by 9948

Abstract

L-carnitine transports fatty acids into the mitochondria for oxidation and also buffers excess acetyl-CoA away from the mitochondria. Thus, L-carnitine may play a key role in maintaining liver function, by its effect on lipid metabolism. The importance of L-carnitine in liver health is supported by the observation that patients with primary carnitine deficiency (PCD) can present with fatty liver disease, which could be due to low levels of intrahepatic and serum levels of L-carnitine. Furthermore, studies suggest that supplementation with L-carnitine may reduce liver fat and the liver enzymes alanine aminotransferase (ALT) and aspartate transaminase (AST) in patients with Non-Alcoholic Fatty Liver Disease (NAFLD). L-carnitine has also been shown to improve insulin sensitivity and elevate pyruvate dehydrogenase (PDH) flux. Studies that show reduced intrahepatic fat and reduced liver enzymes after L-carnitine supplementation suggest that L-carnitine might be a promising supplement to improve or delay the progression of NAFLD. Full article

(This article belongs to the Special Issue Diet and Nutrition for Hepatitis)

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22 pages, 1718 KiB

Open AccessReview

Current Trends of Essential Trace Elements in Patients with Chronic Liver Diseases

by Takashi Himoto and Tsutomu Masaki

Nutrients 2020, 12(7), 2084; https://doi.org/10.3390/nu12072084 - 14 Jul 2020

Cited by 51 | Viewed by 6006

Abstract

Essential trace elements play crucial roles in the maintenance of health, since they are involved in many metabolic pathways. A deficiency or an excess of some trace elements, including zinc, selenium, iron, and copper, frequently causes these metabolic disorders such as impaired glucose tolerance and dyslipidemia. The liver largely regulates most of the metabolism of trace elements, and accordingly, an impairment of liver functions can result in numerous metabolic disorders. The administration or depletion of these trace elements can improve such metabolic disorders and liver dysfunction. Recent advances in molecular biological techniques have helped to elucidate the putative mechanisms by which liver disorders evoke metabolic abnormalities that are due to deficiencies or excesses of these trace elements. A genome-wide association study revealed that a genetic polymorphism affected the metabolism of a specific trace element. Gut dysbiosis was also responsible for impairment of the metabolism of a trace element. This review focuses on the current trends of four trace elements in chronic liver diseases, including chronic hepatitis, liver cirrhosis, nonalcoholic fatty liver disease, and autoimmune liver diseases. The novel mechanisms by which the trace elements participated in the pathogenesis of the chronic liver diseases are also mentioned. Full article

(This article belongs to the Special Issue Diet and Nutrition for Hepatitis)

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20 pages, 1059 KiB

Open AccessReview

Oxidative Stress Management in Chronic Liver Diseases and Hepatocellular Carcinoma

by Daisuke Uchida, Akinobu Takaki, Atsushi Oyama, Takuya Adachi, Nozomu Wada, Hideki Onishi and Hiroyuki Okada

Nutrients 2020, 12(6), 1576; https://doi.org/10.3390/nu12061576 - 28 May 2020

Cited by 51 | Viewed by 6225

Abstract

Chronic viral hepatitis B and C and non-alcoholic fatty liver disease (NAFLD) have been widely acknowledged to be the leading causes of liver cirrhosis and hepatocellular carcinoma. As anti-viral treatment progresses, the impact of NAFLD is increasing. NAFLD can coexist with chronic viral hepatitis and exacerbate its progression. Oxidative stress has been recognized as a chronic liver disease progression-related and cancer-initiating stress response. However, there are still many unresolved issues concerning oxidative stress, such as the correlation between the natural history of the disease and promising treatment protocols. Recent findings indicate that oxidative stress is also an anti-cancer response that is necessary to kill cancer cells. Oxidative stress might therefore be a cancer-initiating response that should be down regulated in the pre-cancerous stage in patients with risk factors for cancer, while it is an anti-cancer cell response that should not be down regulated in the post-cancerous stage, especially in patients using anti-cancer agents. Antioxidant nutrients should be administered carefully according to the patients’ disease status. In this review, we will highlight these paradoxical effects of oxidative stress in chronic liver diseases, pre- and post-carcinogenesis. Full article

(This article belongs to the Special Issue Diet and Nutrition for Hepatitis)

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