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A special issue of Nutrients (ISSN 2072-6643).

Deadline for manuscript submissions: closed (30 September 2014) | Viewed by 125760

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Dr. Leanne Hodson

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Associate Professor, Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford Churchill Hospital, Headington OX3 7LE, UK
Interests: lipids; fatty acids; lipoproteins; postprandial metabolism; human in vivo; liver; adipose tissue; biomarkers

Special Issue Information

Dear Colleagues,

The liver is the chief metabolic visceral organ that performs a vast range of different functions that including: metabolism of lipids, carbohydrates, and vitamins. In humans, diseases of the liver are a global public health issue and burden and non-alcoholic fatty liver disease (NAFLD), is one of the most prevalent liver diseases in developed countries. NAFLD represents a spectrum of conditions ranging from simple fatty liver (hepatic steatosis) through to severe liver disease such as cirrhosis and potentially hepatocellular carcinoma (HCC). Dietary patterns, for example overconsumption of dietary fat and carbohydrate, along with specific dietary components have all been implicated in the initiation and progression of liver disease.

Dr. Leanne Hodson
Guest Editor

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Keywords

Liver disease
Hepatobiliary disease
Inherited metabolic/genetic liver diseases
Cholestasis
Malnutrition
Parenteral Nutrition, Intestinal Failure
Nutrients
Nutraceuticals
Substrate dietary restriction; Depleted product replenishment; Branched chain amino acids, Mean chain tryglicerides
Inflammatory Bowel Disease; Celiac disease; Cystic Fibrosis

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Published Papers (10 papers)

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Research

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254 KiB

Open AccessArticle

Non-Alcoholic Fatty Liver Disease in Children: Focus on Nutritional Interventions

by Min Yang, Sitang Gong, Shui Qing Ye, Beth Lyman, Lanlan Geng, Peiyu Chen and Ding-You Li

Nutrients 2014, 6(11), 4691-4705; https://doi.org/10.3390/nu6114691 - 28 Oct 2014

Cited by 28 | Viewed by 11339

Abstract

With increasing prevalence of childhood obesity, non-alcoholic fatty liver disease (NAFLD) has emerged as the most common cause of liver disease among children and adolescents in industrialized countries. It is generally recognized that both genetic and environmental risk factors contribute to the pathogenesis of NAFLD. Recently, there has been a growing body of evidence to implicate altered gut microbiota in the development of NAFLD through the gut-liver axis. The first line of prevention and treatment of NAFLD in children should be intensive lifestyle interventions such as changes in diet and physical activity. Recent advances have been focused on limitation of dietary fructose and supplementation of antioxidants, omega-3 fatty acids, and prebiotics/probiotics. Convincing evidences from both animal models and human studies have shown that reduction of dietary fructose and supplement of vitamin E, omega-3 fatty acids, and prebiotics/probiotics improve NAFLD. Full article

(This article belongs to the Special Issue Nutrition and Liver Disease)

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Open AccessArticle

Effects of Dietary Fat and Saturated Fat Content on Liver Fat and Markers of Oxidative Stress in Overweight/Obese Men and Women under Weight-Stable Conditions

by Anna Marina, Anize Delfino Von Frankenberg, Seda Suvag, Holly S. Callahan, Mario Kratz, Todd L. Richards and Kristina M. Utzschneider

Nutrients 2014, 6(11), 4678-4690; https://doi.org/10.3390/nu6114678 - 28 Oct 2014

Cited by 35 | Viewed by 9156

Abstract

Dietary fat and oxidative stress are hypothesized to contribute to non-alcoholic fatty liver disease and progression to steatohepatitis. To determine the effects of dietary fat content on hepatic triglyceride, body fat distribution and markers of inflammation and oxidative stress, overweight/obese subjects with normal glucose tolerance consumed a control diet (CONT: 35% fat/12% saturated fat/47% carbohydrate) for ten days, followed by four weeks on a low fat (LFD (n = 10): 20% fat/8% saturated fat/62% carbohydrate) or high fat diet (HFD (n = 10): 55% fat/25% saturated fat/27% carbohydrate). Hepatic triglyceride content was quantified by MRS and abdominal fat distribution by MRI. Fasting biomarkers of inflammation (plasma hsCRP, IL-6, IL-12, TNFα, IFN-γ) and oxidative stress (urinary F2-α isoprostanes) were measured. Body weight remained stable. Compared to the CONT, hepatic triglyceride decreased on the LFD (mean (95% CI): change −2.13% (−3.74%, −0.52%)), but did not change on the HFD and there was no significant difference between the LFD and HFD. Intra-abdominal fat did not change significantly on either diet, but subcutaneous abdominal fat increased on the HFD. There were no significant changes in fasting metabolic markers, inflammatory markers and urinary F2-α isoprostanes. We conclude that in otherwise healthy overweight/obese adults under weight-neutral conditions, a diet low in fat and saturated fat has modest effects to decrease liver fat and may be beneficial. On the other hand, a diet very high in fat and saturated fat had no effect on hepatic triglyceride or markers of metabolism, inflammation and oxidative stress. Full article

(This article belongs to the Special Issue Nutrition and Liver Disease)

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Dietary Fructose Reduction Improves Markers of Cardiovascular Disease Risk in Hispanic-American Adolescents with NAFLD

by Ran Jin, Jean A. Welsh, Ngoc-Anh Le, Jeffrey Holzberg, Puneet Sharma, Diego R. Martin and Miriam B. Vos

Nutrients 2014, 6(8), 3187-3201; https://doi.org/10.3390/nu6083187 - 8 Aug 2014

Cited by 104 | Viewed by 14872

Abstract

Nonalcoholic fatty liver disease (NAFLD) is now thought to be the most common liver disease worldwide. Cardiovascular complications are a leading cause of mortality in NAFLD. Fructose, a common nutrient in the westernized diet, has been reported to be associated with increased cardiovascular risk, but its impact on adolescents with NAFLD is not well understood. We designed a 4-week randomized, controlled, double-blinded beverage intervention study. Twenty-four overweight Hispanic-American adolescents who had hepatic fat >8% on imaging and who were regular consumers of sweet beverages were enrolled and randomized to calorie-matched study-provided fructose only or glucose only beverages. After 4 weeks, there was no significant change in hepatic fat or body weight in either group. In the glucose beverage group there was significantly improved adipose insulin sensitivity, high sensitivity C-reactive protein (hs-CRP), and low-density lipoprotein (LDL) oxidation. These findings demonstrate that reduction of fructose improves several important factors related to cardiovascular disease despite a lack of measurable improvement in hepatic steatosis. Reducing dietary fructose may be an effective intervention to blunt atherosclerosis progression among NAFLD patients and should be evaluated in longer term clinical trials. Full article

(This article belongs to the Special Issue Nutrition and Liver Disease)

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Open AccessArticle

The Effects of Choline on Hepatic Lipid Metabolism, Mitochondrial Function and Antioxidative Status in Human Hepatic C3A Cells Exposed to Excessive Energy Substrates

by Jie Zhu, Yang Wu, Qingya Tang, Yan Leng and Wei Cai

Nutrients 2014, 6(7), 2552-2571; https://doi.org/10.3390/nu6072552 - 9 Jul 2014

Cited by 58 | Viewed by 10866

Abstract

Choline plays a lipotropic role in lipid metabolism as an essential nutrient. In this study, we investigated the effects of choline (5, 35 and 70 μM) on DNA methylation modifications, mRNA expression of the critical genes and their enzyme activities involved in hepatic lipid metabolism, mitochondrial membrane potential (Δψm) and glutathione peroxidase (GSH-Px) in C3A cells exposed to excessive energy substrates (lactate, 10 mM; octanoate, 2 mM and pyruvate, 1 mM; lactate, octanoate and pyruvate-supplemented medium (LOP)). Thirty five micromole or 70 μM choline alone, instead of a low dose (5 μM), reduced hepatocellular triglyceride (TG) accumulation, protected Δψm from decrement and increased GSH-Px activity in C3A cells. The increment of TG accumulation, reactive oxygen species (ROS) production and Δψm disruption were observed under LOP treatment in C3A cells after 72 h of culture, which were counteracted by concomitant treatment of choline (35 μM or 70 μM) partially via reversing the methylation status of the peroxisomal proliferator-activated receptor alpha (PPARα) gene promoter, upregulating PPARα, carnitine palmitoyl transferase-I (CPT-I) and downregulating fatty acid synthase (FAS) gene expression, as well as decreasing FAS activity and increasing CPT-I and GSH-Px activities. These findings provided a novel insight into the lipotropic role of choline as a vital methyl-donor in the intervention of chronic metabolic diseases. Full article

(This article belongs to the Special Issue Nutrition and Liver Disease)

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Sasa borealis Stem Extract Attenuates Hepatic Steatosis in High-Fat Diet-induced Obese Rats

by Yuno Song, Soo-Jung Lee, Sun-Hee Jang, Ji Hee Ha, Young Min Song, Yeoung-Gyu Ko, Hong-Duck Kim, Wongi Min, Suk Nam Kang and Jae-Hyeon Cho

Nutrients 2014, 6(6), 2179-2195; https://doi.org/10.3390/nu6062179 - 5 Jun 2014

Cited by 18 | Viewed by 9761

Abstract

The aim of the current study is to examine the improving effect of Sasa borealis stem (SBS) extract extracts on high-fat diet (HFD)-induced hepatic steatosis in rats. To determine the hepatoprotective effect of SBS, we fed rats a normal regular diet (ND), HFD, and HFD supplemented with 150 mg/kg body weight (BW) SBS extracts for five weeks. We found that the body weight and liver weight of rats in the HFD + SBS group were significantly lower than those in the HFD group. Significantly lower serum total cholesterol (TC) and triglyceride (TG) concentrations were observed in the SBS-supplemented group compared with the HFD group. We also found that the HFD supplemented with SBS group showed dramatically reduced hepatic lipid accumulation compared to the HFD alone group, and administration of SBS resulted in dramatic suppression of TG, TC in the HFD-induced fatty liver. In liver gene expression within the SBS treated group, PPARα was significantly increased and SREBP-1c was significantly suppressed. SBS induced a significant decrease in the hepatic mRNA levels of PPARγ, FAS, ACC1, and DGAT2. In conclusion, SBS improved cholesterol metabolism, decreased lipogenesis, and increased lipid oxidation in HFD-induced hepatic steatosis in rats, implying a potential application in treatment of non-alcoholic fatty liver disease. Full article

(This article belongs to the Special Issue Nutrition and Liver Disease)

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Review

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334 KiB

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Simple Sugar Intake and Hepatocellular Carcinoma: Epidemiological and Mechanistic Insight

by Juan Carlos Laguna, Marta Alegret and Núria Roglans

Nutrients 2014, 6(12), 5933-5954; https://doi.org/10.3390/nu6125933 - 22 Dec 2014

Cited by 32 | Viewed by 9531

Abstract

Sugar intake has dramatically increased during the last few decades. Specifically, there has been a clear trend towards higher consumption of fructose and high fructose corn syrup, which are the most common added sugars in processed food, soft drinks and other sweetened beverages. Although still controversial, this rising trend in simple sugar consumption has been positively associated with weight gain and obesity, insulin resistance and type 2 diabetes mellitus and non-alcoholic fatty liver disease. Interestingly, all of these metabolic alterations have also been related to the development of hepatocellular carcinoma. The purpose of this review is to discuss the evidence coming from epidemiological studies and data from animal models relating the consumption of simple sugars, and specifically fructose, with an increased risk of hepatocellular carcinoma and to gain insight into the putative molecular mechanisms involved. Full article

(This article belongs to the Special Issue Nutrition and Liver Disease)

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The Role of Dietary Sugars and De novo Lipogenesis in Non-Alcoholic Fatty Liver Disease

by J. Bernadette Moore, Pippa J. Gunn and Barbara A. Fielding

Nutrients 2014, 6(12), 5679-5703; https://doi.org/10.3390/nu6125679 - 10 Dec 2014

Cited by 111 | Viewed by 13888

Abstract

Dietary sugar consumption, in particular sugar-sweetened beverages and the monosaccharide fructose, has been linked to the incidence and severity of non-alcoholic fatty liver disease (NAFLD). Intervention studies in both animals and humans have shown large doses of fructose to be particularly lipogenic. While fructose does stimulate de novo lipogenesis (DNL), stable isotope tracer studies in humans demonstrate quantitatively that the lipogenic effect of fructose is not mediated exclusively by its provision of excess substrates for DNL. The deleterious metabolic effects of high fructose loads appear to be a consequence of altered transcriptional regulatory networks impacting intracellular macronutrient metabolism and altering signaling and inflammatory processes. Uric acid generated by fructose metabolism may also contribute to or exacerbate these effects. Here we review data from human and animal intervention and stable isotope tracer studies relevant to the role of dietary sugars on NAFLD development and progression, in the context of typical sugar consumption patterns and dietary recommendations worldwide. We conclude that the use of hypercaloric, supra-physiological doses in intervention trials has been a major confounding factor and whether or not dietary sugars, including fructose, at typically consumed population levels, effect hepatic lipogenesis and NAFLD pathogenesis in humans independently of excess energy remains unresolved. Full article

(This article belongs to the Special Issue Nutrition and Liver Disease)

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Open AccessReview

The Role of Intestinal Bacteria Overgrowth in Obesity-Related Nonalcoholic Fatty Liver Disease

by Silvia M. Ferolla, Geyza N. A. Armiliato, Cláudia A. Couto and Teresa C. A. Ferrari

Nutrients 2014, 6(12), 5583-5599; https://doi.org/10.3390/nu6125583 - 3 Dec 2014

Cited by 85 | Viewed by 13194

Abstract

Nonalcoholic fatty liver disease (NAFLD) is the most common chronic liver disease worldwide. It is a progressive disorder involving a spectrum of conditions that include pure steatosis without inflammation, nonalcoholic steatohepatitis (NASH), fibrosis and cirrhosis. The key factor in the pathophysiology of NAFLD is insulin resistance that determines lipid accumulation in the hepatocytes, which may be followed by lipid peroxidation, production of reactive oxygen species and consequent inflammation. Recent studies suggest that the characteristics of the gut microbiota are altered in NAFLD, and also, that small intestinal bacterial overgrowth (SIBO) contributes to the pathogenesis of this condition. This review presents the chief findings from all the controlled studies that evaluated SIBO, gut permeability and endotoxemia in human NAFLD. We also discuss the possible mechanisms involving SIBO, lipid accumulation and development of NASH. The understanding of these mechanisms may allow the development of new targets for NASH treatment in the future. Full article

(This article belongs to the Special Issue Nutrition and Liver Disease)

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593 KiB

Open AccessReview

Does Vitamin C Deficiency Promote Fatty Liver Disease Development?

by David Højland Ipsen, Pernille Tveden-Nyborg and Jens Lykkesfeldt

Nutrients 2014, 6(12), 5473-5499; https://doi.org/10.3390/nu6125473 - 1 Dec 2014

Cited by 60 | Viewed by 15208

Abstract

Obesity and the subsequent reprogramming of the white adipose tissue are linked to human disease-complexes including metabolic syndrome and concurrent non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH). The dietary imposed dyslipidemia promotes redox imbalance by the generation of excess levels of reactive oxygen species and induces adipocyte dysfunction and reprogramming, leading to a low grade systemic inflammation and ectopic lipid deposition, e.g., in the liver, hereby promoting a vicious circle in which dietary factors initiate a metabolic change that further exacerbates the negative consequences of an adverse life-style. Large epidemiological studies and findings from controlled in vivo animal studies have provided evidence supporting an association between poor vitamin C (VitC) status and propagation of life-style associated diseases. In addition, overweight per se has been shown to result in reduced plasma VitC, and the distribution of body fat in obesity has been shown to have an inverse relationship with VitC plasma levels. Recently, a number of epidemiological studies have indicated a VitC intake below the recommended daily allowance (RDA) in NAFLD-patients, suggesting an association between dietary habits, disease and VitC deficiency. In the general population, VitC deficiency (defined as a plasma concentration below 23 μM) affects around 10% of adults, however, this prevalence is increased by an adverse life-style, deficiency potentially playing a broader role in disease progression in specific subgroups. This review discusses the currently available data from human surveys and experimental models in search of a putative role of VitC deficiency in the development of NAFLD and NASH. Full article

(This article belongs to the Special Issue Nutrition and Liver Disease)

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214 KiB

Open AccessReview

The Influence of Dietary Fat on Liver Fat Accumulation

by Charlotte J. Green and Leanne Hodson

Nutrients 2014, 6(11), 5018-5033; https://doi.org/10.3390/nu6115018 - 10 Nov 2014

Cited by 97 | Viewed by 16747

Abstract

Obesity is a known risk factor for the development of non-alcoholic fatty liver disease (NAFLD); however, it has been suggested that dietary fat, both amount and composition, may play a pivotal role in its development, independent of body fatness. Studies that have investigated the role of dietary fat on liver fat accumulation are reasonably sparse. We review here the available work that has investigated the impact of dietary fat: amount, composition and frequency, on liver fat accumulation in human observational and intervention studies. Overall, it would seem that total calorie consumption, rather than dietary fat composition, is an important factor in the development of fatty liver disease in humans. Full article

(This article belongs to the Special Issue Nutrition and Liver Disease)

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