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Nutrition for Non-Alcoholic Fatty Liver Disease

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

Deadline for manuscript submissions: closed (15 September 2020) | Viewed by 34793

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Prof. Dr. M. Angeles Zulet

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Department of Nutrition, Food Sciences and Physiology, Centre for Nutrition Research, Faculty of Pharmacy and Nutrition, University of Navarra, 31008 Pamplona, Spain
Centro de Investigación Biomédica en Red de la Fisiopatología de la Obesidad y Nutrición (CIBERobn), Instituto de Salud Carlos III, 28029 Madrid, Spain
Navarra Institute for Health Research (IdiSNA), 31008 Pamplona, Spain
Interests: non-alcoholic fatty liver disease; metabolic syndrome; obesity; insulin resistance; cardiovascular disease; body composition; dietary patterns; precision nutrition; personalized nutrition; lifestyle intervention
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Dr. María U. Moreno Zulategui

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Guest Editor

1. Program of Cardiovascular Diseases, Centre for Applied Medical Research, University of Navarra, Pamplona, Spain
2. Department of Biochemistry and Genetics, University of Navarra, Pamplona, Spain
3. Navarra Institute for Health Research (IdiSNA), 31008 Pamplona, Spain
Interests: oxidative stress; cardiovascular diseases; heart failure; hypertension; myocardial fibrosis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Non-alcoholic fatty liver disease (NAFLD) is becoming the major cause of liver-related morbidity. Its prevalence is increasing worldwide, rising conjointly with obesity, insulin resistance, and cardiovascular risk. The pathogenesis is multifactorial, involving a combination of genetic, clinical, and environmental factors. The management of NAFLD is mainly focused on weight loss, but the optimal characteristics of the diet demand further investigation. The aim of this Special Issue, “Nutrition and Non-Alcoholic Fatty Liver Disease”, is to provide a literature compilation evaluating the evidence behind dietary strategies and components, including energy intake; fat, protein, and carbohydrate quantity and quality; and antioxidants and bioactive molecules, which could be a trigger to development and progression of the NAFLD and related comorbidities, such as obesity and insulin resistance, among others. Original research, systematic reviews, and meta-analyses should have a clear focus linking nutrition and NAFLD prevention, progression, treatment, and/or reversion. Potential topics involving experimental animals or humans throughout the life cycle are as follows:

Dietary patterns and NAFLD
Dietary components and NAFLD
Lifestyle intervention and NAFLD
Nutrition, underlying mechanisms, and NAFLD
Nutrition, microbioma, prebiotics, probiotics, and NAFLD
Nutrition, genetic condition, and NAFLD
Nutrition, adipose tissue, and NAFLD
Nutrition, epigenetics, and NAFLD
Nutrition, aging, and NAFLD
Nutrition, emotional well-being, and NAFLD

Prof. Dr. M. Angeles Zulet
Prof. Dr. María J. Moreno-Aliaga
Guest Editors

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Keywords

Non-alcoholic fatty liver disease
Non-alcoholic steatohepatitis
Energy restriction
Hypocaloric diets
Macronutrient distribution
Fat intake
Carbohydrate intake
Protein intake
Vitamins
Minerals
Antioxidants
Lifestyle intervention
Gene variants
Microbiota
Obesity and related comorbidities

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Published Papers (7 papers)

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Research

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11 pages, 305 KiB

Open AccessArticle

Implication between Genetic Variants from APOA5 and ZPR1 and NAFLD Severity in Patients with Hypertriglyceridemia

by Virginia Esteve-Luque, Ariadna Padró-Miquel, Marta Fanlo-Maresma, Emili Corbella, Xavier Corbella, Xavier Pintó and Beatriz Candás-Estébanez

Nutrients 2021, 13(2), 552; https://doi.org/10.3390/nu13020552 - 8 Feb 2021

Cited by 9 | Viewed by 2683

Abstract

Background: Lipid metabolism disorders, especially hypertriglyceridemia (HTG), are risk factors for non-alcoholic fatty liver disease (NAFLD). However, the association between genetic factors related to HTG and the risk of NAFLD has been scarcely studied. Methods: A total of 185 subjects with moderate HTG were prospectively included. We investigated the association between genetic factors’ (five allelic variants with polygenic hypertriglyceridemia) clinical and biochemical biomarkers with NAFLD severity. The five allelic variants’ related clinical and biochemical data of HTG were studied in all the subjects. NAFLD was assessed by abdominal ultrasound and patients were divided into two groups, one with no or mild NAFLD and another with moderate/severe NAFLD. Results: Patients with moderate/severe NAFLD had higher weight and waist values and a higher prevalence of insulin resistance than patients with no or mild NAFLD. Moderate/severe NAFLD was independently associated with APOA5 rs3134406 and ZPR1 rs964184 variants, and also showed a significant inverse relationship with lipoprotein(a) [Lp(a)] concentrations. Conclusions: APOA5 rs3135506 and ZPR1 rs964184 variants and lipoprotein(a) are associated with moderate/severe NAFLD. This association was independent of body weight, insulin resistance, and other factors related to NAFLD. Full article

(This article belongs to the Special Issue Nutrition for Non-Alcoholic Fatty Liver Disease)

19 pages, 2261 KiB

Open AccessArticle

Effects of Long-Term DHA Supplementation and Physical Exercise on Non-Alcoholic Fatty Liver Development in Obese Aged Female Mice

by Jinchunzi Yang, Neira Sáinz, Elisa Félix-Soriano, Eva Gil-Iturbe, Rosa Castilla-Madrigal, Marta Fernández-Galilea, J. Alfredo Martínez and María J. Moreno-Aliaga

Nutrients 2021, 13(2), 501; https://doi.org/10.3390/nu13020501 - 3 Feb 2021

Cited by 22 | Viewed by 5689

Abstract

Obesity and aging are associated to non-alcoholic fatty liver disease (NAFLD) development. Here, we investigate whether long-term feeding with a docosahexaenoic acid (DHA)-enriched diet and aerobic exercise, alone or in combination, are effective in ameliorating NAFLD in aged obese mice. Two-month-old female C57BL/6J mice received control or high fat diet (HFD) for 4 months. Then, the diet-induced obese (DIO) mice were distributed into four groups: DIO, DIO + DHA (15% dietary lipids replaced by a DHA-rich concentrate), DIO + EX (treadmill running), and DIO + DHA + EX up to 18 months. The DHA-rich diet reduced liver steatosis in DIO mice, decreasing lipogenic genes (Dgat2, Scd1, Srebp1c), and upregulated lipid catabolism genes (Hsl/Acox) expression. A similar pattern was observed in the DIO + EX group. The combination of DHA + exercise potentiated an increase in Cpt1a and Ppara genes, and AMPK activation, key regulators of fatty acid oxidation. Exercise, alone or in combination with DHA, significantly reversed the induction of proinflammatory genes (Mcp1, Il6, Tnfα, Tlr4) in DIO mice. DHA supplementation was effective in preventing the alterations induced by the HFD in endoplasmic reticulum stress-related genes (Ern1/Xbp1) and autophagy markers (LC3II/I ratio, p62, Atg7). In summary, long-term DHA supplementation and/or exercise could be helpful to delay NAFLD progression during aging in obesity. Full article

(This article belongs to the Special Issue Nutrition for Non-Alcoholic Fatty Liver Disease)

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14 pages, 1587 KiB

Open AccessArticle

Differential Effects of Chronic Ingestion of Refined Sugars versus Natural Sweeteners on Insulin Resistance and Hepatic Steatosis in a Rat Model of Diet-Induced Obesity

by Marion Valle, Philippe St-Pierre, Geneviève Pilon and André Marette

Nutrients 2020, 12(8), 2292; https://doi.org/10.3390/nu12082292 - 30 Jul 2020

Cited by 19 | Viewed by 7900

Abstract

While the detrimental effect of refined sugars on health has been the subject of many investigations, little is known about the long-term impact of natural sweeteners on metabolic disorders. In this study we compared the metabolic responses to chronic ingestion of refined sugars compared to various natural sweeteners in diet-induced obese rats. Wistar rats were fed a high-fat high-sucrose diet (HFHS) for 8 weeks and daily gavaged with a solution containing 1 g of total carbohydrates from refined sugar (sucrose or fructose) or six different natural sugar sources, followed by assessment of glucose homeostasis, hepatic lipid accumulation, and inflammation. While glucose tolerance was similar following treatments with refined and natural sugars, lowered glucose-induced hyperinsulinemia was observed with fructose. Consumption of fructose and all-natural sweeteners but not corn syrup were associated with lower insulin resistance as revealed by reduced fasting insulin and homeostatic model assessment of insulin resistance (HOMA-IR) compared to sucrose treatment of HFHS-fed rats. All-natural sweeteners and fructose induced similar liver lipid accumulation as sucrose. Nevertheless, maple syrup, molasses, agave syrup, and corn syrup as well as fructose further reduced hepatic IL-1β levels compared to sucrose treatment. We conclude that natural sweeteners and especially maple syrup, molasses, and agave syrup attenuate the development of insulin resistance and hepatic inflammation compared to sucrose in diet-induced obese rats, suggesting that consumption of those natural sweeteners is a less harmful alternative to sucrose in the context of obesity. Full article

(This article belongs to the Special Issue Nutrition for Non-Alcoholic Fatty Liver Disease)

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12 pages, 567 KiB

Open AccessArticle

Eating Fast Is Associated with Nonalcoholic Fatty Liver Disease in Men But Not in Women with Type 2 Diabetes: A Cross-Sectional Study

by Fuyuko Takahashi, Yoshitaka Hashimoto, Rena Kawano, Ayumi Kaji, Ryosuke Sakai, Yuka Kawate, Takuro Okamura, Emi Ushigome, Noriyuki Kitagawa, Saori Majima, Takafumi Sennmaru, Hiroshi Okada, Naoko Nakanishi, Masahide Hamaguchi, Mai Asano, Masahiro Yamazaki and Michiaki Fukui

Nutrients 2020, 12(8), 2174; https://doi.org/10.3390/nu12082174 - 22 Jul 2020

Cited by 15 | Viewed by 3214

Abstract

Non-alcoholic fatty liver disease (NAFLD), often complicated by type 2 diabetes mellitus (T2DM), is reported to be associated with diet habits, including eating speed, in the general population. However, the association between eating speed and NAFLD in patients with T2DM, especially sex difference, has not been reported so far. This cross-sectional study included 149 men and 159 women with T2DM. Eating speed was evaluated by a self-reported questionnaire and divided into three groups: fast, moderate, and slow eating. Nutrition status was evaluated by a brief-type self-administered diet history questionnaire. NAFLD was defined as the hepatic steatosis index ≥36 points. Body mass index and carbohydrate/fiber intake in the fast-eating group were higher than those in the slow-eating group in men, whereas this difference was absent in women. In men, compared with eating slowly, eating fast had an elevated risk of the presence of NAFLD after adjusting for covariates (odds ratio (OR) 4.48, 95% confidence interval (CI) 1.09–18.5, p = 0.038). In women, this risk was not found, but fiber intake was found to be negatively associated with the presence of NAFLD (OR 0.85, 95% Cl 0.76–0.96, p = 0.010). This study indicates that eating speed is associated with the presence of NAFLD in men but not in women. Full article

(This article belongs to the Special Issue Nutrition for Non-Alcoholic Fatty Liver Disease)

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16 pages, 1725 KiB

Open AccessArticle

Association of the SH2B1 rs7359397 Gene Polymorphism with Steatosis Severity in Subjects with Obesity and Non-Alcoholic Fatty Liver Disease

by Nuria Perez-Diaz-del-Campo, Itziar Abete, Irene Cantero, Bertha Araceli Marin-Alejandre, J. Ignacio Monreal, Mariana Elorz, José Ignacio Herrero, Alberto Benito-Boillos, Jose I. Riezu-Boj, Fermín I. Milagro, Josep A. Tur, J. Alfredo Martinez and M. Angeles Zulet

Nutrients 2020, 12(5), 1260; https://doi.org/10.3390/nu12051260 - 29 Apr 2020

Cited by 12 | Viewed by 4378

Abstract

Non-alcoholic fatty liver disease (NAFLD) is a major cause of liver disease worldwide. Some genetic variants might be involved in the progression of this disease. The study hypothesized that individuals with the rs7359397 T allele have a higher risk of developing severe stages of NAFLD compared with non-carriers where dietary intake according to genotypes could have a key role on the pathogenesis of the disease. SH2B1 genetic variant was genotyped in 110 overweight/obese subjects with NAFLD. Imaging techniques, lipidomic analysis and blood liver biomarkers were performed. Body composition, general biochemical and dietary variables were also determined. The SH2B1 risk genotype was associated with higher HOMA-IR p = 0.001; and Fatty Liver Index (FLI) p = 0.032. Higher protein consumption (p = 0.028), less mono-unsaturated fatty acid and fiber intake (p = 0.045 and p = 0.049, respectively), was also referred to in risk allele genotype. Lipidomic analysis showed that T allele carriers presented a higher frequency of non-alcoholic steatohepatitis (NASH) (69.1% vs. 44.4%; p = 0.006). In the genotype risk group, adjusted logistic regression models indicated a higher risk of developing an advanced stage of NAFLD measured by FLI (OR 2.91) and ultrasonography (OR 4.15). Multinomial logistic regression models showed that risk allele carriers had higher liver fat accumulation risk (RRR 3.93) and an increased risk of NASH (RRR 7.88). Consequently, subjects carrying the T allele were associated with a higher risk of developing a severe stage of NAFLD. These results support the importance of considering genetic predisposition in combination with a healthy dietary pattern in the personalized evaluation and management of NAFLD. Full article

(This article belongs to the Special Issue Nutrition for Non-Alcoholic Fatty Liver Disease)

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Review

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19 pages, 858 KiB

Open AccessReview

Fructose, Omega 3 Fatty Acids, and Vitamin E: Involvement in Pediatric Non-Alcoholic Fatty Liver Disease

by Gigliola Alberti, Juan Cristóbal Gana and José L. Santos

Nutrients 2020, 12(11), 3531; https://doi.org/10.3390/nu12113531 - 17 Nov 2020

Cited by 8 | Viewed by 4606

Abstract

Non-alcoholic fatty liver disease (NAFLD) is currently the most common form of liver disease in both adults and children, becoming the leading cause for liver transplant in many countries. Its prevalence has increased considerably in recent years, mainly due to the explosive increase in pediatric obesity rates. NAFLD is strongly associated with central obesity, diabetes, dyslipidemia and insulin resistance, and it has been considered as the hepatic manifestation of the metabolic syndrome. Its complex pathophysiology involves a series of metabolic, inflammatory and oxidative stress processes, among others. Given the sharp increase in the prevalence of NAFLD and the lack of an appropriate pharmacological approach, it is crucial to consider the prevention/management of the disease based on lifestyle modifications such as the adoption of a healthy nutrition pattern. Herein, we review the literature and discuss the role of three key nutrients involved in pediatric NAFLD: fructose and its participation in metabolism, Omega-3 fatty acids and its anti-inflammatory effects and vitamin E and its action on oxidative stress. Full article

(This article belongs to the Special Issue Nutrition for Non-Alcoholic Fatty Liver Disease)

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23 pages, 1264 KiB

Open AccessReview

Physiopathology of Lifestyle Interventions in Non-Alcoholic Fatty Liver Disease (NAFLD)

by David Carneros, Guillermo López-Lluch and Matilde Bustos

Nutrients 2020, 12(11), 3472; https://doi.org/10.3390/nu12113472 - 12 Nov 2020

Cited by 29 | Viewed by 5554

Abstract

Non-alcoholic fatty liver disease (NAFLD) is a major health problem, and its prevalence has increased in recent years. Diet and exercise interventions are the first-line treatment options, with weight loss via a hypocaloric diet being the most important therapeutic target in NAFLD. However, most NAFLD patients are not able to achieve such weight loss. Therefore, the requisite is the investigation of other effective therapeutic approaches. This review summarizes research on understanding complex pathophysiology underlying dietary approaches and exercise interventions with the potential to prevent and treat NAFLD. Full article

(This article belongs to the Special Issue Nutrition for Non-Alcoholic Fatty Liver Disease)

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