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Review
. 2019 Jan 1;15(2):265-276.
doi: 10.7150/ijbs.30121. eCollection 2019.

Role of Nutrition in the Pathogenesis and Prevention of Non-alcoholic Fatty Liver Disease: Recent Updates

Rahim Ullah  1   2 , Naveed Rauf  1   2 , Ghulam Nabi  3 , Hamid Ullah  4 , Yi Shen  2 , Yu-Dong Zhou  2 , Junfen Fu  1
Affiliations
Review

Role of Nutrition in the Pathogenesis and Prevention of Non-alcoholic Fatty Liver Disease: Recent Updates

Rahim Ullah et al. Int J Biol Sci. .

Abstract

Non-alcoholic fatty liver disease (NAFLD) is an acquired metabolic disease characterized by triglycerides (TGs) deposition in liver induced by other factors rather than alcohol consumption. NAFLD significantly contributes to liver diseases in children and adults. NAFLD pathogenesis is associated with age, gender, race and ethnicity. Insulin resistance, hyperinsulinemia, elevated plasma free fatty acids (FFAs), fatty liver, hepatocyte injury, liver inflammation, oxidative stress, mitochondrial dysfunction, imbalanced pro-inflammatory cytokines, and fibrosis are the characteristics of NAFLD. Factors including genetic and epigenetic pathways, sedentary lifestyle, sleep, and diet composition affect NAFLD pathogenesis. In this review, we discuss the aetiology, risk factors and pathogenesis of NAFLD. Special focus is given to macro and micro nutrition as causing factors and their role in the prevention of NAFLD pathogenesis.

Keywords: NAFLD pathogenesis; hepatic inflammation; nutrition; prevention.

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Conflict of interest statement

Competing Interests: The authors have declared that no competing interest exists.

Figures

Figure 1
Figure 1
Convergence of fats and carbohydrates induced key signalling molecules on NAFLD pathogenesis. Here, fats and carbohydrates mean a high intake or intake of harmful components of fats and carbohydrates supporting NAFLD pathogenesis. Fats and carbohydrates directly or indirectly induce metabolic stress and related signalling cascade that collectively induce insulin resistance and support overall NAFLD pathogenesis. FFAs= free fatty acids, IKK β= inhibitor of κB kinase-β, NF-κB= nuclear factor kappa B, Mac= macrophages, TNF-α = tumor necrosis factor-α , IL-6= interleukin 6, IL-1 β= interleukin 1 β, ER= endoplasmic reticulum, IR= insulin resistance, TGs= triglycerides, NASH= non-alcoholic steatohepatitis, HSC= hepatic stellate cells, KC= Kupffer cells.
Figure 2
Figure 2
Contribution of various factors in the development of obesity and NAFLD. The above factors trigger NAFLD pathogenesis directly or indirectly through obesity. Abbreviation: CVD= cardiovascular diseases, G= genetics, IR= Insuline resistance, T2D= type 2 diabetes, D= diet, LS= lifestyle, EF= environmental factors, PD= parental diet, NASH= non-alcoholic steatoheptitis, CRHS= cirrhosis. Single sided arrows mean unidirectional, whereas double sided arrows mean bidirectional interaction.
Figure 3
Figure 3
Contribution of macro and micronutrients in NAFLD pathogenesis. The above nutrition types support or prevent NAFLD pathogenesis and NAFLD related metabolic complications. Abbreviations: NAFLD= non-alcoholic fatty liver disease, GI= glycemic index, SFAs= saturated fatty acids, trans FAs= trans fatty acids, MUFAs= monounsaturated fatty acids, PUFAs= polyunsaturated fatty acids. Positive (+) means to support NAFLD pathogenesis, Negative (-) means to prevent NAFLD.
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