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Review
. 2017 Sep 26;9(10):1065.
doi: 10.3390/nu9101065.

Isocaloric Dietary Changes and Non-Alcoholic Fatty Liver Disease in High Cardiometabolic Risk Individuals

Giuseppe Della Pepa  1 , Claudia Vetrani  2 , Gianluca Lombardi  3 , Lutgarda Bozzetto  4 , Giovanni Annuzzi  5 , Angela Albarosa Rivellese  6
Affiliations
Review

Isocaloric Dietary Changes and Non-Alcoholic Fatty Liver Disease in High Cardiometabolic Risk Individuals

Giuseppe Della Pepa et al. Nutrients. .

Abstract

Non-alcoholic fatty liver disease (NAFLD) incorporates an extensive spectrum of histologic liver abnormalities, varying from simple triglyceride accumulation in hepatocytes non-alcoholic fatty liver (NAFL) to non-alcoholic steatohepatitis (NASH), and it is the most frequent chronic liver disease in the industrialized world. Beyond liver related complications such as cirrhosis and hepatocellular carcinoma, NAFLD is also an emerging risk factor for type 2 diabetes and cardiovascular disease. Currently, lifestyle intervention including strategies to reduce body weight and to increase regular physical activity represents the mainstay of NAFLD management. Total caloric intake plays a very important role in both the development and the treatment of NAFLD; however, apart from the caloric restriction alone, modifying the quality of the diet and modulating either the macro- or micronutrient composition can also markedly affect the clinical evolution of NAFLD, offering a more realistic and feasible treatment alternative. The aim of the present review is to summarize currently available evidence from randomized controlled trials on the effects of different nutrients including carbohydrates, lipids, protein and other dietary components, in isocaloric conditions, on NAFLD in people at high cardiometabolic risk. We also describe the plausible mechanisms by which different dietary components could modulate liver fat content.

Keywords: NAFLD; NASH; carbohydrates; isocaloric dietary changes; monounsaturated fatty acids; polyphenols; polyunsaturated fatty acids; vitamins.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Pathogenesis of NAFLD. Based on the “multiple hit” model, dietary habits, insulin resistance, visceral adiposity, inflammatory state, oxidative stress, alteration in microbiome, and genetic predisposition, are all recognized risk factors for NAFLD. DNL: de novo lipogenesis; FFA: free fatty acids; IL-6: interleukin-6; IL-1β: interleukin-1β; LPS: lipopolysaccharide; NAFLD: non-alcoholic fatty liver disease; NASH: non-alcoholic steatohepatitis; TNF-α: tumor necrosis factor-α.
Figure 2
Figure 2
Possible sites of action of dietary nutrients in the nutritional treatment and prevention of NAFLD. Nutrients and dietary composition can modulate many key aspects in the pathophysiology of NAFLD: simple sugars promote DNL, produce inflammation and activate cellular stress pathways. Contrarily, LGI meals can improve insulin resistance and can positively modulate the microbiome. SFA could induce lipogenesis, oxidative stress, and apoptosis of hepatocytes; conversely, MUFA and PUFA can improve FFA β-oxidation and can reduce DNL, improve insulin sensitivity and reduce inflammation. Polyphenols could inhibit DNL and increase FFA β-oxidation. Furthermore, polyphenols can improve insulin sensitivity, reduce the transcription of inflammatory cytokines, and can mitigate the oxidative stress involved in NAFLD progression. Vitamin C and vitamin E could avoid the progression of NAFLD and improve NASH acting as powerful antioxidants; furthermore, vitamin E could reduce plasma levels of cytokines involved in inflammation and liver fibrosis. Vitamin D can reduce the transcription of inflammatory cytokines and improve FFA β-oxidation. Furthermore, it has been observed that vitamin D increases adiponectin secretion, decreases lipolysis in adipose tissue, and improves insulin resistance. DNL: de novo lipogenesis; LGI: low glycemic index; MUFA: monounsaturated fatty acids; NAFLD: non-alcoholic fatty liver disease; NASH: non-alcoholic steatohepatitis; PUFA: polyunsaturated fatty acids; SFA: saturated fatty acids.
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