The consequences of poor dietary patterns on the proliferation of non-alcoholic fatty liver disease

Figures & data

Figure 1. A persistent lack of vitamin C causes a disturbance in the hepatic de novo lipogenesis pathway by impairing the conversion of bile acid to cholesterol. The current research’ straightforward graphical abstract. Normal hepatocytes exhibit de novo lipogenesis in the left panel. Right panel: Impaired de novo lipogenesis in long-term vitamin C–deficient hepatocytes. CYP7A1: cholesterol 7α-hydroxylase; ER: endoplasmic reticulum; FAS: fatty acid synthase; SCAP: SREBP cleavage-activating protein; SRE: sterol regulatory element; SREBP-1c: sterol regulatory element-binding protein-1c; SVCT-1: sodium-dependent vitamin C transporter 1; TG: triglycerides (Source: Lee et al., 2021).

Figure 2. Through several possible interrelated processes, vitamin D may slow the course of NAFLD (Source: Gorman et al., 2015).

Figure 3. Function of Vitamin E in regulating NAFLD (Source: Banini & Sanyal, 2019).

Table 1. Displays documented studies on the benefits of vitamin E in people with NAFLD.

Authors	Design	Intervention	Histology	Duration	Liver Enzyme	Imaging result of fatty liver
Lavine (2000)	OL	Vitamin E	NA	4–10	Yes	NA
Sanyal et al. (2010)	RCT	Contrasts between vitamin E, pioglitazone, and placebo	Alleviated inflammation & steatosis (NS vs pioglitazone)	24	Improved	NA
Zöhrer et al. (2017)	RCT	Lifestyle modification, Vitamin E	Yes (fibrosis) No inflammation/necrosis	6	Yes	NA
Foster et al. (2011)	RCT	Compared to placebo, atorvastatin + antioxidants (vitamins E and C)	NA	48	NA	CT scans with improving steatosis
Lavine et al. (2011)	RCT	Vitamin E versus metformin versus Placebo	Enhanced ballooning and NASH activities, with no impact on lobular fibrosis or inflammation	24	NA	NA
Vajro et al. (2004)	RCT	Compared to a low-calorie diet, vitamin E	No	5	Yes but NS	NA
Kawanaka et al. (2004)	Open-label	Vitamin E	NA	6	Yes	NA

N/A: Not available; RCT: randomized controlled trial; OL: open label and NS: non-significant (Source: Al-Busafi et al., 2012).

Figure 4. Consequences of western and healthy dietary patterns on the onset of non-alcoholic steatohepatitis (NASH) and non-alcoholic fatty liver disease (NAFLD). HODE: hydroxyoctadecadienoic acids; oxidized LDL: lipid oxidation products; TNF: tuber necrosis factor; IL-6: Interleukin 6; VLDL: very low density lipoproteins; FFA: free fatty acids; CRP: C-reactive proteins.

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Data availability statement

The data that support the findings of this study are available on request from the corresponding author.