Qualitative and Quantitative Evaluation of Dietary Intake in Patients with Non-Alcoholic Steatohepatitis

Federico, Alessandro; Dallio, Marcello; Caprio, Giovanni Di; Gravina, Antonietta Gerarda; Picascia, Desirée; Masarone, Mario; Persico, Marcello; Loguercio, C.

doi:10.3390/nu9101074

Cited by 18 publications

(16 citation statements)

References 73 publications

(80 reference statements)

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“…The first hit of lipid deposition in the liver is induced via dietary intake. Advanced NAFLD patients have been shown to consume more carbohydrates/energy higher saturated fatty acid and lower polyunsaturated fatty acids [77,78]. Adipose tissue in NAFLD produces adipokines, such as tumor necrosis factor alpha (TNFα), resistin, and adiponectin.…”

Section: Oxidative Stress In the Pathogenesis Of Nafld-related Steatomentioning

confidence: 99%

Oxidative Stress Management in Chronic Liver Diseases and Hepatocellular Carcinoma

et al. 2020

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Chronic viral hepatitis B and C and non-alcoholic fatty liver disease (NAFLD) have been widely acknowledged to be the leading causes of liver cirrhosis and hepatocellular carcinoma. As anti-viral treatment progresses, the impact of NAFLD is increasing. NAFLD can coexist with chronic viral hepatitis and exacerbate its progression. Oxidative stress has been recognized as a chronic liver disease progression-related and cancer-initiating stress response. However, there are still many unresolved issues concerning oxidative stress, such as the correlation between the natural history of the disease and promising treatment protocols. Recent findings indicate that oxidative stress is also an anti-cancer response that is necessary to kill cancer cells. Oxidative stress might therefore be a cancer-initiating response that should be down regulated in the pre-cancerous stage in patients with risk factors for cancer, while it is an anti-cancer cell response that should not be down regulated in the post-cancerous stage, especially in patients using anti-cancer agents. Antioxidant nutrients should be administered carefully according to the patients’ disease status. In this review, we will highlight these paradoxical effects of oxidative stress in chronic liver diseases, pre- and post-carcinogenesis.

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Section: Oxidative Stress In the Pathogenesis Of Nafld-related Steatomentioning

confidence: 99%

Oxidative Stress Management in Chronic Liver Diseases and Hepatocellular Carcinoma

et al. 2020

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“…Similar to VC and VD, VB6 was also negatively correlated with the risk of NAFLD. Federico et al found that patients with NASH had a less daily intake of VB6 than those in the control group ( 41 ). A prospective clinical study suggested that an oral VB6 supplement could significantly ameliorate liver fat accumulation in patients with NAFLD ( 42 ).…”

Section: Discussionmentioning

confidence: 99%

Associations of serum multivitamin levels with the risk of non-alcoholic fatty liver disease: A population-based cross-sectional study in U.S. adults

et al. 2022

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Vitamins were closely associated with non-alcoholic fatty liver disease (NAFLD) development, but no study had explored the association of serum multivitamin levels with NAFLD risk. We assessed the association between serum levels of both single-vitamin and multivitamins (VA, VB6, VB9, VB12, VC, VD, and VE) and the risk of NAFLD, using the database of National Health and Nutrition Examination Survey (NHANES) (cycles 2003–2004 and 2005–2006). We employed multivariable logistic regression and weighted quantile sum (WQS) regression models to explore the association of serum multivitamin levels with NAFLD. Among all 2,294 participants, 969 participants with NAFLD were more likely to be male, older, less educated, or have hypertension/high cholesterol/diabetes. After adjustment of covariates, serum VC/VD/VB6/VB9 levels were negatively correlated with NAFLD risk, while serum VA/VE levels were positively correlated with NAFLD risk. In the WQS model, elevated serum VA/VE levels and lowered serum VC/VD/VB6 levels were linearly associated with increased NAFLD risk. There was a non-linear relationship between serum VB9/VB12 levels and NAFLD risk. There were evident associations between serum multivitamin levels and reduced NAFLD risk, which was mainly driven by VD/VB9/VC. In conclusion, our findings suggested that serum multivitamin levels were significantly associated with the risk of NAFLD.

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“…High levels of carbohydrates, especially fructose, worsen insulin sensitivity and increase de novo lipogenesis (DNL). Unbalanced lipid intake leads to alterations in redox status and ROS production [ 30 , 31 ].…”

Section: Triggers Of Liver Inflammationmentioning

confidence: 99%

Chronic Inflammation—A Link between Nonalcoholic Fatty Liver Disease (NAFLD) and Dysfunctional Adipose Tissue

et al. 2022

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Nonalcoholic fatty liver disease (NAFLD) is a new challenge in modern medicine, due to its high prevalence in the world. The pathogenesis of NAFLD is a complex dysmetabolic process, following the “multiple-hit” hypothesis that involves hepatocytes excessive accumulation of triglycerides, insulin resistance (IR), increased oxidative stress, chronic low-grade inflammatory response and lipotoxicity. In this review, we provide an overview of the interrelation of these processes, the link between systemic and local inflammation and the role of dysfunctional adipose tissue (AT) in the NAFLD development. Multiple extrahepatic triggers of the pathophysiological mechanisms of NAFLD are described: nutritional deficiency or malnutrition, unhealthy food intake, the dysfunction of the liver–gut axis, the involvement of the mesenteric adipose tissue, the role of adipokines such as adiponectin, of food intake hormone, the leptin and leptin resistance (LR) and adipose tissue’s hormone, the resistin. In addition, a wide range of intrahepatic players are involved: oxidative stress, fatty acid oxidation, endoplasmic reticulum stress, mitochondrial dysfunction, resident macrophages (Kupffer cells), neutrophils, dendritic cells (DCs), B and T lymphocytes contributing to the potential evolution of NAFLD to nonalcoholic steatohepatitis (NASH). This interdependent approach to complex dysmetabolic imbalance in NAFLD, integrating relevant studies, could contribute to a better clarification of pathogenesis and consequently the development of new personalized treatments, targeting de novo lipogenesis, chronic inflammation and fibrosis. Further studies are needed to focus not only on treatment, but also on prevention strategy in NAFLD.

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Qualitative and Quantitative Evaluation of Dietary Intake in Patients with Non-Alcoholic Steatohepatitis

Cited by 18 publications

References 73 publications

Oxidative Stress Management in Chronic Liver Diseases and Hepatocellular Carcinoma

Oxidative Stress Management in Chronic Liver Diseases and Hepatocellular Carcinoma

Associations of serum multivitamin levels with the risk of non-alcoholic fatty liver disease: A population-based cross-sectional study in U.S. adults

Chronic Inflammation—A Link between Nonalcoholic Fatty Liver Disease (NAFLD) and Dysfunctional Adipose Tissue

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