Underrated enemy – from nonalcoholic fatty liver disease to cancers of the gastrointestinal tract

Derra, Aleksandra; Bator, Martyna; Menżyk, Tomasz; Kukla, Michał

doi:10.5114/ceh.2018.75955

Cited by 9 publications

(7 citation statements)

References 206 publications

(204 reference statements)

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“…In addition, NAFLD is strongly associated with features of the metabolic syndrome, including obesity, insulin resistance, type 2 diabetes (DM2) and dyslipidemia 1,2. NAFLD represents a new emerging risk factors for the onset of extra-hepatic tumors, particularly in the development of tumors of the gastro-intestinal tract 3,4. Risk factors associated with the development of NAFLD include bad eating habits associated with a sedentary lifestyle.…”

Section: Introductionmentioning

confidence: 99%

Obesity, Nonalcoholic Fatty Liver Disease and Adipocytokines Network in Promotion of Cancer

Divella¹,

Mazzocca²,

Daniele³

et al. 2019

Int. J. Biol. Sci.

131

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Western populations are becoming increasingly sedentary and the incidence of nonalcoholic fatty liver disease (NAFLD) is increasing and becoming one of the most common causes of liver disease worldwide. Also, NAFLD is considered one the new emerging risk factors for development of tumors of the gastro-intestinal tract, particularly hepatocellular carcinoma (HCC). Visceral obesity is an important risk factor for the onset of NAFLD. An accumulation of ectopic fat, including visceral obesity and fatty liver leads to a dysfunction of the adipose tissue with impaired production of adipocytokines which, in turn, favor an increase in pro-inflammatory cytokines. In this review, we discuss how the obesity-related chronic state of low-grade inflammation and the presence of NAFLD lead to the emergence of a microenvironment favorable to the development of cancer.

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Section: Introductionmentioning

confidence: 99%

Obesity, Nonalcoholic Fatty Liver Disease and Adipocytokines Network in Promotion of Cancer

Divella¹,

Mazzocca²,

Daniele³

et al. 2019

Int. J. Biol. Sci.

131

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“…Evident dysregulation of serum cytokines levels, altered gut microbiota and bile acids composition are also connected to metabolic syndrome. Dysregulation of adipose tissue derived hormones (adipocytokines/adipokines) might also be involved in obesity-related liver carcinogenesis [3][4][5][6][7]. Adipokines disbalance, such as dysregulation in level of adiponectin, leptin, resistin, chemerin, visfatin and some others, have been identified as a factor increasing fibrosis progression, inflammation and steatosis in chronic liver diseases including NAFLD/NASH, CHB and alcoholic liver disease (ALD) [4][5][6][7][8][9].…”

Section: Introductionmentioning

confidence: 99%

Serum visfatin and vaspin levels in hepatocellular carcinoma (HCC)

et al. 2020

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Hepatocellular carcinoma (HCC) is the most common liver cancer, accountable for 90% cases. Visfatin and vaspin are adipocytokines with various suggested functions and proven significant correlations between BMI and percentage of body fat. The aim was to assess visfatin and vaspin serum levels in HCC patients and controls, compare their levels in patients with different cancer etiology and grade assessed according to the Barcelona-Clinic Liver Cancer (BCLC) staging system. The additional aim was to analyze relationship between analyzed adipokines and metabolic abnormalities and liver disfunction severity. The study was performed on 69 cirrhotic patients (54 males/15 females) with HCC, aged 59.0 ± 12.1 years, and with BMI 29.0 ± 4.5 kg/m 2 compared to 20 healthy volunteers. Serum visfatin and vaspin concentrations were significantly increased in HCC patients compared to controls (p = 0.01 and p = 0.02, respectively). Serum vaspin was significantly higher in HCC patients with viral compared to those with non-viral etiology (p = 0.02), with more evident increase in chronic hepatitis C patients (CHC). Serum visfatin levels were significantly higher in patients with higher insulin resistance (p = 0.04) and with platelets count > 100 000/mm 3 (p<0.001). Patients with BMI >30 kg/m 2 had markedly up-regulated vaspin levels (p = 0.04). There was no difference in vaspin and visfatin serum levels with respect to liver dysfunction and BCLC classification. In conclusion, our study revealed serum vaspin and visfatin to be significantly increased in HCC patients independently of cancer etiology compared to controls. Additionally, serum vaspin was elevated in viral disease, especially in CHC. Vaspin up-regulation can be a compensatory mechanism against IR in HCC patients. Serum visfatin and vaspin, although up-regulated, seem not to be associated with cancer grade and cirrhosis severity.

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“…NAFLD is the most common chronic liver disease in developed countries. The estimated prevalence of NAFLD ranges from 10% to 25% [6]. Until now, there has been no effective treatment of NAFLD.…”

Section: Introductionmentioning

confidence: 99%

“…Until now, there has been no effective treatment of NAFLD. The only way to deal with this disease is weight loss and treatment of comorbid conditions [6]. Thus, dietary strategies that prevent the development of liver steatosis or its progression to NASH are critically needed [7].…”

Section: Introductionmentioning

confidence: 99%

Green tea extract prevents the development of nonalcoholic liver steatosis in rats fed a high-fat diet

Karolczak¹,

Seget²,

Bajerska³

et al. 2019

pjp

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Green tea contains many polyphenolic constitutes, which might prevent non-alcoholic fatty liver disease (NAFLD). We aimed to investigate whether green tea extract (GTE) given at doses reflecting habitual consumption of green tea beverages prevents development of NAFLD in rats fed a high-fat diet (HFD). Twenty-four male Wistar rats were randomly divided into four equal groups (two study and two control groups). The study groups received a HFD (approximately 50% energy from fat), enriched with 1.1% and 2.0% GTE, respectively, for a total of 56 days. The control groups were fed a HFD alone and normal standardised diet (low-fat diet), respectively, for the same period of time. The percentage of hepatocytes affected by steatosis in the HFD group (median [1 st-3 rd quartile]: 25% [12-34%]) was higher (p < 0.033 and p < 0.050, respectively) than in the HFD-2.0%GTE group (9% [3-18%]) and normal diet group (10% [5-18%]). No significant differences were observed for the group consuming HFD-1.1%GTE, in which intermediate results were observed (15% [4-30%]). This finding points towards the hepatoprotective potential of GTE in preventing dietary-induced liver steatosis. In view of the increasing incidence of overweight and obesity a simple and cheap dietary modification, such as GTE supplementation, could prove to be useful clinically.

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Underrated enemy – from nonalcoholic fatty liver disease to cancers of the gastrointestinal tract

Cited by 9 publications

References 206 publications

Obesity, Nonalcoholic Fatty Liver Disease and Adipocytokines Network in Promotion of Cancer

Obesity, Nonalcoholic Fatty Liver Disease and Adipocytokines Network in Promotion of Cancer

Serum visfatin and vaspin levels in hepatocellular carcinoma (HCC)

Green tea extract prevents the development of nonalcoholic liver steatosis in rats fed a high-fat diet

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