Histopathological Evaluation of Non-Alcoholic Fatty Liver
Disease: Mini-Review of Literature

Andrade, Raíssa Silva Bacelar de; Rodrigues, Ayane Araújo; França, Luíz Felipe de Carvalho; Vasconcelos, Daniel Fernando Pereira

doi:10.17554/j.issn.2224-3992.2018.07.752

Cited by 2 publications

(3 citation statements)

References 31 publications

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“…The cafeteria diet model used in the present study was effective in inducing hepatic steatosis, using a cheaper and more standardized diet. It should also be noted that the imbalance in the organ's redox state indicates that had the diet been maintained for a longer time, an inflammatory process could have developed, with the liver status being classified as Hepatic steatosis and redox imbalance NASH (Bellentani, 2017;Silva Bacelar de Andrade et al, 2018). The results obtained in this study allow the use of this model to study the pathways of diet fat accumulation in the liver.…”

Section: Discussionmentioning

confidence: 83%

“…In humans, NAFLD can also be subdivided according to the level of liver involvement: when there is less than 5% fat accumulation in liver tissue, it is called hepatic steatosis. However, when there is fat accumulation (>5%) and also the presence of inflammation and fibrosis, it is classified as non-alcoholic steatohepatitis (NASH) (Bellentani, 2017;Silva Bacelar de Andrade et al, 2018;Younossi et al, 2018).…”

Section: Introductionmentioning

confidence: 99%

“…Obesogenic diets are used to investigate the development and progression of hepatic steatosis or NASH, which are also directly associated with the onset of obesity and/or metabolic syndrome. In more severe cases, cirrhosis or hepatocellular carcinoma may further develop (Bellentani, 2017;Silva Bacelar de Andrade et al, 2018). The cafeteria diet is a model of obesogenic diet commonly used in rodents, being rich in sugars and saturated fats, and poor in vitamins, minerals and fibers.…”

Section: Introductionmentioning

confidence: 99%

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Cafeteria diet from birth to adulthood promotes hepatic steatosis and redox imbalance in Wistar rats

Gomes

Costa

Rocha-Gomes

et al. 2020

NFS

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Purpose The purpose of this paper is to evaluate the pathological, biochemical and redox state parameters of liver tissue in Wistar rats treated from birth to adulthood (119 days) with cafeteria diet. Design/methodology/approach During the lactation, 6 liters of Wistar rats (dam + 8 pups each) were fed one of two diets: control (CTRL; n = 3) or cafeteria (CAF; n = 3) diets and water ad libitum. After weaning, the males were placed in individual cages, receiving the same diet offered to their respective dams (CTRL or CAF; n = 18) until adulthood. The following parameters were evaluated: absolute and relative liver weight; blood, liver and feces biochemistry; liver histology; and redox state of the liver. Findings When assessing the relative and absolute organ weight, no significant differences were found between the groups. The Cafeteria group exhibited higher values of serum LDL-c (p = 0.008), VLDL-c (p = 0.03) and triglycerides (p = 0.01), as well as several micro and macrovacuoles of fat accumulation, higher hepatic lipid (p = 0.03) and cholesterol (p = 0.0001) levels regarding Control group. Cafeteria group showed greater expression of glutathione-s-transferase (p = 0.03) and superoxide dismutase (p = 0.005) enzymes compared to the control group. In the case of the markers of oxidative stress, there was no difference between the groups. Originality/value A simple and standardized cafeteria diet caused an accumulation of fatty acids in liver tissue, inducing a state of hepatic steatosis besides an increased expression of antioxidant enzymes.

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Section: Discussionmentioning

confidence: 83%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Cafeteria diet from birth to adulthood promotes hepatic steatosis and redox imbalance in Wistar rats

Gomes

Costa

Rocha-Gomes

et al. 2020

NFS

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High‐fat diet aggravates the liver disease caused by periodontitis in rats

Andrade

França

Pessoa

et al. 2019

Journal of Periodontology

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Background: Periodontitis is an inflammatory disease that causes periodontium and hepatic alterations. Liver disease is related to the intake of foods rich in fat and sugars (high-fat). The objective of this study was to evaluate whether a high-fat diet can aggravate the liver disease caused by ligature-induced periodontitis in rats.Methods: Twenty-one female rats were divided into three groups (n = 7 in each group): control; periodontitis (periodontitis induced with ligature) and high-fat + periodontitis (received hypercaloric diet and induction of periodontitis). The rats were submitted to the analyses of the following periodontal parameters: gingival bleeding index (GBI), probing pocket depth (PPD), tooth mobility (TM), and alveolar bone height. In the hepatic tissue, the levels of malondialdehyde (MDA), glutathione (GSH), total cholesterol, and myeloperoxidase activity (MPO) were measured. Liver samples were also histopathologically evaluated. Finally, blood levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), glucose, total cholesterol, cholesterol high-density lipoprotein (HDL), and uric acid were measured. Results:The high-fat + periodontitis group presented an increase in the steatosis score (P < 0.05) for the histopathologic evaluation, when compared with the periodontitis group. MDA, uric acid and ALT levels also increased, whereas GSH and HDL levels showed lower values. Conclusion:A high-fat diet aggravates the liver disease caused by ligature-induced periodontitis in rats.

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Histopathological Evaluation of Non-Alcoholic Fatty Liver Disease: Mini-Review of Literature

Cited by 2 publications

References 31 publications

Cafeteria diet from birth to adulthood promotes hepatic steatosis and redox imbalance in Wistar rats

Cafeteria diet from birth to adulthood promotes hepatic steatosis and redox imbalance in Wistar rats

High‐fat diet aggravates the liver disease caused by periodontitis in rats

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