Upregulation of caveolin-1 and SR-B1 in mice with non-alcoholic fatty liver disease

Qiu, Yan; Liu, Shan; Chen, Hong-Tan; Yu, Chaohui; Teng, Xiaodong; Yao, Huaiying; Xu, Guofan

doi:10.1016/s1499-3872(13)60099-5

Cited by 39 publications

(26 citation statements)

References 33 publications

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“…Another important purpose of this study is to clarify the role of caveolin-1 on MMP-1 expression in the pathophysiology of NASH because up-regulation of caveolin-1 expression was reported in a murine NAFLD model [21]. The results of the present study also suggest co-localization of MMP-1 and caveolin-1 in caveolae under pathological conditions.…”

Section: Discussionsupporting

confidence: 65%

Spatiotemporal expression of matrix metalloproteinase-1 in progression of nonalcoholic steatohepatitis

Yokomori¹,

Inagaki²,

Ando³

et al. 2016

J Mod Hum Pathol.

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Section: Discussionsupporting

confidence: 65%

Spatiotemporal expression of matrix metalloproteinase-1 in progression of nonalcoholic steatohepatitis

Yokomori¹,

Inagaki²,

Ando³

et al. 2016

J Mod Hum Pathol.

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“…Caveolin 1 was increased in the liver of mice with NAFLD, and located mainly in the centrilobular zone 3, where the steatosis was most severe [27]. Similarly, zone 3 predominant hepatic steatosis is reported in adult NAFLD patients [28].…”

Section: Hepatic Lipid Uptakementioning

confidence: 99%

Molecular mechanisms of hepatic lipid accumulation in non-alcoholic fatty liver disease

Ipsen

Lykkesfeldt

Tveden‐Nyborg

2018

Cell. Mol. Life Sci.

927

757

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Non-alcoholic fatty liver disease (NAFLD) is currently the world’s most common liver disease, estimated to affect up to one-fourth of the population. Hallmarked by hepatic steatosis, NAFLD is associated with a multitude of detrimental effects and increased mortality. This narrative review investigates the molecular mechanisms of hepatic steatosis in NAFLD, focusing on the four major pathways contributing to lipid homeostasis in the liver. Hepatic steatosis is a consequence of lipid acquisition exceeding lipid disposal, i.e., the uptake of fatty acids and de novo lipogenesis surpassing fatty acid oxidation and export. In NAFLD, hepatic uptake and de novo lipogenesis are increased, while a compensatory enhancement of fatty acid oxidation is insufficient in normalizing lipid levels and may even promote cellular damage and disease progression by inducing oxidative stress, especially with compromised mitochondrial function and increased oxidation in peroxisomes and cytochromes. While lipid export initially increases, it plateaus and may even decrease with disease progression, sustaining the accumulation of lipids. Fueled by lipo-apoptosis, hepatic steatosis leads to systemic metabolic disarray that adversely affects multiple organs, placing abnormal lipid metabolism associated with NAFLD in close relation to many of the current life-style-related diseases.

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“…The fat distribution may be diffuse or focal on the liver parenchyma. It possesses similarities with alcoholic liver disease, although it occurs in individuals without significant alcohol ingestion [Qiu et al, 2013;Augustin et al, 2017;Ferramosca et al, 2017]. It is a common disease that affects approximately 27% of the general population [Khoshbaten et al, 2010].…”

Section: Introductionmentioning

confidence: 99%

“…Obesity, diabetes mellitus, and dyslipidemia are known risk factors that contribute to NAFLD development. Insulin resistance seems to play a fundamental role in the pathogenesis of these conditions, and it has been suggested that NAFLD should be included as a marker for the diagnosis of metabolic syndrome [Qiu et al, 2013;Mantovani and Targher, 2017;Massart et al, 2017].…”

Section: Introductionmentioning

confidence: 99%

Grape Leucoanthocyanidin Protects Liver Tissue in Albino Rabbits with Nonalcoholic Hepatic Steatosis

Franklin

Bispo

Sousa‐Rodrigues

et al. 2018

Cells Tissues Organs

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Nonalcoholic fatty liver disease (NAFLD) is a common ailment. It is usually found in association with diabetes or obesity. There are no approved drugs to treat this condition. The study of flavonoid consumption has increased over the decades due to their antioxidative properties, although the literature is scarce when it comes to their effects in liver tissue. The purpose of this study was to evaluate the role of leucoanthocyanidin in nonalcoholic hepatic steatosis. Thirty male albino rabbits were divided in 3 groups. Group 1 had a regular commercial diet. The second group had a regular diet and 10 mL of egg yolk and 1.5 g of pure cholesterol. The rabbits of the third group were on the same regimen as the second, but were also treated with grape leucoanthocyanidin (50 mg/kg/day) for 100 days. On the last day of the experiment, the animals were euthanized, and the livers excised and fixated in a 10% formalin solution. Afterwards, fragments of each liver were removed and histologically processed and analyzed. The stereological evaluation showed that leucoanthocyanidin reduced NAFLD in comparison with the nontreated group. This was also observed in the histological analysis of the liver tissue, as the treated group had less foci of fatty tissue. Leucoanthocyanidin may therefore be a promising substance to treat NAFLD, although further studies are needed.

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Upregulation of caveolin-1 and SR-B1 in mice with non-alcoholic fatty liver disease

Cited by 39 publications

References 33 publications

Spatiotemporal expression of matrix metalloproteinase-1 in progression of nonalcoholic steatohepatitis

Spatiotemporal expression of matrix metalloproteinase-1 in progression of nonalcoholic steatohepatitis

Molecular mechanisms of hepatic lipid accumulation in non-alcoholic fatty liver disease

Grape Leucoanthocyanidin Protects Liver Tissue in Albino Rabbits with Nonalcoholic Hepatic Steatosis

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