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FGF21 induces autophagy-mediated cholesterol efflux to inhibit atherogenesis via RACK1 up-regulation.
In this study, ApoE-/- mice were fed a high-fat diet (HFD) with or without FGF21 and FGF21 + 3-Methyladenine (3MA) for 12 weeks. Our results showed that FGF21 inhibited AS in HFD-fed ApoE-/- mice, which was reversed by 3MA treatment. Moreover, FGF21 increased plaque RACK1 and autophagy-related protein (LC3 and beclin-1) expression in ApoE-/- mice, thus preventing AS. However, these proteins were inhibited by LV-RACK1 shRNA injection. Foam cell development is a crucial determinant of AS, and cholesterol efflux from foam cells represents an important defensive measure of AS. In this study, foam cells were treated with FGF...
Source: J Cell Mol Med - March 29, 2020 Category: Molecular Biology Authors: Xiaolong L, Dongmin G, Liu M, Zuo W, Huijun H, Qiufen T, XueMei H, Wensheng L, Yuping P, Jun L, Zhaolin Z Tags: J Cell Mol Med Source Type: research

Targeting endothelial thioredoxin-interacting protein (TXNIP) protects from metabolic disorder-related impairment of vascular function and post-ischemic revascularisation
ConclusionCollectively, these results show that targeting endothelial TXNIP in metabolic disorders is essential to maintaining endothelial function, vascular function and improving ischemia-induced revascularisation, making TXNIP a potential therapeutic target for therapy of vascular complications related to metabolic disorders.
Source: Angiogenesis - January 2, 2020 Category: Molecular Biology Source Type: research

CYP3A suppression during diet-induced nonalcoholic fatty liver disease is independent of PXR regulation.
Abstract Cytochrome P450 3A (CYP3A) activity is inhibited, and its expression is suppressed during many diseases, including nonalcoholic fatty liver disease (NAFLD). However, the mechanism is controversial. Here, we report that PXR may not take part in the downregulation of CYP3A during NAFLD. Hepatic CYP3A11 (major subtype of mouse CYP3A) mRNA and protein expression was significantly decreased in both mice fed a high-fat diet (HFD) for 8 weeks and palmitate (PA)-treated mouse primary hepatocytes. Similarly, in HepG2 cells, PA treatment significantly suppressed the CYP3A4 (major subtype of human CYP3A) mRNA level ...
Source: Chemico-Biological Interactions - July 23, 2019 Category: Molecular Biology Authors: Zeng H, Lin Y, Gong J, Lin S, Gao J, Li C, Feng Z, Zhang H, Zhang J, Li Y, Yu C Tags: Chem Biol Interact Source Type: research

Pro-atherogenic proteoglycanase ADAMTS-1 is down-regulated by lauric acid through PI3K and JNK signaling pathways in THP-1 derived macrophages.
Abstract The prevalence of atherosclerosis has increased significantly in the recent years due to sedentary lifestyle and high-fat diet. However, the association between saturated fat intake and the increased risk for atherosclerotic cardiovascular diseases remains heavily debated. Lauric acid belongs to the saturated fatty acid group and its unique medium chain fatty acid properties are proven to be beneficial to humans in many ways. Thus, the aim of this project is to investigate the effect of lauric acid on the expression of a disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS) genes-ADAMTS-1,...
Source: Molecular Biology Reports - April 14, 2019 Category: Molecular Biology Authors: Ong MH, Wong HK, Tengku-Muhammad TS, Choo QC, Chew CH Tags: Mol Biol Rep Source Type: research

High-fat diet consumption reduces hepatic folate transporter expression via nuclear respiratory factor-1
AbstractFolate is an essential micronutrient for biological function. The liver, a primary organ for folate metabolism and storage, plays an important role in folate homeostasis. Proton-coupled folate transporter (PCFT) and reduced folate carrier (RFC) are the major folate transporters responsible for folate uptake at basolateral membrane of hepatocytes. Low serum folate levels are frequently associated with obesity. We investigated the mechanism that regulated folate status in a mouse model with diet-induced obesity. Mice (C57BL/6J) were fed a high-fat diet (60% kcal fat) for 8  weeks. Mice displayed increased hepatic li...
Source: Journal of Molecular Medicine - September 4, 2018 Category: Molecular Biology Source Type: research

ERK5/KLF2 activation is involved in the reducing effects of puerarin on monocyte adhesion to endothelial cells and atherosclerotic lesion in apolipoprotein E-deficient mice
Publication date: August 2018Source: Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease, Volume 1864, Issue 8Author(s): Yan Deng, Tingwen Lei, Hongmei Li, Xiaochuan Mo, Zhuting Wang, Hailong OuAbstractPuerarin has properties of anti-oxidation and anti-inflammation, which has been demonstrated protective effects in atherosclerosis and other cardiovascular diseases. However, the detail molecular mechanism still remains unclear. Here, we determined whether the atheroprotective effect of puerarin was by reducing monocyte adhesion and explored the underlying mechanism. The results showed that puerarin dose- and ti...
Source: Biochimica et Biophysica Acta (BBA) Molecular Basis of Disease - July 10, 2018 Category: Molecular Biology Source Type: research

Cannabinoid receptor type 1 mediates high-fat diet-induced insulin resistance by increasing forkhead box O1 activity in a mouse model of obesity.
Abstract Hepatic glucose production is promoted by forkhead box O1 (FoxO1) under conditions of insulin resistance. The overactivity of cannabinoid receptor type 1 (CB1R) partly causes increased liver fat deposits and metabolic dysfunction in obese rodents by decreasing mitochondrial function. The aim of the present study was to investigate the role of FoxO1 in CB1R-mediated insulin resistance through the dysregulation of mitochondrial function in the livers of mice with high-fat diet (HFD)-induced obesity. For this purpose, male C57BL/6 mice were randomly assigned to groups and either fed a standard diet (ST...
Source: International Journal of Molecular Medicine - January 29, 2016 Category: Molecular Biology Authors: Chen CC, Lee TY, Kwok CF, Hsu YP, Shih KC, Lin YJ, Ho LT Tags: Int J Mol Med Source Type: research

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