2017
DOI: 10.1002/mnfr.201600456
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Alleviating VLDL overproduction is an important mechanism for Laminaria japonica polysaccharide to inhibit atherosclerosis in LDLr−/− mice with diet‐induced insulin resistance

Abstract: These results suggested that LJP61A ameliorated HFD-induced insulin resistance to attenuate VLDL overproduction possibly via regulating insulin signaling, leading to the inhibition of atherosclerosis.

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Cited by 24 publications
(15 citation statements)
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“…In current research, miRNA-FoxO1 interference decreased the relative gene expression and the protein content of CPT1 and ACOX1, which indicated that fatty acid oxidation decreased after FoxO1 interference, which is in line with a previous study that FoxO1 proteins exerted important effects on fatty acid oxidation via the regulation of adipose triacylglycerol lipase reported by Zhang et al (2016). Zha et al (2017) reported that regulating PI3K-Akt-Foxo1 signaling pathway mediated by insulin receptor substrate alleviated VLDL overproduction. In this study, FoxO1 interference decreased the gene expression of MTP and ApoB, decreased the protein content of MTP, decreased VLDL-TG secretion and increased the intracellular TG content, which led to excessive fat accumulation in the liver cells.…”
Section: Discussionsupporting
confidence: 90%
“…In current research, miRNA-FoxO1 interference decreased the relative gene expression and the protein content of CPT1 and ACOX1, which indicated that fatty acid oxidation decreased after FoxO1 interference, which is in line with a previous study that FoxO1 proteins exerted important effects on fatty acid oxidation via the regulation of adipose triacylglycerol lipase reported by Zhang et al (2016). Zha et al (2017) reported that regulating PI3K-Akt-Foxo1 signaling pathway mediated by insulin receptor substrate alleviated VLDL overproduction. In this study, FoxO1 interference decreased the gene expression of MTP and ApoB, decreased the protein content of MTP, decreased VLDL-TG secretion and increased the intracellular TG content, which led to excessive fat accumulation in the liver cells.…”
Section: Discussionsupporting
confidence: 90%
“…However, because the roles of mTOR in lipogenesis and insulin signaling are also blocked, common side effects of their use are dyslipidemia and insulin resistance, which are both risk factors for atherosclerosis. In order to minimize these effects, which would lead to an increase of low-density lipoprotein cholesterol levels, additional use of cholesterol lowering drugs is a recommended strategy [195,196,197].…”
Section: Mtor and Age-related Diseasesmentioning
confidence: 99%
“…(1 (Figure 1) [13]. LJP61A has been proved to suppressing atherosclerosis via the regulation of cellular lipid metabolism, inhibition of cellular inflammation and alleviation of insulin resistance [13,14]. Additionally, we have demonstrated that LJP61A could ameliorate vascular calcification via preventing osteoblastic differentiation of vascular smooth muscle cells [15].…”
Section: Introductionmentioning
confidence: 87%