Obesity-driven prepartal hepatic lipid accumulation in dairy cows is associated with increased CD36 and SREBP-1 expression

Prodanović, Radivoje; Korićanac, Goran; Vujanac, Ivan; Djordjević, Ana; Pantelić, Marija; Romić, Snježana; Stanimirović, Zoran; Kirovski, Danijela

doi:10.1016/j.rvsc.2016.04.007

Cited by 24 publications

(19 citation statements)

References 28 publications

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“…Moreover, lipid trafficking relies on the biofunction of liver lipoprotein lipase (LPL) and fatty acid translocase (CD36) in the liver. The hepatocellular LPL regulates lipid intake via hydrolyzing lipoproteins, and hepatic CD36 plays key role in transporting the lipids from blood into the liver (Scott, 2015;Prodanović et al, 2016). As results, notable upregulation of LPL and CD36 expressions both in mRNA and protein levels were observed in PFOA-exposed liver.…”

Section: Accepted Manuscriptmentioning

confidence: 76%

The impact of exposure to environmental contaminant on hepatocellular lipid metabolism

Hui

Chen

2017

Gene

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Section: Accepted Manuscriptmentioning

confidence: 76%

The impact of exposure to environmental contaminant on hepatocellular lipid metabolism

Hui

Chen

2017

Gene

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“…The SREBP-1c is a master transcriptional regulator of lipid synthesis by stimulating the expression of lipogenic genes ACC1, FAS, SCD1, DGAT1, and DGAT2 (Li et al, 2014. Increased expression of hepatic SREBP-1c is relevant in lipid accumulation in the liver of dairy cows (Prodanović et al, 2016), we therefore detected the expression levels of SREBP-1c and its target genes (ACC1, FAS, SCD1, DGAT1, and DGAT2). The results showed that the protein expression of SREBP-1c and gene expression of TG synthesis genes, SREBP1, DGAT1, and DGAT2, in the liver of CK cows were markedly higher than those of control cows, which was consistent with increased TG accumulation in CK cows.…”

Section: Discussionmentioning

confidence: 99%

Expression patterns of hepatic genes involved in lipid metabolism in cows with subclinical or clinical ketosis

Zhu¹,

Liu²,

et al. 2019

Journal of Dairy Science

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“…SREBP-1c is a major transcription regulator of lipid synthesis. It has been shown in cows that increasing the expression of SREBP-1c in liver correlates with lipid accumulation [26]. In addition, the expression of SREBP-1c increased significantly in the case of liver triglyceride accumulation [27].…”

Section: Discussionmentioning

confidence: 99%

ACSL1 affects Triglyceride Levels through the PPARγ Pathway

Li¹,

Li²,

Meng³

et al. 2020

Int. J. Med. Sci.

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In clinical cohort studies, high expression of long-chain acyl-coenzyme A synthetases 1 (ACSL1 gene) in peripheral white blood cells of patients with acute myocardial infarction (AMI) has been utilized as molecular markers of myocardial infarction diagnosis. The plasma triglyceride level of AMI patients is significantly higher than that of healthy individuals. We hypothesized that the high expression of ACSL1 increases the level of triglyceride, which is one of the pathogenesis of AMI promoted by ACSL1. In this report, cell culture based methods were adopted to test the hypothesis and further investigate the effect and mechanism of ACSL1 on lipid metabolism. In this study, liver cells of healthy individuals were cultured, the overexpression and the knockdown vectors of ACSL1 were constructed and transfected into liver cells. The transfection was verified at the mRNA and protein level. Intracellular triglyceride content was quantitatively analyzed using ELISA. Changes of genes related to lipid metabolism were subsequently measured through PCR array. Overexpression of ACSL1 led to higher gene expression and protein levels compared to control and the triglyceride content was significantly increased in overexpressing cells. The expression level of fatty acid oxidation pathway PPARγ was significantly down-regulated compared with the control group, as were genes associated with fatty acid synthesis pathways: SREBP1, ACC, FAS, and SCD1. ACSL1 knockdown decreased the content of triglyceride whereas PPARγ was up-regulated and SREBP1, ACC, FAS, and SCD1 were down-regulated compared with the control group. In summary, high expression of ACSL1 reduced fatty acid β-oxidation through the PPARγ pathway, thereby increasing triglyceride levels.

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Obesity-driven prepartal hepatic lipid accumulation in dairy cows is associated with increased CD36 and SREBP-1 expression

Cited by 24 publications

References 28 publications

The impact of exposure to environmental contaminant on hepatocellular lipid metabolism

The impact of exposure to environmental contaminant on hepatocellular lipid metabolism

Expression patterns of hepatic genes involved in lipid metabolism in cows with subclinical or clinical ketosis

ACSL1 affects Triglyceride Levels through the PPARγ Pathway

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