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Several abnormalities of lipid metabolism, ..

T1 - Increased catabolism of VLDL-apolipoprotein B and synthesis of bile acids in a case of hypobetalipoproteinemia

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while HCV-LDL induced an increased TG synthesis.

Hepatocytes play a crucial role in regulating lipid metabolism by exporting cholesterol and triglyceride into plasma through secretion of very low density lipoproteins (VLDL). VLDL production is also required for release of hepatitis C virus (HCV) from infected hepatocytes. Here, we show that long chain acyl-CoA synthetase 3 (ACSL3) plays a crucial role in secretion of VLDL and HCV from hepatocytes. In cultured human hepatoma Huh7 cells, ACSL3 is specifically required for incorporation of fatty acids into phosphatidylcholine. In cells receiving small interfering RNA targeting ACSL3, secretion of apolipoprotein B, the major protein component of VLDL, was inhibited and the lipoprotein was rapidly degraded. This inhibition in secretion was completely eliminated when these cells were treated with phosphatidylcholine. Treatment of cells with small interfering RNA targeting ACSL3 also inhibited secretion of HCV from Huh7-derived cells. These results identify ACSL3 as a new enzymatic target to limit VLDL secretion and HCV infection.

T1 - Effect of 3-thiadicarboxylic acid on lipid metabolism in experimental nephrosis

T1 - Long chain Acyl-CoA synthetase 3-mediated phosphatidylcholine synthesis is required for assembly of very low density lipoproteins in human hepatoma Huh7 cells

Synthesis of VLDL-triglycerides was also ..

Gebhard RL, Clayman RV, Prigge WF, et al:Abnormal cholesterol metabolism in renal clear cell carcinoma. JLipid Res. 28:1177–1184. 1987.

Hyperglycemia is the major factor, inducing metabolic lipid changes by increasing hepatic synthesis of triglycerides and promoting lipoprotein and apolipoprotein glycosylation and oxidation.

AB - The effect of the sulfur-substituted fatty acid analogue 1,10 bis(carboxymethylthio)decane, also known as 3-thiadicarboxylic acid, on puromycin aminonucleoside-induced nephrotic hyperlipidemia was studied in rats. Treatment with 3-thiadicarboxylic acid (250 mg/kg) for 5 days reduced plasma levels of triglycerides from 5.8 to 2.7 mmol/L and cholesterol from 11.0 to 7.7 mmol/L. This was accounted for by decreases in very-low-density lipoprotein triglycerides, very-low-density lipoprotein cholesterol, and low-density lipoprotein cholesterol, without any major changes in the composition of plasma lipoproteins. The activities of two enzymes involved in fatty acid synthesis (ATP:citrate lyase and fatty acid synthetase) were inhibited by 3-thiadicarboxylic acid treatment, whereas acetyl-coenzyme A carboxylase activity was unchanged. In contrast, treatment with the sulfur-substituted fatty acid analogue induced the peroxisomal β-oxidation of fatty acids ninefold and the mitochondrial β-oxidation by 54% to 73%, depending on the substrate used. This was accompanied by a 26% reduction in hepatic triglyceride secretion rate. The hepatic phosphatidate phosphohydrolase activity was unchanged. 3-Thiadicarboxylic acid treatment suppressed the activity of the rate-limiting enzyme in cholesterol biosynthesis, 3-hydroxy-3-methylglutaryl-coenzyme A reductase, by 58%, whereas hepatic LDL receptor expression was unaltered. The activities of lipoprotein lipase and hepatic lipase were unchanged by treatment. These results demonstrated that treatment with 3-thiadicarboxylic acid ameliorates hyperlipidemia in experimental nephrosis primarily by decreasing the overproduction of very-low-density lipoprotein present. The data also indicate that hepatic very-low-density lipoprotein synthesis and secretion is strongly influenced by the availability of the fatty acid substrate under the same hyperlipidemic conditions.

The source of the fatty acids for TG synthesis has ..

Kidney cancer is the third most common genitourinarycancer with 64,770 new cases per year in the US in 2012 (,). Themajority (75%) are renal clear cell carcinomas (RCC), which havethe highest mortality to incidence ratios or all urologicmalignancies resulting in 13,570 deaths per year due to theirextreme insensitivity to chemo- and radiation therapy. Theincidence is twice as high in men than women and associated withrisk factors such as: advanced age, tobacco use, and obesity(,). In the majority of RCC, the HIF1complex is constitutively activated due to mutation of the VonHippel-Lindau tumor suppressor (VHL), gene and inactivation of theprolyl hydro-xylation that targets the HIFs to be degraded(,). As a result of HIF1 stabilization,there is an induction of a hypoxic gene expression program (GLUT1,VEGF, iNOS, EPO) that support proteins involved in angiogenesis andoxygenation (,,).This had led to therapies targeting angiogenesis which haveachieved only partial responses (,),and the necessity for further research into new factors involved inRCC progression. A role for elevated tumor cell cholesterol andaltered lipid metabolism has been implicated in the etiology anddisease progression in renal clear cell cancer based on itspotential for apoptotic interference (,–).Currently favored theories propose that RCC consists of a group ofdiseases of abnormal metabolism relating to oxygen, iron, energyand nutrient sensing pathways (,,).The concept of an aberrant metabolic phenotype of RCC has beenfurther supported by several studies elaborating mechanisms ofdefects in mitochondrial metabolism in the TCA cycle that lead tometabolic imbalance and HIF1 stabilization (–).Our current study of the role of TERE1 in RCC is based on its rolein synthesis of menaquinone ()that exerts profound influence on mitochondrial function, oxidativeand nitrosative stress, and regulation of lipid metabolism viaactivation of SXR nuclear receptor signaling, and several othermechanisms that lead to growth inhibition and increased apoptosis().

Studies performed with insulin dependent children showed early changes in lipid metabolism, usually correlated and aggravated by poor glycemic control.

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  • Reduced insulin-mediated inhibition of VLDL secretion …

    KW - Lipoprotein synthesis

  • to very low-density lipoprotein (VLDL) and low-density ..

    The effects of pharmacological LXR ligands on insulin's action on hepatic lipid metabolism ..

  • The activities of two enzymes involved in fatty acid synthesis ..

    VLDL-TG synthesis, ..

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Lipid and lipoprotein levels of his ..

N2 - Hepatocytes play a crucial role in regulating lipid metabolism by exporting cholesterol and triglyceride into plasma through secretion of very low density lipoproteins (VLDL). VLDL production is also required for release of hepatitis C virus (HCV) from infected hepatocytes. Here, we show that long chain acyl-CoA synthetase 3 (ACSL3) plays a crucial role in secretion of VLDL and HCV from hepatocytes. In cultured human hepatoma Huh7 cells, ACSL3 is specifically required for incorporation of fatty acids into phosphatidylcholine. In cells receiving small interfering RNA targeting ACSL3, secretion of apolipoprotein B, the major protein component of VLDL, was inhibited and the lipoprotein was rapidly degraded. This inhibition in secretion was completely eliminated when these cells were treated with phosphatidylcholine. Treatment of cells with small interfering RNA targeting ACSL3 also inhibited secretion of HCV from Huh7-derived cells. These results identify ACSL3 as a new enzymatic target to limit VLDL secretion and HCV infection.

lipid changes by increasing hepatic synthesis of ..

AB - Hepatocytes play a crucial role in regulating lipid metabolism by exporting cholesterol and triglyceride into plasma through secretion of very low density lipoproteins (VLDL). VLDL production is also required for release of hepatitis C virus (HCV) from infected hepatocytes. Here, we show that long chain acyl-CoA synthetase 3 (ACSL3) plays a crucial role in secretion of VLDL and HCV from hepatocytes. In cultured human hepatoma Huh7 cells, ACSL3 is specifically required for incorporation of fatty acids into phosphatidylcholine. In cells receiving small interfering RNA targeting ACSL3, secretion of apolipoprotein B, the major protein component of VLDL, was inhibited and the lipoprotein was rapidly degraded. This inhibition in secretion was completely eliminated when these cells were treated with phosphatidylcholine. Treatment of cells with small interfering RNA targeting ACSL3 also inhibited secretion of HCV from Huh7-derived cells. These results identify ACSL3 as a new enzymatic target to limit VLDL secretion and HCV infection.

Effects of glucose metabolism on the regulation of …

Glucose disposal induces a signal that modulates the transcriptional regulation of genes involved in the glycolysis and lipogenesis pathways. To investigate the role of glucose metabolism on hepatic gene expression independently from insulin action, we overexpressed glucokinase, the limiting enzyme in the glycolysis pathway, in the liver of streptozotocin-induced type 1 diabetic rats. By microarray analysis, we observed that critical genes such as liver-type pyruvate kinase, malic enzyme, fatty acid synthase, and stearoyl-CoA desaturase 1 were enhanced multiple-fold, whereas genes involved in mitochondrial fatty acid oxidation and the Krebs cycle were downregulated. Despite the increase in expression of fatty acid synthesis genes and the presence of steatosis, no major alterations to the levels of genes involved in VLDL assembly and secretion, such as diacylglycerol acyltransferases 1 and 2 and microsomal triglyceride transfer protein, were observed. Overall, our data suggest that the gene expression pattern induced by glucose metabolism favors fatty acid storage in the liver rather than secretion into the circulation.

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