Effects of Acipimox on the metabolism of free fatty acids and very low density lipoprotein triglyceride

In hepatocyte cultures maintained in the absence of extracellular fatty acids, at least 70% of the secreted very-low-density lipoprotein (VLDL) triacylglycerol was derived via lipolysis of intracellular triacylglycerol. This proportion was unchanged when the cells were exposed for 24 h to insulin or glucagon, hormones which decreased the overall secretion of intracellular triacylglycerol, or to chloroquine or tolbutamide, agents which inhibit lysosomal lipolysis. The rate of intracellular lipolysis was 2-3-fold greater than that required to maintain the observed rate of triacylglycerol secretion. Most of the fatty acids released were returned to the intracellular pool. Neither insulin nor glucagon had any significant effect on the overall lipolysis and re-esterification of intracellular triacylglycerol. In these cases a greater proportion of the released fatty acids re-entered the cellular pool, rather than being recruited for VLDL assembly. Tolbutamide inhibited intracellular lipolysis, but suppressed VLDL secretion to a greater extent. 3,5-Dimethylpyrazole did not affect lipolysis or VLDL secretion. The increased secretion of VLDL triacylglycerol observed after exposure of cells to insulin for 3 days was not accompanied by an increased rate of intracellular lipolysis. However, a larger proportion of the triacylglycerol secreted under these conditions may not have undergone prior lipolysis.

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Chronic treatment of curcumin improves hepatic lipid metabolism and alleviates the renal damage in adenine-induced chronic kidney disease in Sprague-Dawley rats

BMC Nephrology ◽

10.1186/s12882-019-1621-6 ◽

2019 ◽

Vol 20 (1) ◽

Cited By ~ 5

Author(s):

Hardik Ghelani ◽

Valentina Razmovski-Naumovski ◽

Dennis Chang ◽

Srinivas Nammi

Keyword(s):

Chronic Kidney Disease ◽

Fatty Acids ◽

Kidney Disease ◽

Free Fatty Acids ◽

Kidney Function ◽

Low Density Lipoprotein ◽

Density Lipoprotein ◽

Atherogenic Index ◽

Low Density ◽

Cardiovascular Morbidity And Mortality

Abstract Background Chronic kidney disease (CKD), including nephrotic syndrome, is a major cause of cardiovascular morbidity and mortality. The literature indicates that CKD is associated with profound lipid disorders due to the dysregulation of lipoprotein metabolism which progresses kidney disease. The objective of this study is to evaluate the protective effects of curcumin on dyslipidaemia associated with adenine-induced chronic kidney disease in rats. Methods Male SD rats (n = 29) were divided into 5 groups for 24 days: normal control (n = 5, normal diet), CKD control (n = 6, 0.75% w/w adenine-supplemented diet), CUR 50 (n = 6, 50 mg/kg/day curcumin + 0.75% w/w adenine-supplemented diet), CUR 100 (n = 6, 100 mg/kg/day curcumin + 0.75% w/w adenine-supplemented diet), and CUR 150 (n = 6, 150 mg/kg/day curcumin + 0.75% w/w adenine-supplemented diet). The serum and tissue lipid profile, as well as the kidney function test, were measured using commercial diagnostic kits. Results The marked rise in total cholesterol, low-density lipoprotein (LDL) cholesterol, very low-density lipoprotein (VLDL) cholesterol, triglycerides and free fatty acids in serum, as well as hepatic cholesterol, triglyceride and free fatty acids of CKD control rats were significantly protected by curcumin co-treatment (at the dose of 50, 100 and 150 mg/kg). Furthermore, curcumin significantly increased the serum high-density lipoprotein (HDL) cholesterol compared to the CKD control rats but did not attenuate the CKD-induced weight retardation. Mathematical computational analysis revealed that curcumin significantly reduced indicators for the risk of atherosclerotic lesions (atherogenic index) and coronary atherogenesis (coronary risk index). In addition, curcumin improved kidney function as shown by the reduction in proteinuria and improvement in creatinine clearance. Conclusion The results provide new scientific evidence for the use of curcumin in CKD-associated dyslipidaemia and substantiates the traditional use of curcumin in preventing kidney damage.

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Inflammatory effects of very low-density lipoprotein and fatty acids

Future Cardiology ◽

10.2217/14796678.2.3.315 ◽

2006 ◽

Vol 2 (3) ◽

pp. 315-323

Author(s):

Mikko PS Ares ◽

Maria M Stollenwerk

Keyword(s):

Fatty Acids ◽

Low Density Lipoprotein ◽

Density Lipoprotein ◽

Very Low Density Lipoprotein ◽

Low Density

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Stimulation of triacylglycerol synthesis in rat adipocytes by plasma very-low-density lipoproteins

Biochemical Journal ◽

10.1042/bj1760169 ◽

1978 ◽

Vol 176 (1) ◽

pp. 169-174 ◽

Cited By ~ 5

Author(s):

P Thomopoulos ◽

M Berthelier ◽

D Lagrange ◽

M J Chapman ◽

M H Laudat

Keyword(s):

Fatty Acids ◽

Low Density Lipoprotein ◽

Density Lipoprotein ◽

Low Density Lipoproteins ◽

High Density Lipoproteins ◽

Very Low Density Lipoprotein ◽

Low Density ◽

Very Low Density Lipoproteins ◽

Rat Adipocytes ◽

Triacylglycerol Synthesis

The effect of human plasma lipoproteins on lipogenesis from glucose has been studied in isolated rat adipocytes. The very-low-density lipoproteins increased lipogenesis specifically, whereas low-density lipoproteins and high-density lipoproteins were without effect. Such stimulation could be reproduced with partially delipidated very-low-density lipoproteins. Nod-esterified fatty acids and glycerol were also without effect. Pretreatment of the adipocytes with trypsin did not alter the effect of very-low-density lipoprotein. The presence of Ca2+ was required for the full activation of lipogenesis. The synthesis of acylglycerol fatty acids and of acylglycerol glycerol were equally increased. The effect of very-low-density lipoprotein was not additive to that of insulin. It is suggested that very-low-density lipoprotein may directly stimulate lipogenesis in fat-cells, particularly in states when the lipoproteins are present at high concentration in the circulation.

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