Catabolic defect of triglyceride is associated with abnormal very-low-density lipoprotein in experimental nephrosis

Furukawa, Seiichi; Hirano, Tsutomu; Mamo, John; Nagano, Seishi; Takahashi, Takehiro

doi:10.1016/0026-0495(90)90155-6

Cited by 55 publications

(33 citation statements)

References 34 publications

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“…1416 - 47 ' 48 As shown in Fig 1, 3-thiadicarboxylic acid treatment decreased hepatic VLDL triglyceride secretion by 26%. Interestingly, this decrease was of the same magnitude as the increase in the VLDL secretion rate reported in experimental nephrosis, 45 indicating that drug treatment rectified the VLDL overproduction present in the nephrotic syndrome. It is noteworthy that the specific mechanisms underlying the increase in VLDL synthesis present in nephrosis are still largely unknown.…”

Section: Discussionsupporting

confidence: 61%

“…45 Since 3-thiadicarboxylic acid decreases VLDL triglyceride production in normal rats, 12 it was of interest to investigate whether this was also the case under the present hyperlipidemic conditions. For this purpose, rats were injected with Triton WR 1339, a detergent that inhibits the action of lipoprotein lipase on triglyceride-rich lipoproteins.…”

Section: Resultsmentioning

confidence: 99%

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

Al‐Shurbaji

Skorve

Berge

et al. 1993

Arterioscler Thromb

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The effect of the sulfur-substituted fatty acid analogue 1,10 6i?(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 /3-oxidation of fatty acids ninefold and the mitochondrial /3-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.

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Section: Discussionsupporting

confidence: 61%

Section: Resultsmentioning

confidence: 99%

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

Al‐Shurbaji

Skorve

Berge

et al. 1993

Arterioscler Thromb

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“…The scarcity of cholesterol ester-rich HDL in nephrotic syndrome contributes to an impairment of VLDL and chylo micron metabolism, and limits the delivery of lipids to myocytes for energy production and to adipose tissue for storage 48 . The contribution of HDL abnormalities to the pathogenesis of impaired VLDL metabolism in nephrotic syndrome has been clearly demonstrated in vivo, where impaired endothelial binding and LPLmediated lipolysis of VLDL in nephrotic rats could be corrected by infusion of HDL from healthy animals 49,50 . These findings have been further supported by in vitro experiments that showed defective maturation of nascent VLDL in the presence of nephrotic HDL and its subsequent correction with the addition of normal HDL 40 .…”

Section: Consequences Hdl Abnormalitiesmentioning

confidence: 99%

HDL abnormalities in nephrotic syndrome and chronic kidney disease

2015

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| Normal HDL activity confers cardiovascular and overall protection by mediating reverse cholesterol transport and through its potent anti-inflammatory, antioxidant, and antithrombotic functions. Serum lipid profile, as well as various aspects of HDL metabolism, structure, and function can be profoundly altered in patients with nephrotic range proteinuria or chronic kidney disease (CKD). These abnormalities can, in turn, contribute to the progression of cardiovascular complications and various other comorbidities, such as foam cell formation, atherosclerosis, and/or glomerulosclerosis, in affected patients. The presence and severity of proteinuria and renal insufficiency, as well as dietary and drug regimens, pre-existing genetic disorders of lipid metabolism, and renal replacement therapies (including haemodialysis, peritoneal dialysis, and renal transplantation) determine the natural history of lipid disorders in patients with kidney disease. Despite the adverse effects associated with dysregulated reverse cholesterol transport and advances in our understanding of the underlying mechanisms, safe and effective therapeutic interventions are currently lacking. This Review provides an overview of HDL metabolism under normal conditions, and discusses the features, mechanisms, and consequences of HDL abnormalities in patients with nephrotic syndrome or advanced CKD.

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“…Thus, the TG levels are assumed to be regulated by factors other than hepatic FA synthesis and FA mobilization. Such factors may include: (a) increased FA oxidation in the liver, (b) increased clearance of TG-rich lipoproteins by lipoprotein lipase (LPL), and (c) normalization of abnormal lipoprotein composition which is observed in nephrosis and retards the hydrolysis of lipoprotein-TG by LPL (30,31). Further studies are needed to clarify these aspects.…”

Section: Discussionmentioning

confidence: 99%

Reduction of Hypercholesterolemia and Proteinuria in Nephritic Rats by Low-Meat-Protein Diets.

Yagasaki

Ebara

Fujisawa

et al. 1994

Journal of Nutritional Science and Vitaminology, J Nutr Sci Vit

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SummaryThe effects of low-meat-protein diets on hypercholesterol emia and proteinuria were studied in rats with nephrotoxic serum nephri tis. After an injection of nephrotoxic serum, rats were given either a 20% meat-protein diet (20M), an 8.5%-meat-protein diet (8.5M), or a valine (0.05%)-supplemented 8.5%-meat-protein diet (8.5MV) for 12days. Urinary protein excreted from the 20M-fed, nephritic control rats in creased rapidly and linearly during the initial 3days, and thereafter the high excretion rate was maintained for up to 12days. Two low-meat protein diets (8.5M, 8.5MV) commenced to suppress proteinuria 3days after feeding and the suppression was preserved during the rest of the experimental periods. Compared with the 20M, both low-meat-protein diets significantly improved hypercholesterolemia induced in this nephrit ic model. These two diets significantly enhanced the fecal excretion of neutral sterols. They caused neither fatty liver nor severe growth retarda tion. These effects of 8.5MV were identical to those of 8.5M. The results suggest that low-meat-protein feeding, without amino acid supplementa tion, improves hypercholesterolemia and proteinuria in nephritis without severe protein malnutrition. The results also suggest that the hypochole sterolemic effect of the low-meat-protein diets may be, at least in part, attributed to increased fecal excretion of steroids.

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Catabolic defect of triglyceride is associated with abnormal very-low-density lipoprotein in experimental nephrosis

Cited by 55 publications

References 34 publications

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

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

HDL abnormalities in nephrotic syndrome and chronic kidney disease

Reduction of Hypercholesterolemia and Proteinuria in Nephritic Rats by Low-Meat-Protein Diets.

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