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Very Low-density Lipoprotein (very + low-density_lipoprotein)
Terms modified by Very Low-density Lipoprotein Selected AbstractsFate of fatty acids at rest and during exercise: regulatory mechanismsACTA PHYSIOLOGICA, Issue 4 2003M. D. Jensen Abstract Fatty acids are a major fuel source for humans both at rest and during exercise. Plasma free fatty acids (FFA), although present only in micromolar concentrations, are the major circulating lipid fuel. FFA availability can increase two- to four-fold with moderate intensity exercise. Other potential sources of fatty acids include circulating very low-density lipoprotein (VLDL) triglycerides (TGs) (,1/5 the fuel availability of FFA) and intramyocellular TGs (,2 mmol kg,1 muscle). At rest ,40% of systemic FFA uptake occurs in the splanchnic bed and uptake in legs is ,15,20%. During leg exercise the uptake of FFA in leg tissue increases to 30,60% of systemic uptake and splanchnic uptake decreases to 15%. The fate of VLDL TG fatty acids has not been adequately studied. Intramyocellular TG hydrolysis increases during exercise, but the factors that regulate this response are not clear. The fact that contraction of isolated muscles can stimulate the hydrolysis and oxidation of intramyocellular TGs (in the absence of hormonal or neural input) suggests an intracellular regulation of this process. Additional regulation from changes in catecholamines and insulin may also occur. During moderate intensity exercise circulating FFA and intramyocellular TG provide roughly equal portions of fatty acids for oxidation. In addition to endurance training, dietary factors have been shown to modulate the fatty acid oxidation response to exercise. Much remains to be learned about fatty acid trafficking during exercise. What role do VLDL TG play? How is the oxidation of intramyocellular TGs regulated? Techniques to address these questions in humans are only now becoming available. [source] Glibenclamide improves postprandial hypertriglyceridaemia in Type 2 diabetic patients by reducing chylomicrons but not the very low-density lipoprotein subfraction levelsDIABETIC MEDICINE, Issue 10 2001I. Skrapari Abstract Aim, There are scarce data dealing with the degree of postprandial lipaemia after sulphonylurea administration. The aim of this study was to examine the effect of acute glibenclamide administration on postprandial lipaemia in Type 2 diabetic patients. Methods, Eight randomly selected Type 2 diabetic individuals, aged 43,65 years (mean, 54 years), who had never received any anti-diabetic drug, were included in the study. Each patient was given a 485 kcal mixed meal (45% fat, 40% carbohydrate and 15% protein) twice on separate days after an overnight fast: once with placebo and once with 5 mg glibenclamide, per os, in a random order. The two tests were performed with an interval of 7 days. Venous blood samples were drawn just before and 2 h, 4 h and 6 h after meal consumption. Total triglyceride levels in plasma, in chylomicrons (CM), in CM-deficient plasma, in very low-density lipoprotein (VLDL) subfractions (VLDL-1, VLDL-2) and in intermediate-density lipoprotein (IDL) were determined. Free fatty acid (FFA) and total cholesterol levels in plasma, as well as high-density lipoprotein (HDL) cholesterol and low-density lipoprotein (LDL) cholesterol levels in CM-deficient plasma, were also measured. Finally, serum glucose, insulin and C-peptide concentrations were measured in each sample. Results, As expected there was a significant decrease in postprandial glycaemia after glibenclamide administration compared to placebo (mean area under the curve values: AUC = 53.3 ± 18.2 and 69.1 ± 21.6 mm/h, P = 0.00009). In addition, the mean AUC values of insulin and C-peptide were significantly greater after drug administration. The AUC values of total plasma triglyceride and of CM triglyceride following glibenclamide administration were significantly lower compared to placebo, while the AUC values of postprandial triglyceride in CM-deficient plasma and of postprandial triglyceride in VLDL-1, VLDL-2 and IDL were not different after drug administration compared to placebo. Finally, no significant differences were noted in the AUC values of total cholesterol, LDL cholesterol, HDL cholesterol and plasma FFA levels after glibenclamide administration. Conclusions, These results demonstrate that glibenclamide administration improves postprandial hypertriglyceridaemia acutely by reducing postprandial triglycerides of intestinal origin. Diabet. Med. 18, 781,785 (2001) [source] Metabolism of cholesterol ester of apolipoprotein B100-containing lipoproteins in dogs: evidence for disregarding cholesterol ester transferEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 8 2004E. Bailhache Abstract Background, It has been shown that dogs exhibit no cholesterol ester transfer protein (CETP) activity in vitro, in contrast to humans. The aim of our study was to determine modalities of in vivo plasma cholesterol ester turnover in this species, using a kinetic approach with stable isotopes. Materials and methods, Kinetics of very low-density lipoprotein (VLDL) and low-density lipoprotein (LDL) were studied in seven adult male Beagle dogs using a dual isotope approach through endogenous labelling of both their cholesterol moiety and their protein moiety. A primed constant infusion of both [1,213C]acetate and [5,5,5- 2H3]leucine enabled us to obtain measurable deuterium enrichments by gas chromatography-mass spectrometry for plasma leucine and apoB100, as well as measurable 13C enrichment by gas chromatography-combustion-isotopic ratio mass spectrometry for unesterified cholesterol and cholesterol ester in the VLDL and LDL. Two identical multicompartmental models (SAAM II) were used together for the analysis of tracer kinetics' data of proteins and cholesterol. Results, Characterization of the apoB100-containing lipoprotein cholesterol ester model allowed determination of kinetic parameters of VLDL and LDL cholesterol ester metabolism. We succeeded in modelling VLDL and LDL cholesterol ester metabolism and apoB100 metabolism simultaneously. Fractional catabolic rate (FCR) of apoB100 and CE had the same values. Introducing cholesterol ester transfer between lipoproteins in the model did not significantly improve the fit. Total VLDL FCR was 2·97 ± 01·47 h,1. Approximately one-quarter corresponded to the direct removal of VLDL (0·81 ± 00·34 h,1) and the remaining three-quarters corresponded to the fraction of VLDL converted to LDL, which represented a conversion of VLDL into LDL of 2·16 ± 01·16 h,1. Low-density lipoproteins were produced exclusively from VLDL conversion and were then removed (0·031 ± 0·004 h,1) from plasma. Conclusion, These kinetic data showed that VLDL cholesterol ester and LDL cholesterol ester metabolism followed VLDL and LDL apoB100 metabolism, and that consequently there is no in vivo transfer of cholesterol ester in dogs. [source] LIPID-LOWERING EFFICACY OF PIPERINE FROM PIPER NIGRUM L. IN HIGH-FAT DIET AND ANTITHYROID DRUG-INDUCED HYPERCHOLESTEROLEMIC RATSJOURNAL OF FOOD BIOCHEMISTRY, Issue 4 2006RAMASAMY SUBRAMANIAM VIJAYAKUMAR ABSTRACT Male Wistar rats were divided into two groups: control diet group and high-fat diet group (HFD). Both groups were divided into four subgroups, each consisted of 10 animals, and the diets were supplemented with the following ingredients for 10 weeks: (1) 1% carboxymethyl cellulose; (2) 10 mg carbimazole (CM)/kg body weight; (3) 10 mg CM + 40 mg piperine/kg body weight; and (4) 10 mg CM + 2 mg atorvastatin/kg body weight. Feeding HFD to rats significantly (P < 0.05) elevated plasma total cholesterol, triglycerides, phospholipids, free fatty acids, low-density lipoprotein (LDL), very low-density lipoprotein (VLDL) and the activity of 3-hydroxy 3-methyl glutaryl coenzyme A (HMG CoA) reductase in the liver, heart and aorta, while the activities of plasma and tissue lipoprotein lipase (LPL) and plasma lecithin cholesterol acyl transferase (LCAT) and high-density lipoprotein were significantly (P < 0.05) lowered compared to control rats. Supplementing piperine with HFD significantly (P < 0.05) reduced the levels of plasma total cholesterol, LDL, VLDL tissue HMG CoA reductase and significantly (P < 0.05) elevated the levels of LPL and LCAT compared to rats that did not receive piperine. Fecal bile acids and neutral sterols were also elevated in HFD-fed rats as compared to control animals, while simultaneous supplementation of piperine significantly (P < 0.05) enhanced further excretion of bile acids and neutral sterols. The results indicate that piperine can prevent the accumulation of plasma lipids and lipoproteins significantly by modulating the enzymes of lipid metabolism. [source] l -carnitine supplementation and lipid metabolism of rats fed a hyperlipidaemic dietJOURNAL OF ANIMAL PHYSIOLOGY AND NUTRITION, Issue 3 2000K. Eder Summary Until now, there has been no clear knowledge about the effect of dietary carnitine supplementation on lipid metabolism. Therefore, this study was conducted to investigate the effect of a dietary l -carnitine supplementation (500 mg/kg) onx the lipid metabolism of adult rats. Rats fed a hyperlipidaemic basal diet containing 15% lard and 1% cholesterol were used as an animal model. The feeding period was 6 weeks. As parameters of lipid metabolism, the concentrations of individual lipids in plasma, lipoproteins and liver and the fatty acid composition of liver and erythrocyte total lipids were determined. There were no significant differences between the control group and the group receiving the diet supplemented with carnitine on parameters of animal performance (daily body weight gains and feed conversion ratio). As expected, plasma, very low-density lipoproteins (VLDL) and liver exhibited high concentrations of cholesterol. Concentrations of triglycerides and phospholipids in plasma and individual lipoproteins as well as the concentrations of triglycerides, cholesterol and phospholipids in the liver were not significantly altered by dietary carnitine supplementation. The concentration of cholesterol in plasma and liver was increased by dietary carnitine. The fatty acid composition of liver and erythrocyte total lipids was not influenced by dietary carnitine supplementation. In conclusion, this study does not indicate a lipid-lowering effect of dietary carnitine supplementation in hyperlipidaemic rats. Probably, the essential functions of carnitine in metabolism were realized by carnitine which was synthesized endogenously. [source] Apolipoprotein B: a clinically important apolipoprotein which assembles atherogenic lipoproteins and promotes the development of atherosclerosisJOURNAL OF INTERNAL MEDICINE, Issue 5 2005S.-O. OLOFSSON Abstract. Apolipoprotein (apo) B exists in two forms apoB100 and apoB48. ApoB100 is present on very low-density lipoproteins (VLDL), intermediate density lipoproteins (IDL) and LDL. ApoB100 assembles VLDL particles in the liver. This process starts by the formation of a pre-VLDL, which is retained in the cell unless converted to the triglyceride-poor VLDL2. VLDL2 is secreted or converted to VLDL1 by a bulk lipidation in the Golgi apparatus. ApoB100 has a central role in the development of atherosclerosis. Two proteoglycan-binding sequences in apoB100 have been identified, which are important for retaining the lipoprotein in the intima of the artery. Retention is essential for the development of the atherosclerotic lesion. [source] | |||||||||||||