Triglycerides VLDLs

Apo, apolipoprotein C, cholesterol HDL, high-density lipoprotein LDL, low-density lipoprotein TG, triglyceride VLDL, very low-density lipoprotein. 

Hyperlipidemia with skin xanthomas elevation of triglycerides (VLDL)... 

Figure 3.10 Uptake of blood constituents by the mammary gland CoA, coenzyme A G-3-P, glycerol-3-phosphate FFA, free fatty acid FA, fatty acid TG, triglyceride, VLDL, very low density lipoprotein (from Hawke and Taylor, 1995).

In a prospective study of lipid changes in 36 patients with chronic hepatitis C treated with interferon alfa for 6 months, the most prominent findings included increases in triglycerides, VLDL cholesterol, and apolipoprotein B, and falls in HLD cholesterol and apolipoprotein Al... 

Cholesterol is found in all lipoprotein particles but is relatively concentrated in LDL and HDL, whereas triglycerides are relatively concentrated in chylomicrons and VLDL. Heart disease appears to correlate with increased LDL and decreased HDL. Elevated HDL generally is a favorable finding, as HDL shunts excess cholesterol back to the liver (via LDL remnant particles) where it can be excreted. Chylomicrons, VLDL, and LDL, on the other hand, carry triglycerides and cholesterol to the periphery (fig. 6.4). The more significant clinical conditions involve elevation of cholesterol, triglycerides, VLDL, LDL, and/or chylomicrons, rather than HDL. 

Niacin (but not niacinamide) is also indicated in hyperlipidemia to lower uiglycerides and cholesterol. Triglycerides. VLDL.S, and LDLs are reduced HDLs are increased. The exact mechanism is not known. Because niacin at high doses has a direct vasodilatory effect believed to be mediated through the prostaglandins, the dose required (1 to 3 g 3 times daily) often limits the usefiilne.ss. 

Woifrum, C., and Stoffel, M. Coactivation of Foxa2 through Pgc-lbeta promotes liver fatty acid oxidation and triglyceride/VLDL secretion. Ceil Metab 3 (2006) 99-110. 

ABBREVIATIONS apo, apoHpoprotein CHOL, cholesterol HDL, high-density lipoproteins IDL, intermediate-density lipoproteins Lp(a), lipoprotein(a) LDL, low-density lipoproteins NS, not significant (triglyceride is less than 5% of LDL and HDL) TG, triglyceride VLDL, very-low-density lipoproteins HL, hepatic lipase LPL, lipoprotein lipase. 

Cholestyramine (Questran) Forms insoluble complex with bile salts, excreted in feces. Body compensates by increasing LDL receptors and oxidizing cholesterol to bile acids. LDL > 190 mg/dl (160 with 2 risk factors) provided that 6 month trial of low lipid diet has failed. i Cholesterol, LDL T Triglycerides, VLDL, HDL ... 

Table 3. Effect of dietary EPA, DHA and palmitic acid on serum very-low density lipoprotein triglycerides (VLDL-TG) and hepatic volume fractions of mitochondria and peroxisomes.

Protein that transfers lipids among lipoproteins, especially cholesteryl ester from HDL to VLDL in exchange for triglycerides. 

Lipoprotein formed by hydrolysis of triglycerides in VLDL elevated in type III hyperlipoproteinemia. 

PLTP is responsible for the majority of phospholipid transfer activity in human plasma. Specifically, it transfers surface phospholipids from VLDL to HDL upon lipolysis of triglycerides present in VLDL. The exact mechanism by which PLTP exerts its activity is yet unknown. The best indications for an important role in lipid metabolism have been gained from knockout experiments in mice, which show severe reduction of plasma levels of HDL-C and apoA-I. This is most likely the result of increased catabolism of HDL particles that are small in size as a result of phospholipid depletion. In addition to the maintenance of normal plasma HDL-C and apoA-I concentration, PLTP is also involved in a process called HDL conversion. Shortly summarized, this cascade of processes leads to fusion of HDL... 

Endothelial anchored enzyme in muscle and adipose tissue primarily responsible for hydrolysis of chylomicron and VLDL triglycerides. 

Disorders of lipoprotein metabolism involve perturbations which cause elevation of triglycerides and/or cholesterol, reduction of HDL-C, or alteration of properties of lipoproteins, such as their size or composition. These perturbations can be genetic (primary) or occur as a result of other diseases, conditions, or drugs (secondary). Some of the most important secondary disorders include hypothyroidism, diabetes mellitus, renal disease, and alcohol use. Hypothyroidism causes elevated LDL-C levels due primarily to downregulation of the LDL receptor. Insulin-resistance and type 2 diabetes mellitus result in impaired capacity to catabolize chylomicrons and VLDL, as well as excess hepatic triglyceride and VLDL production. Chronic kidney disease, including but not limited to end-stage... 

Lipoprotein fraction containing triglycerides and to a lesser degree cholesterol. VLDL is produced by the liver. The main structural protein connected to this lipoprotein class is apolipoprotein B. 

A daily intake of 25 and 30 g of GA for 21 to 30 days reduced total cholesterol by 6 and 10.4%, respectively (Ross et al., 1983, Sharma 1985). The decrease was limited only to LDL and VLDL, with no effect on HDL and triglycerides. However, Topping et al. (1985) reported that plasma cholesterol concentrations were not affected by the supply of GA, but triglyceride concentration in plasma was significantly lower than in controls. 

This approach can be used only for fat-soluble compounds that follow the same lymphatic route to be transported to the liver as carotenoids. The bioavailability of the compound of interest is determined by monitoring the appearance of the compound and its newly formed intestinal metabolites in the postprandial chylomicron fraction of plasma [also called the density < 1.006 kg/L fraction or triglyceride-rich lipoprotein (TRL) fraction because it is generally a mixture of chylomicrons (CMs) and very low density lipoproteins (VLDLs)] as a function of the time after ingestion. 

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