Glycerides serum

Lipoproteins. The lipid moiety of lipoproteins is quite variable both qualitatively and quantitatively. The a-lipoprotein of serum contains glyceride, phosphatide and cholesterol to about 30 -40% of the total complex. The -lipoprotein of serum contains some glyceride but the phosphatide and cholesterol account for nearly 75% of the total. 

Ellerbe PM, Sniegoski LT, and Welch MJ (1995) Isotope dilution mass spectrometry as a candidate definitive method for determining total glycerides and triglycerides in serum. Clin Chem 41 397-404. 

All serum Tipids, which consist of free cholesterol, glycerides, cholesterol ester and phospholipids, circulate in association with specific proteins (apo-lipoproteins) to form lipid-protein complexes. These macromolecular complexes are called "lipoproteins" and have remarkable hydrophilic properties, in spite of high lipid contents. Therefore, water insoluble lipids are transported from their organs for synthesis to their sites for utilization. Most serum lipoproteins have a molecular weight range from approximately 200,000 to 10,000,000 and contain from 40 % to 95 % of lipids. Studies of the factors affecting lipoprotein levels are very important for health and diseases, because lipoprotein levels are closely related to atherosclerosis and its clinical manifestations. 

Essential hyperlipemia is a term used for various syndromes associated with elevation of plasma glycerides, usually well in excess of other plasma lipids and not secondary to other known disease. Hyperglyceridemia, if marked, results in turbid or milky appearance of the serum. 

An enzyme which catalyses the hydrolysis of glycerides int( glycerol and fatty acids. Several types of lipase may be present ii normal plasma, including pancreatic lipase and lipoproteii lipase. Increased serum levels are found in acute pancreatitis ii much the same way as serum amylase. 

The extent of the work done on the relationship between dietary carbohydrates and serum glycerides in animals is small, but it seems that carbohydrates probably play a bigger part in determining the level of serum glycerides than in determining the level of serum cholesterol. 

Many dietary experiments in man are limited in time and it is obvious from some of the changes produced in the seram lipid levels that the elevations found cannot continue if the subject is to survive. The limitation in time is the result of the comparative diseomfort of subjects on a diet. However, Antonis and Bersohn (1961) were able to overcome this diflBculty to a certain extent by the use of volunteer prisoners who consumed a low-fat hi -carbohydrate diet for 39 weeks. They found that die volunteers on diis high-carbohydrate diet ( the nature of the carbohydrate is not disclosed) showed immediate and signifieant rises in their fasting serum glycerides, with peak values after 5 weeks on the diet. These high levels then subsided slowly and in some subjeets it took 32 weeks before the glyceride level returned to the base level. 

About this time Ahrens et al. (1961) postulated that there were two kinds of hyperlipemia in man one was fat-induced, and the other was carbohydrate-induced. The latter was associated widi a raised serum glyceride concentration, and this carbohydrate-induced type of lipemia is now well-established. 

It seems quite clear from these studies in man that a high-carbohydrate diet, accompanied as it is by a reduced fat intake, is associated with a fall in the serum phospholipid concentration unless the carbohydrate is sucrose as this tends to prevent the fall or even to raise the phospholipid level. After feeding C -labeled carbohydrate the serum phospholipid fraction shows more activity than other serum lipid fractions examined, and there is some evidence to suggest that, unlike the glycerides, most of the labeling is in the fatty acid portion. 

An unusual approach to the study of dietary carbohydrate lipid interrelationships is the estimation in tissue culture of intracellular lipid disposition in human aortic cells grown in the serum from men subjected to various dietary procedures (Rutstein et al., 1964). It was found that carbohydrate ingestion was followed by a suppression of intracellular lipid deposition and that this occurred in the absence of any changes in the concentration of glycerides, phospholipids, or cholesterol in the serum. 

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