Plasma triacylglycerol concentration

The increased mobilisation of fatty acids from adipose tissue raises the plasma concentration, which increases the rate of fat oxidation by muscle. It also releases some essential fatty acids from the store in the triacylglycerol in adipose tissue. These are required for formation of new membranes in proliferating cells and those involved in repairing the wound (e.g. fibroblasts) (Chapters 11 and 21 Figure 21.22). 

Measurement of the plasma concentration of phylloquinone gives some information about stams, but reflects not only intake but also plasma triacyl-glycerol, because most is carried in chylomicrons and chylomicron remnants. The plasma concentration of phylloquinone is higher in older subjects, but the phylloquinone triacylglycerol ratio is lower than in younger people (Booth andSuttie, 1998). 

The free fatty acids (FFA, nonesterified fatty acids, im-esterified fatty acids) arise in the plasma from hpolysis of triacylglycerol in adipose tissue or as a result of the action of hpoprotein hpase during uptake of plasma tri-acylglycerols into tissues. They are found in combination with albumin, a very effective solubilizer, in concentrations varying between 0.1 and 2.0 ieq/mL of plasma. Levels are low in the ftiUy fed condition and rise to 0.7-0.8 leq/mL in the starved state. In uncontrolled diabetes mellitus, the level may rise to as much as 2 Ieq/mL. 

HDL concentrations vary reciprocally with plasma triacylglycerol concentrations and directly with the activity of lipoprotein lipase. This may be due to surplus surface constituents, eg, phospholipid and apo A-I being released during hydrolysis of chylomicrons and VLDL and contributing toward the formation of preP-HDL and discoidal HDL. HDLj concentrations are inversely related to the incidence of coronary atherosclerosis, possibly because they reflect the efficiency of reverse cholesterol transport. HDL, (HDLj) is found in... 

The free fatty acids formed by lipolysis can be reconverted in the tissue to acyl-CoA by acyl-CoA synthetase and reesterified with glycerol 3-phosphate to form triacylglycerol. Thus, there is a continuous cycle of lipolysis and reesterification within the tissue. However, when the rate of reesterification is not sufficient to match the rate of lipolysis, free fatty acids accumulate and diffuse into the plasma, where they bind to albumin and raise the concentration of plasma free fatty acids. 

Otfier fiormones accelerate tfie release of free fatty acids from adipose tissue and raise tfie plasma free fatty acid concentration by increasing the rate of lipolysis of the triacylglycerol stores (Figure 25—8). These include epinephrine, norepinephrine, glucagon, adrenocorticotropic hormone (ACTH), a- and P-melanocyte-stimulat-ing hormones (MSH), thyroid-stimulating hormone (TSH), growth hormone (GH), and vasopressin. Many of these activate the hormone-sensitive hpase. For an optimal effect, most of these lipolytic processes require the presence of glucocorticoids and thyroid hormones. These hormones act in a facilitatory or permissive capacity with respect to other lipolytic endocrine factors. 

Hypolipemic activity. Fiber, administered orally to nine adults with ileostomies at a dose of 13 g/day, increased the excretion of cholesterol " Petroleum ether extract of the fresh fruit, administered to pigs at a concentration of 3.5 g/kg of diet, was inactive "" . Purified green barley extract, in human mononuclear culture of cells isolated from perithelial blood and synovial fluid of patients with rheumatoid arthritis, was active . Leaf essence, administered to atherosclerotic New Zealand White male rabbits at a dose of 1% of diet, produced a decrease of plasma total cholesterol, triacylglycerol, lucigenin-chemilumines-cence, and luminal-chemiluminescence levels. The value of Tj of red blood cell hemolysis and the lag phase of LDL oxidation increased in barley-treated group compared with the control. Ninety percent of the intimal surface of the thoracic aorta was covered with atherosclerotic lesions in the... 

Asai et al. (1999) determined that phospholipid hydroperoxides (PLOOH) are key products for oxidative injury in membranous phospholipid layers in the plasma, red blood cells (RBC), and liver of mice. The formation and accumulation of PLOOH have been confirmed in several cellular disorders, various diseases, and in aging. A lower PLOOH level was found in RBC of the spice-extract-fed mice (65 to 74% of the nonsupplemented control mice). The liver lipid peroxidizability induced with Fe2+/ascorbic acid was effectively suppressed in mice by dietary supplementation with the turmeric and capsicum extracts. Although no difference in the plasma lipids was observed, the liver triacylglycerol concentration of the turmeric-extract-fed mice was markedly reduced to half of the level in the control mice. These findings suggest that these spice extracts could act antioxidatively in vivo by food supplementation, and that the turmeric extract has the ability to prevent the deposition of triacylglycerols in the liver. 

R2. Rajaram, O. V., and Barter, P. J., Influence of lipoprotein concentration on the exchanges of triacylglycerol between rabbit plasma low density and high density lipoproteins. Biochim. Biophys. Acta 620, 438-448 (1980). 

Letexier, D., Diraison, F., and Beylot, M., Addition of inulin to a moderately high-carbohydrates diet reduces hepatic lipogenesis and plasma triacylglycerol concentrations in humans, Am. J. Clin. Nutr., 77, 559-564, 2003. 

Several excellent reviews have summarized the well-established ability of phytosterols to lower serum cholesterol concentrations in humans.The consumption of food products supplemented with 1.6 to 3.5 g/d of phytosterols has been shown to consistently decrease serum total cholesterol and LDL-C concentrations by up to 15%, without affecting HDL-C and triacylglycerol concentrations (Table 8.6). About 1 g of mixed phytosterols per day is needed to decrease cholesterol by at least 5%, but phytosterol intakes exceeding 2.5 g/d decrease plasma cholesterol and LDL-C by up to 15%. 

GIP is synthesized and released by K cells located in the duodenal and jejunal mucosa. Plasma GIP is increased by oral administration of glucose, triacylglycerols, or intraduo-denai infusions of solutions containing a mixture of amino acids none of these, however, increases GIP concentrations when given intravenously. Protein ingestion does not significantly increase GIP. For food components to stimulate GIP release, they must be absorbed by the intestinal mucosa. 

Lipoproteins are often called pseudomicellar because their outer shell is in part composed of amphipathic phospholipid molecules. Unlike simple micelles, lipoproteins contain apolipoproteins, or apoproteins, in their outer shell and a hydrophobic core of triacylglycerol and cholesteryl esters. Unesterified, or free, cholesterol, which contains a polar group, can be found as a surface component and in the region between the core and surface (Figure 20-1). Most lipoproteins are spherical. However, newly secreted high-density lipoproteins (HDLs) from the liver or intestine are discoidal and require the action of lecithin-cholesterol acyltransferase (LCAT) in plasma to expand their core of neutral lipid and become spherical. The hydrophobic core of the low-density lipoprotein (LDL) molecule may contain two concentric layers one of triacylglycerol and another of cholesteryl ester. 

A high-carbohydrate diet results in substantial elevation of plasma VLDL concentration. A high-cholesterol diet alters the composition of VLDL, with cholesterol esters substituting for triacylglycerol as core components, and leads to a marked increase in apo E synthesis. 

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