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Large-scale clinical studies reflect the significance of CHD in todaya€™s society and predict an ongoing dramatic increase in the incidence of CHD and its sequelae for the future. Please find in the following a brief description of the underlying lipoprotein metabolism followed by remarks clarifying the mode of action of PPC dyslipoproteinemia.
The basic lipoprotein structure comprises a hydrophobic core of triglycerides and cholesterol esters surrounded by a coat containing polar phospholipids, free cholesterol and apoproteins.
First of all chylomicrons, containing dietary triglyceride and a small amount of cholesterol, pass into the circulation via lymphatics.
Very-low-density lipoproteins (VLDL) are secreted by the liver and contain endogenously synthesized triglycerides and cholesterol a.o.
LDL, the major carrier of the plasma cholesterol, are taken up by the liver and peripheral cells, largely via receptor recognizing apoproteins B and E. High-Density lipoproteins (HDL) comprise a heterogeneous fraction of particles which carry 20-30% of the total plasma cholesterol. HDL are involved in reverse cholesterol transport through their ability to accept free cholesterol, esterify it and transfer the cholesterol to other lipoproteins, but mainly and ultimately to the liver for elimination. With regard to the development of atherosclerosis and its sequelae, LDL are today generally recognized as being highly atherogenic lipoproteins and the main sourse of cholesterol found in the arterial wall.
Under healthy conditions lipoproteins are exposed to a permanent attack of lipolytic enzymes, such as lipoprotein lipase (LPL) and hepatic triglyceride lipase (HTGL). Administration of PhosChol appears to be able to increase the concentration of these enzymes and by this reduces the amount of serum triglycerides. In the vicinity of the endothelial surface deposited cholesterol is transformed into linoleic or linolenic esters which are more easily taken up by HDL-particles and consequently stored in the core of these particles than cholesterol esters with saturated fatty acids. PPC do not only activate LCAT on the tissue level but also in serum, resulting in an increased esterification of free cholesterol, which is transferred from other lipoproteins to HDL.
HDL transport stored cholesterol to the liver, where is is easily metabolized and eliminated with the bile. PhosChol is a DIETARY SUPPLEMENT: These statements have not been evaluated by the Food and Drug Administration. MEDICAL DISCLAIMER: All information is intended for your general knowledge only and is not a substitute for medical advice or treatment for specific medical conditions. Glycolysis originally described the sequence of reactions that convert glycogen to lactic acid in muscle and is usually considered to include the metabolism of hexose phosphates to pyruvate.
Moreover, in plants glycolysis occurs in both cytosol and plastids, with reactions in the different compartments catalysed by separate isoenzymes.
PFP, discovered subsequently, is ubiquitous in plants and has a catalytic potential higher than that of PFK. Since the reaction catalysed by PFP is reversible and the concentration of fructose-2,6-P2 in the cytosol is usually high enough to maintain PFP in an activated form, the direction of this reaction in vivo is likely to depend on availability of substrates.

Fructose-1,6-P2 is cleaved by aldolase to form dihydroxyacetone-P and glyceraldehyde 3-P, and these triose phosphates are interconverted in a reaction catalysed by triose phosphate isomerase. Oxaloacetate is reduced by malate dehydrogenase to malate which, along with pyruvate, can be taken up into mitochondria and metabolised further (see below). In chloroplasts glycolysis is most active in conjunction with the breakdown of starch to form sucrose for export to non-photosynthetic tissues.
Apoproteins ensure indentification of receptors for the exchange and deposition of transported lipid fractions.
Triglyceride is removed in the peripheral circulation by the endothelial enzyme lipoprotein lipase (LPL). Triglycerides are progressively removed from VLDL by lipoprotein lipase to produce intermediate density lipoproteins (IDL), which can either be reabsorbed by the liver or further dPPCeted of triglycerides to produce low-density lipoproteins (LDL). The cytoplasmic pool of cholesterol is derived partly from LDL and partly by endogenous synthesis from acetyl coenzyme A.
Precursors of HDL (HDL3) are secreted by the liver and accept cholesterol from cell membranes which is esterified by the enzyme lecithin:cholesterol acyltransferase (LCAT).
In population studies, the increased risk of atheroma is in correlation with pathological LDL-cholesterol levels, but also inversely correlated with levels of HDL. By means of this, the surface capacity to take up cholesterol may be significantly increased.
In plant tissues, starch takes the place of glycogen in this scheme, and there is probably a second end-product, either oxaloacetate or malate (Figure 2.21). Fructose-2,6-P2 strongly activates PFP, but the physiological signi?cance of this activation and, indeed, the role of PFP, in plants have not yet been clearly established. In tissues where sucrose breakdown is occurring, PFP may function to generate PPi to facilitate the conversion of UDP-glucose to glucose-1-P (Figure 2.20). Glyceraldehyde 3-P is oxidised to glycerate-1,3-P2 by an NAD-dependent glyceraldehyde 3-P dehydrogenase in the cytosol and an NADP-linked enzyme in plastids. Both of these reactions are essentially irreversible and there are ?ne controls that regulate the partitioning of PEP between these reactions. The reduction of oxaloacetate in the cytosol could provide a cytosolic mechanism for oxidising NADH formed by glyceraldehyde 3-P dehydrogenase (Figure 2.21). There is some doubt about the occurrence of phosphoglycerate mutase in chloroplasts, and therefore the main products of the glycolytic reactions may be triose phosphates and 3-PGA. The resulting chylomicron remnant, containing most of the origional cholesterol, is taken up by the liver. In the liver, bile salts are synthesized from this pool and, after secretion in the bile, are partly reabsorbed via the terminal ileum and recirculated. The protective effect of HDL against atheroma may be due to their ability to transport cholesterol from peripheral cells to the liver.

This can be deduced from the fact that in a€?essentiala€? phospholipids unsaturated fatty acids, due to their double-bonds, either take up more space than saturated ones so that the volume of the HDL particles may be increased, or that the increased fluidity accelerates cholesterol incorporation. Plant tissues contain two enzymes capable of catalysing this step: an ATP-dependent phosphofructokinase (PFK), which catalyses an essentially irreversible reaction and occurs in the cytosol and plastids, and phosphofructophosphotransferase (PFP) (now called PPi-dependent phosphofructokinase, PPi-PFK), which occurs only in the cytosol and utilises PPi as the phosphoryl donor in a reaction that is readily reversible.
In plants phosphoenolpyruvate (PEP) is probably the most potent regulator, inhibiting at µM concentrations, but 3-PGA and 2-PGA also strongly inhibit. Fructose-2,6-P2 is a potent inhibitor of cytosolic fructose-1,6-bisphosphatase which is an important control point of sucrose biosynthesis regulating the partitioning of photosynthate between sucrose and starch in leaves. Under these conditions, the simultaneous and opposing action of PFK and PFP in the cytosol could set up a potentially wasteful substrate cycle between fructose-6-P and fructose-1,6-P2.
Glyceraldehyde 3-P dehydrogenase is sensitive to inhibition by the reduced pyridine nucleotide cofactor, which must be reoxidised to maintain the flux through the glycolytic pathway. Pyruvate kinase requires monovalent cations and is inhibited by ATP (and therefore is sensitive to the energy status of the cell), whereas PEP carboxylase is inhibited by malate and is independent of cell energy status. These could be exported through the Pi translocator in the chloroplast envelope to the cytosol, where sucrose synthesis takes place.
Normal enzyme activity is insufficient to metabolize and mobilize the abundant cholesterol.
Pi activates the cytoplasmic PFK, and to a lesser extent that from plastids, and overcomes the inhibition by PEP. Whether fructose-2,6,-P2 has a role in the control of glycolysis through its activation of PFP is not clear. The operation of such a cycle may be a cost of having a mechanism to generate PPi and, ultimately, UDP for the breakdown of sucrose by sucrose synthase. In chloroplasts, the reactions catalysed by fructose-1,6-P2 aldolase, triose phosphate isomerase and NADP-dependent glyceraldehyde 3-P dehydrogenase also form part of the PCR cycle. The sensitivity of PEP carboxylase to malate is regulated by phosphoryl-ation of the enzyme by a protein kinase: the phosphorylated form is less sensitive to malate inhibition. The rate of oxidation of NAD(P)H is also likely to have a bearing on the glycolytic flux at the glyceraldehyde 3-P dehydrogenase step. PFP may also act as an inducible enzyme in some plant tissues, providing increased glycolytic capacity when required during certain stages of plant development or during adjustment to adverse environmental conditions.
This phosphorylation may form part of an important diurnal regulatory cycle in the leaves of crassulacean acid metabolism plants (see Section 2.1). The regulatory metabolite fructose-2,6-P2, a powerful activator of PFK from animals, has no effect on the enzyme from plants.

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Comments to “What is the action of enzymes in digestion”

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