DIGESTIONE E ASSORBIMENTO DEI LIPIDI PDF

DIGESTIONE E ASSORBIMENTO DEI LIPIDI I lipidi passano praticamente immodificati attraverso la bocca e lo stomaco. La loro digestione avviene. Inoltre, tutte le sostanze caloricamente rilevanti: proteine, lipidi e zuccheri poi la loro digestione prosegue nello stomaco sottoposti a lipasi gastrica ed infine si L’assorbimento degli acidi grassi avviene quasi esclusivamente nel tratto. Nel sistema endocrino, è responsabile della produzione dei parecchi ormoni, la secrezione degli enzimi digestivi che aiutano la digestione e l’assorbimento le sostanze nutrienti diverse dalla dieta, quali i carboidrati, i lipidi e le proteine.

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HDL originates in the liver or the intestine or from remnant lipoprotein products released during the hydrolysis of lipoproteins by plasma liporotein lipase. Sul progetto SlidePlayer Condizioni di utilizzo. This results in activation or suppression of transcription of a target gene. Several mouse studies have implicated the 4 1-integrin also known as VLA-4 and its cognate ligand VCAM-1 in these high-affinity interactions.

Fibrates have several effects on lipid metabolism, all of whihc are thought to result assorbimenyo PPARalpha-mediated changes in gene transcription. First, cholesterol decreases the activity of HGM CoA reductase, the rate-limiting enzyme in cholesterol synthesis. Using apoAI as a cofactor, plasma lecithin: To use this website, you must agree to our Privacy Policyincluding cookie policy.

Alternatively, LDL can be oxidized and taken up by macrophages, in a reaction that depends on the scavenger receptor-A SR-A ; this reaction results in the formation of foam cells. Niacin also increases the half-life of apoAI, an important apolipoprotein in HDL the increased apoAI levels directly increases levels of plasma HDL, and may also augment reverse cholesterol transport, delivery of cholesterol from HDL to the liver and excretion opf cholesterol in the bile.

LDL-R is recycled to the cell surface, whilethe lipoprotein particle is hydrolyzed into aminoacids and free cholestero. In eigestione absence of ligand, the heterodimer forms high-affinity complexes with nuclear co-repressor proteins, such as nuclear receptor co-repressor N-CoRwhich prevent transcriptional activation by sequestration of the receptor complex from the promoter. On activation of monocytes by endothelial cell products assorbomento as chemokines, monocyte integrins achieve high-affinity interactions with endothelial adhesion molecules, and cells arrest on the endothelial surface.

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This decreased free fatty acid flux results assorblmento decrease epatic triglyceride synthesis and decrease VLD synthesis.

Apolipoprotein apo A-I may be shed from the particle in this process. Note the many points of intersection between HDL and endogenous lipid metabolism. Registrazione Hai dimenticato la passaword? The realtive triglycerdie rich HDL can then be eliminated by one of three mechanisms. The cytokine-activated endothelium expresses adhesion molecules that lead to the recruitment of peripheral blood monocytes to the inflammatory site.

After lipoprotein lipase has removed a large proportion of the triglyceride core, chylomicrons lose many of their apolipoproteins; the resulting lipoprotein is termed a chylomicron remnant.

This results in the formation of nascent high-density lipoprotein HDL particles, which undergo further modification by the lecithin-cholesterol acyltransferase LCAT enzyme and develop into spherically shaped HDL2 larger, less dense particles or HDL3 smaller, more dense particleswhich, in turn, can act as acceptors for ABCG1-mediated cholesterol efflux from macrophages, resulting in further cholesterol enrichment of HDL, before returning to the circulation.

The decrease apoCIII, combined with incerased lipoprotein lipase expression in muscle vascular beds, leads to increased fatty acid uptake in muscle cells and increased fatty acid oxidation.

Fibrates have been shown to increase the expression of apoA-I in human hepatocytes. These lipids are then esterified and packed into chylomicrons in association with the apolipoproteins apoB48 and apoAI.

As macrophages accumulate, they take up lipoproteins and actively accumulate lipid to become foam cells. Oxidized LDL has a number of deleterious effects on vascular function.

L’INTESTINO: assorbe colesterolo dal cibo o dalla bile IL FEGATO:

The end result of these metabolic alterations is a decrease in plasma triglyceride levels and an increase in plasma HDL levels. There are also data to suggest that apo A-I may be in a more dissociable form on TG-enriched HDL, possibly due to a change in the particle stability.

Oxidized LDL can also cause foam cell necrosis, with release of numerous proteolyitic enzymes that can damage the intima E. Per scaricarla, consigliatela, per favore ai vostri amici su un qualsiasi social network.

The liver takes up these remnants in an interactions mediated by apoE binding to the LDL receptor or to the LDL-related receptor not shown. Statins competitively inhibit HGM CoA reductase, the enzyme that catalyzes a crucial step in cholesterol synthesis. Cytosolic FC is kept in appropriate equilibrium with cholesterol ester CE through the action of two enzymes: Several pleiotropic effects of HDL in the vasculature may underlie its anti-atherogenicity.

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HDL metabolism in hypertriglyceridemic states: LOD levels also decrease modestly because of a decrease in hepatic fatty acid and triglyceride synthesis not shown.

Expression of this transporter can also be stimulated by LXR activation. To make this website work, we log user data and share it with processors. Second, hepatic lipase can hydrolyze the triglyceride core, regenerating small HDL. The catabolism of HDL can also be inhibited by nicotinic acid through a mechanism that is largely qssorbimento. HDL becomes larger as it accumulates more cholestery esters.

L’INTESTINO: assorbe colesterolo dal cibo o dalla bile IL FEGATO: – ppt scaricare

In response to these chemokine gradients, cells migrate through the endothelium. Nascent HDL circulates in the plasma and receives free cholesterol from cholesterol laden cells,including macrophages, by a process that is depndent on the enzyme ATP-binding cassette transporter A!

Third, cholesterol inhibits the transcription of the gene encoding the LDL receptor, and thereby decreases further uptake of cholesterol by the cell. Le mie presentazioni Profilo Feed-back Uscire. The mechanisms are grossly simplified but focus on components for example, cell adhesion molecules, macrophages, connective tissue elements, lipid core and fibrin and processes for example, apoptosis, proteolysis, angiogenesis and thrombosis in plaques that have been imaged or that present useful potential imaging targets.

On entering the sub-endothelial space, lipid-free or lipid-poor apolipoprotein A-I apoA-I can bind to the ABC transporter A1 ABCA1 on the cell surface of macrophages in the arterial wall and promote efflux of free cholesterol and phospholipids from these cells. Autorizzarsi attraverso i social network: Infusion of apoA-I has been shown to attenuate atherosclerosis in animals and possibly in humans.

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