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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Copiare nel buffer di scambio. On the basis of studies in genetically modified mice, E- and P-selectins have been implicated in the development of vascular lesions.

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!

First, cholesterol decreases the activity of HGM CoA reductase, the rate-limiting enzyme in cholesterol synthesis. Dissociation of co-repressors occurs as a consequence of a ligand-induced conformational change, and the activated heterodimer can then bind to the PPRE. The endocytosed particles are transported to the lysosomes, and free cholesterol FC digestoine then released into the cytosol. The triglyceride core of VLDL is removed by the action of lipoprotein lipase on the endothelial cells of adipose and muscle tissue.

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

On activation of monocytes by endothelial cell products such as chemokines, monocyte integrins achieve high-affinity interactions with endothelial adhesion molecules, and cells arrest on the endothelial surface. The molecular mechanismo of niacin action is unknown, but niacin has been shown to decrease hormone-sensitive lipase activity in adipose tissue, leading to decreased free fatty acid flux to the liver.

Oxidized LDL can directly injure endothelial cells and cause endothelial dysfunction D. Although inter-conversion of HDL subspecies is depicted as occurring in the arterial wall, it probably also occurs in the plasma. Decreased hepatocyte cholesterol concentration leads to protease activation and cleavage of the sterol regulatory element binding assorbimrnto SREBPwhich is a transcription factor that normally xei in the cytoplasm.

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The liver takes up these remnants in an interactions mediated by apoE binding zssorbimento the LDL receptor or to the LDL-related receptor not shown.

In the 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.

Using apoAI as a cofactor, plasma lecithin: Sul progetto SlidePlayer Condizioni di utilizzo. 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.

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

Recently, co-activators such as PPAR- co-activator 1 PGC-1 have been identified, which promote the assembly of an effective transcriptional complex that includes histone acetyltransferases HATs and steroid receptor co-activator-1 SR Circulating chylomicrons are depleted of triglycerides by the action of lipoprotein lipase, in a reaction that is dependent on apoCII.

Infusion of apoA-I has been shown to attenuate atherosclerosis in animals and possibly in humans. These lipids are then esterified and packed into chylomicrons in association with the apolipoproteins apoB48 and apoAI. 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.

The end result of these metabolic alterations is a decrease in plasma triglyceride levels and an increase in plasma HDL levels. Pensiamo che vi sia piaciuta questa presentazione. The realtive triglycerdie rich HDL can then be eliminated by one of three mechanisms. 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.

HDL originates in the liver or the intestine or from remnant lipoprotein products released during the hydrolysis of lipoproteins by plasma liporotein lipase.

Registrazione Hai dimenticato la passaword? Resident monocyte-macrophages bind to oxidized LDL via a scavenger receptor SR-Aresulting in the formation of lipid-laden foam cells C. Third, cholesterol inhibits the transcription of the gene encoding the LDL receptor, and thereby decreases further uptake of cholesterol by the cell.

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Activated macrophages within the lesion secrete chemotactic products, including chemokines. Oxidized LDL can also cause foam cell necrosis, with release of numerous asosrbimento enzymes that can damage the intima E.

LOD levels also decrease modestly because of a decrease in hepatic fatty acid and triglyceride synthesis not shown. Several pleiotropic effects of HDL in the vasculature may underlie its anti-atherogenicity. Statins competitively inhibit HGM CoA reductase, the enzyme that catalyzes a crucial step in cholesterol synthesis. 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.

Native LDL that migrates into the subendothelial space can undergo chemical transformation tyo oxidized LDL via lipid peroxidation and fragmentation of apoB Low-affinity interactions between monocytes and the endothelium, which are mediated by selectins and integrins, lead to capture and rolling of monocytes on the endothelial surface.

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. Oxidized LDL has a number of deleterious effects on vascular assorbimengo. To make this website work, we log user data and share it with processors. Apolipoprotein apo A-I may be shed asskrbimento the particle in this process.

Oxidized LDL promotes monocyte chemotaxis into the subendothelial space A and inhibits digestkone egress from that space B. Per scaricarla, consigliatela, per favore ai vostri amici su un qualsiasi social network. Second, cholesterol activates acetyl CoA: