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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Fibrates have several effects on lipid metabolism, all of whihc are thought to result from PPARalpha-mediated changes in gene transcription. Apolipoprotein apo A-I may be shed from the particle in this process. Expression of this transporter can also be stimulated by LXR activation. Native LDL that migrates into the subendothelial space can undergo chemical transformation tyo oxidized LDL via lipid peroxidation and fragmentation of apoB 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.

They differentiate into the metabolically digestionee, secretory and highly phagocytic inflammatory macrophage.

HDL metabolism in hypertriglyceridemic states: Cytosolic FC is kept in appropriate equilibrium with cholesterol ester CE through the action of two enzymes: 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. Le mie presentazioni Profilo Feed-back S.

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The end result of these metabolic alterations is a decrease in plasma triglyceride levels and an increase in plasma HDL levels. 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, digestikne, angiogenesis and thrombosis in plaques that have been imaged or that present useful potential imaging targets.

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

These diegstione are then esterified and packed into chylomicrons in association with the apolipoproteins apoB48 and apoAI. 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.

As macrophages accumulate, they take up lipoproteins and actively accumulate lipid to become foam cells. These mechanisms may all be responsible to a significant extent for the increased fractional catabolic rate FCR of apo A-I generally seen in hypertriglyceridemic states and ultimately, for the concomitant reductions in plasma HDL cholesterol levels.

HDL becomes larger as it accumulates more cholestery esters.

Sul progetto SlidePlayer Condizioni di utilizzo. Oxidized LDL has a number of deleterious effects on vascular function. 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.

To make this website work, we log user data and share it with processors. Intracellular cholesterol has three regulatory effects on the cell. PPARalpha also increases fatty acid oxidation in hepatocytes. To use this website, you must agree to our Privacy Policyincluding cookie policy.

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

In response to these chemokine gradients, cells migrate through the endothelium. Several pleiotropic effects of HDL in the vasculature may underlie its digextione. LOD levels also decrease modestly because of a decrease in hepatic fatty acid and triglyceride synthesis assorbimejto shown. Oxidized LDL can directly injure endothelial cells and cause endothelial dysfunction D.

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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!

Pubblicato Agnese Capone Modificato 4 anni fa. 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.

Dissociation of co-repressors occurs as a consequence of a ligand-induced conformational change, and the activated heterodimer can then bind to the PPRE. eigestione

HDL originates in the liver or the intestine or from remnant lipoprotein products released during the hydrolysis of lipoproteins by plasma liporotein lipase. Autorizzarsi attraverso i social network: Illustration of processes of atherogenesis ranging from pre-lesional endothelial dysfunction left through monocyte recruitment to the development of advanced plaque complicated by thrombosis right. The catabolism of HDL can also be inhibited by nicotinic acid through a mechanism that is largely unknown.

Note the many points of intersection between HDL and endogenous lipid metabolism. 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.