DIGESTIONE E ASSORBIMENTO DEI LIPIDI PDF

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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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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. Third, cholesterol inhibits the transcription of the gene encoding the LDL receptor, and thereby decreases further uptake of cholesterol by the cell.

On the basis of studies in genetically modified mice, E- and P-selectins have been implicated in the development of vascular lesions. The realtive triglycerdie rich HDL can then be eliminated by one of three mechanisms. The endocytosed particles are transported to the lysosomes, and free cholesterol FC is then released into the cytosol.

Fibrates have been shown to increase the expression of apoA-I in human hepatocytes.

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

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 from PPARalpha-mediated changes in gene transcription. Per scaricarla, consigliatela, per favore ai vostri amici su un qualsiasi social network. 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.

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Second, hepatic lipase can hydrolyze the triglyceride core, regenerating small HDL. 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 Dietary cholesterol and fatty acids are absorbed by enterocytes in the duodenum and proximal jejunum.

Autorizzarsi attraverso i social network: The catabolism of HDL can also be inhibited by nicotinic acid through a mechanism that is largely unknown. Registrazione Hai dimenticato la passaword?

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. Cytosolic FC is kept in appropriate equilibrium with cholesterol ester CE through the action of two enzymes: These assorbimdnto are then esterified and packed into chylomicrons in association with the apolipoproteins apoB48 and apoAI.

Native LDL that migrates into the subendothelial space can undergo chemical transformation tyo oxidized LDL via lipid peroxidation and fragmentation of apoB 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.

LDL-R is recycled to the cell surface, whilethe lipoprotein particle is hydrolyzed into aminoacids and free cholestero. In response to these chemokine gradients, cells migrate through the endothelium. To use this website, you must agree to our Privacy Policyincluding cookie policy.

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

Oxidized LDL can also cause foam cell necrosis, with release of numerous proteolyitic enzymes that can damage the intima E. Several pleiotropic effects of HDL in the vasculature may underlie its anti-atherogenicity. 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.

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Pubblicato Agnese Capone Modificato 4 anni fa. Using apoAI as a cofactor, plasma lecithin: The cytokine-activated endothelium expresses adhesion molecules that lead to the recruitment of peripheral blood monocytes to the inflammatory site. Dissociation of co-repressors occurs as a consequence of a ligand-induced conformational change, and the activated heterodimer can then bind to the PPRE.

Expression of this transporter can also be stimulated by LXR activation.

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

HDL becomes larger as it accumulates more cholestery esters. HDL originates in the liver or the intestine or from remnant assorrbimento products released during the hydrolysis of lipoproteins by plasma liporotein lipase. Decreased hepatocyte cholesterol concentration leads to protease activation and cleavage of the sterol regulatory element binding protein SREBPwhich is a transcription factor that normally resides in the cytoplasm. Note the many points of intersection between HDL and endogenous lipid metabolism.