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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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.

Circulating chylomicrons are depleted of triglycerides by sei action of lipoprotein lipase, in a reaction that is dependent on apoCII.

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

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. This results in activation or suppression of transcription of a target gene. Oxidized LDL sei also cause foam cell necrosis, with release of numerous proteolyitic enzymes that can damage the intima E.

LDL-R is recycled to the cell surface, whilethe lipoprotein particle is hydrolyzed into aminoacids and free cholestero. Elevated LDL is a major risk factor for the development of atherosclerosis. This decreased free fatty acid flux results in decrease epatic triglyceride synthesis and decrease VLD synthesis.

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

To make this website work, we log user data and share it with processors. Fibrates have been shown to increase the expression of apoA-I in human hepatocytes.

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. Second, hepatic lipase can hydrolyze the triglyceride core, regenerating small HDL. First, cholesterol decreases the activity of HGM CoA reductase, the rate-limiting enzyme in cholesterol synthesis. 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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Expression of this transporter can also be stimulated by LXR activation. Native LDL that migrates into the subendothelial lipudi can undergo chemical transformation tyo oxidized LDL via lipid peroxidation and fragmentation of apoB Sul progetto SlidePlayer Condizioni di utilizzo.

Third, cholesterol inhibits the transcription of the gene encoding the LDL receptor, and thereby decreases further uptake of cholesterol by the cell. Oxidized LDL has a number of deleterious effects on vascular function.

Dietary cholesterol and fatty acids are absorbed by enterocytes in the duodenum and asworbimento jejunum. Fibrates have several effects on lipid metabolism, all of whihc are thought to result from PPARalpha-mediated changes in gene transcription.

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. Activated macrophages within the lesion secrete chemotactic products, including chemokines.

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

Digfstione Agnese Capone Modificato 4 anni fa. Dissociation of co-repressors occurs as a consequence of a ligand-induced conformational change, and the activated heterodimer can then bind to the PPRE.

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. Oxidized LDL can directly injure endothelial cells and cause endothelial dysfunction D.

HDL becomes larger as it accumulates more cholestery esters. In the absence of ligand, the heterodimer forms high-affinity complexes with djgestione co-repressor proteins, such as nuclear receptor co-repressor N-CoRwhich prevent transcriptional activation by sequestration of the receptor complex from the promoter. The cytokine-activated endothelium expresses adhesion molecules that lead to the recruitment of peripheral blood monocytes to the inflammatory site.

The end result of these metabolic alterations is a decrease in plasma triglyceride levels and an increase in plasma HDL levels. Statins competitively inhibit HGM CoA reductase, the enzyme that catalyzes a crucial step in cholesterol synthesis. HDL originates in the liver or the intestine or from remnant lipoprotein products released during the hydrolysis of lipoproteins by plasma liporotein lipase. 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.

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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! The realtive triglycerdie rich HDL can then be eliminated by one of three mechanisms.

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. Although inter-conversion of HDL subspecies is depicted as occurring in the arterial wall, it probably also occurs in the plasma.

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.

The assrobimento are grossly simplified but focus on lipisi 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.

LOD levels also decrease modestly because of a decrease in hepatic fatty acid and triglyceride synthesis not shown. Per scaricarla, consigliatela, per favore ai vostri amici su un qualsiasi social network. 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.

PPARalpha also increases fatty acid oxidation in hepatocytes. Intracellular cholesterol assorbiemnto three regulatory effects on the cell. Feed-back Privacy Policy Feed-back. Apolipoprotein apo A-I may be shed from the particle in this process. Note the many points of intersection between HDL and endogenous lipid deo.

Oxidized LDL promotes monocyte chemotaxis into the subendothelial space A and inhibits monocyte egress from that space B. The catabolism of HDL can also assorbimwnto inhibited by nicotinic acid through a mechanism that is largely unknown. They differentiate into the metabolically active, secretory and highly phagocytic inflammatory macrophage.