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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Several mouse studies have implicated the 4 1-integrin also known as VLA-4 and digestionf cognate ligand VCAM-1 in these high-affinity interactions. Oxidized LDL can also cause foam cell necrosis, with release of numerous proteolyitic enzymes that can damage the intima E.

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 deei cholesterol enrichment of HDL, before returning to the circulation.

This decreased free fatty acid flux results in decrease epatic triglyceride synthesis and decrease VLD synthesis. Fibrates have several effects on lipid metabolism, all of whihc are thought to result from PPARalpha-mediated changes in gene transcription. Niacin also increases the half-life of apoAI, an important apolipoprotein in HDL the increased apoAI levels directly increases levels of plasma Ilpidi, and may also augment reverse cholesterol transport, delivery of cholesterol from HDL to the liver and excretion opf cholesterol in the bile.

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. Expression of this transporter can also be stimulated by LXR activation. LDL-R is recycled to the cell surface, whilethe lipoprotein particle is hydrolyzed into aminoacids and free cholestero. First, cholesterol decreases aszorbimento activity of HGM CoA reductase, asssorbimento rate-limiting enzyme in cholesterol synthesis.

Native LDL that migrates into the subendothelial space can undergo chemical transformation tyo oxidized LDL via lipid peroxidation and fragmentation of apoB Note the many points of intersection assorbimenti HDL and endogenous lipid metabolism.

This results in activation or suppression of transcription of a target gene. In response to these chemokine gradients, cells migrate through the endothelium.


The catabolism of HDL can also be inhibited by nicotinic acid through a mechanism that is largely unknown. Elevated LDL is a major risk factor for the development of atherosclerosis. HDL metabolism in hypertriglyceridemic states: As macrophages accumulate, they take up lipoproteins and actively accumulate lipid to become foam cells. Fibrates have been shown to increase the expression of apoA-I in human hepatocytes.

Dietary cholesterol and fatty acids are absorbed by enterocytes in the duodenum and proximal jejunum. 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. HDL becomes larger as it accumulates more cholestery esters.

These lipids are then esterified and packed into chylomicrons in association with the apolipoproteins apoB48 and apoAI. PPARalpha also increases fatty acid oxidation in hepatocytes.

Oxidized LDL promotes monocyte chemotaxis into the subendothelial space A ,ipidi inhibits monocyte egress from that space B. 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.

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

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. Second, hepatic lipase can hydrolyze the triglyceride core, regenerating small HDL. Apolipoprotein apo A-I may be shed from the particle in this process. 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.

On the basis of studies in genetically modified mice, E- and P-selectins have been implicated in the development of vascular lesions. Although inter-conversion of HDL subspecies is depicted as occurring in the arterial wall, it probably also occurs in the plasma.

Pubblicato Agnese Capone Modificato 4 anni fa.

Sul progetto SlidePlayer Condizioni di utilizzo. Activated macrophages within the lesion secrete chemotactic products, including chemokines. LOD levels also decrease modestly because of a decrease in hepatic fatty acid and triglyceride synthesis not shown. 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!


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

Second, cholesterol activates acetyl CoA: Dissociation of co-repressors occurs as a consequence of a ligand-induced conformational change, and the activated heterodimer can then bind to the PPRE. 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.

Copiare nel buffer di scambio. Pensiamo che vi sia piaciuta questa presentazione. The realtive triglycerdie rich HDL can then be eliminated by one of three mechanisms.

Statins competitively inhibit HGM CoA reductase, the enzyme that catalyzes a crucial step in cholesterol synthesis. Resident monocyte-macrophages bind to oxidized LDL via a scavenger receptor SR-Aresulting in the formation of lipid-laden foam cells C.

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

Per scaricarla, consigliatela, per favore ai vostri amici su un qualsiasi social network. 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.

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.

The endocytosed particles are transported to the lysosomes, and free cholesterol FC is then released into the cytosol. The triglyceride core of VLDL is removed by the action of lipoprotein lipase on the endothelial cells of digestikne and muscle tissue.

The cytokine-activated endothelium expresses adhesion molecules that lead to the recruitment of peripheral blood monocytes to the inflammatory site. Using apoAI as a cofactor, plasma lecithin: