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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Using apoAI as a cofactor, plasma lecithin: In response to these chemokine gradients, cells migrate through the endothelium.

Oxidized LDL can also cause foam cell necrosis, with release of numerous proteolyitic enzymes that can damage the intima E. The end result of these metabolic alterations is a decrease in plasma triglyceride levels and an increase in plasma HDL levels.

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. Apolipoprotein apo A-I may be shed from the particle in this process.

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

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. First, cholesterol decreases the activity of HGM CoA reductase, the rate-limiting enzyme in cholesterol synthesis.

HDL metabolism in hypertriglyceridemic states: Circulating chylomicrons are depleted of triglycerides by the action of lipoprotein lipase, in a reaction that is dependent on apoCII. Oxidized LDL has a number of deleterious effects on vascular function.

LOD levels also decrease modestly because of a decrease in hepatic fatty acid and triglyceride synthesis not shown. Feed-back Privacy Policy Feed-back. The cytokine-activated endothelium expresses adhesion molecules that lead to the recruitment of peripheral blood monocytes to the inflammatory site. To make this website work, we log user data and share it with processors. 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.


PPARalpha also increases fatty acid oxidation in hepatocytes. Second, hepatic lipase can hydrolyze the triglyceride core, regenerating small HDL. The endocytosed particles are transported to the lysosomes, and free cholesterol FC is then released into the cytosol. 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. Pensiamo che vi sia piaciuta questa presentazione. The triglyceride core of VLDL is removed by the action of lipoprotein lipase on the endothelial cells of adipose and muscle tissue.

This decreased free fatty acid flux results in decrease epatic triglyceride synthesis and decrease VLD synthesis.

Copiare nel buffer di scambio. Resident monocyte-macrophages bind to oxidized LDL via a scavenger receptor SR-Aresulting in the formation of lipid-laden foam cells C. Decreased hepatocyte cholesterol concentration leads assorbimmento protease activation and cleavage of the sterol regulatory element binding protein SREBPwhich is a transcription factor that normally resides in the cytoplasm.

Oxidized LDL promotes monocyte chemotaxis into the subendothelial space A and inhibits monocyte egress from that space B. Several pleiotropic effects of HDL in the vasculature may underlie its anti-atherogenicity.

They differentiate into assorvimento metabolically active, secretory and highly phagocytic inflammatory macrophage. Recently, co-activators such as PPAR- co-activator 1 PGC-1 have assorbimdnto identified, which promote the assembly of an effective transcriptional complex that includes histone acetyltransferases HATs and steroid receptor co-activator-1 SR 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.


Expression of this transporter can also be stimulated by LXR activation. Second, cholesterol activates acetyl CoA: Third, cholesterol inhibits the transcription of the gene encoding the LDL receptor, and thereby decreases further uptake of figestione by the cell.

The realtive triglycerdie rich HDL can then be eliminated by one of three mechanisms. Autorizzarsi attraverso i social network: Intracellular cholesterol has three regulatory effects on the cell. Sul progetto SlidePlayer Condizioni di utilizzo.

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. 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.

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

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. Le mie presentazioni Profilo Feed-back Uscire.

Registrazione Hai dimenticato la passaword? Statins competitively inhibit HGM CoA reductase, the enzyme that catalyzes a crucial step in cholesterol synthesis. This results in activation or suppression of assornimento of a target gene.