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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Low-affinity interactions between monocytes and the endothelium, which are mediated by selectins and integrins, lead to capture and rolling of monocytes on the endothelial surface. Circulating chylomicrons are depleted of triglycerides by the action of lipoprotein lipase, in a reaction that is dependent on apoCII.

These mechanisms may all be responsible to a significant extent for the increased fractional asorbimento rate FCR of apo A-I generally seen in hypertriglyceridemic states and ultimately, for the concomitant reductions in plasma HDL cholesterol levels.

Activated macrophages within the lesion secrete chemotactic products, including chemokines. Dietary cholesterol and fatty acids are absorbed by lipldi in the duodenum and proximal jejunum.

LDL-R is recycled to the cell surface, whilethe lipoprotein particle is hydrolyzed into aminoacids and free cholestero. To use this website, you must agree to our Privacy Policyincluding cookie policy.

The catabolism of HDL can also be inhibited by assrbimento acid digesgione a mechanism that is largely unknown. 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.

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

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This results in activation or suppression of transcription of a target gene.

Copiare nel buffer di scambio. Intracellular cholesterol has three regulatory effects on the cell.

The end result of these metabolic alterations is a decrease in plasma triglyceride levels and an increase in plasma HDL levels. Pubblicato Lipifi Capone Modificato 4 anni fa. 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.

HDL becomes larger as it accumulates more cholestery esters.

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

Alternatively, LDL can be oxidized and taken up by macrophages, in a reaction that depends on the scavenger receptor-A SR-A ; this s results in the formation digstione foam cells. 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.

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.

Second, cholesterol activates acetyl CoA: Oxidized LDL has a number of deleterious effects on vascular function. Xei 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. Infusion of apoA-I has been shown to attenuate atherosclerosis in animals and possibly in humans. Although inter-conversion of HDL subspecies asosrbimento depicted as occurring in the arterial wall, it probably also occurs in the plasma.

Resident monocyte-macrophages bind to oxidized LDL via a scavenger receptor SR-Aresulting in the formation of lipid-laden foam cells C. Per scaricarla, consigliatela, per favore ai vostri amici su un qualsiasi social network. These lipids are then esterified and packed into chylomicrons in association with the apolipoproteins apoB48 and apoAI.

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Elevated LDL is a major risk factor for the development of atherosclerosis.

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 decrease apoCIII, digestionw with incerased lipoprotein lipase expression in muscle vascular beds, leads to increased fatty acid uptake in muscle cells and increased fatty acid oxidation.

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

Autorizzarsi attraverso i social network: PPARalpha also increases fatty acid oxidation in hepatocytes. Native LDL that migrates into the subendothelial space can undergo chemical transformation tyo oxidized LDL via lipid peroxidation and fragmentation of apoB 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.

The realtive triglycerdie rich HDL can then be eliminated by one of three mechanisms. Expression of this transporter can also be stimulated by LXR activation. Cytosolic FC is kept in appropriate equilibrium with cholesterol ester CE through the action of two enzymes: This decreased free fatty acid flux results in decrease epatic triglyceride synthesis and decrease VLD synthesis.

The endocytosed particles are transported to the lysosomes, and free cholesterol FC is then released into the cytosol.