DIGESTIONE E ASSORBIMENTO DEI LIPIDI PDF

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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Per scaricarla, consigliatela, per favore ai vostri amici su un qualsiasi social network. LDL-R is recycled to the cell surface, whilethe lipoprotein particle is hydrolyzed into aminoacids and free cholestero.

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

Second, hepatic lipase can hydrolyze the triglyceride core, regenerating small HDL. Pensiamo che vi sia piaciuta questa presentazione. The endocytosed particles are transported to the lysosomes, and free cholesterol FC is then released into the cytosol.

Pubblicato Agnese Capone Modificato 4 anni fa. 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.

Autorizzarsi attraverso i 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. The decrease apoCIII, combined with incerased lipoprotein lipase expression in muscle vascular beds, leads to increased fatty acid uptake in muscle cells assorbimmento increased fatty acid oxidation.

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In response to these chemokine gradients, cells migrate through the endothelium.

Copiare nel buffer di scambio. 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.

As macrophages accumulate, they take up lipoproteins sigestione actively accumulate lipid to become foam cells. These lipids are then esterified and packed into chylomicrons in association with the apolipoproteins apoB48 and apoAI.

Circulating chylomicrons are depleted of triglycerides by the action of lipoprotein lipase, in a reaction that is dependent on apoCII. Registrazione Hai dimenticato la passaword? Resident monocyte-macrophages bind to assorbi,ento LDL via a scavenger receptor SR-Aresulting in the formation of lipid-laden foam cells C.

This decreased free fatty acid flux results in assorbimeno epatic triglyceride synthesis and decrease VLD synthesis. Oxidized LDL can directly injure endothelial cells and cause endothelial dysfunction D.

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.

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 HDL originates in the liver or the intestine or from remnant lipoprotein products released during the hydrolysis of lipoproteins by plasma liporotein lipase.

The end result of these metabolic alterations is a decrease in plasma triglyceride levels and an increase in plasma HDL levels. The cytokine-activated endothelium expresses adhesion molecules that lead to the recruitment of peripheral blood monocytes to the inflammatory site. 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!

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

Oxidized LDL has a number of deleterious effects on vascular function. Le mie presentazioni Profilo Feed-back Uscire. This results in activation or suppression diestione transcription of a target gene. Using apoAI as a cofactor, plasma lecithin: The molecular mechanismo of niacin action is unknown, but niacin has been shown to decrease hormone-sensitive lipase activity in asaorbimento tissue, leading to decreased free fatty acid flux to lilidi liver.

PPARalpha also increases fatty acid oxidation in hepatocytes. 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. Several pleiotropic effects of HDL in the vasculature may underlie its anti-atherogenicity. Apolipoprotein apo A-I may be shed from the particle in this process.

The realtive triglycerdie rich HDL can then be eliminated by one of three mechanisms. To use this website, you must agree to our Privacy Policyincluding cookie policy. LOD levels also decrease modestly because of a decrease awsorbimento hepatic fatty acid and triglyceride synthesis not shown.