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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Fibrates have several effects on lipid metabolism, all of whihc are thought to result from PPARalpha-mediated changes in gene transcription.

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. Registrazione Hai dimenticato la passaword? PPARalpha also increases fatty acid oxidation in hepatocytes.

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.

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 To use this website, you must agree to our Privacy Policyincluding cookie policy.

To make this website work, we log user data and share it with processors. The catabolism of HDL can also be inhibited by nicotinic acid through a mechanism that is largely unknown. 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. The endocytosed particles are transported to the lysosomes, and free cholesterol FC is then released into the cytosol.

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Fibrates have been shown to increase the expression of apoA-I in human hepatocytes.

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

Feed-back Privacy Policy Feed-back. Elevated LDL is a major risk factor for the development of atherosclerosis. Using apoAI as a cofactor, plasma lecithin: The molecular mechanismo of niacin action is unknown, but niacin has been shown to decrease ddigestione lipase activity in adipose tissue, leading to decreased free fatty acid flux to the liver.

Oxidized LDL can also cause foam cell digeestione, with release of numerous proteolyitic enzymes that can damage the intima E.

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

Autorizzarsi attraverso i social network: On the basis of studies in genetically modified mice, E- and P-selectins have been implicated in the development of vascular lesions. 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.

They differentiate into the metabolically active, secretory and highly phagocytic inflammatory macrophage. 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!

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. 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.

Per scaricarla, consigliatela, per favore ai vostri amici su un qualsiasi social network. Sul progetto SlidePlayer Condizioni di utilizzo. 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.

Note the many points of intersection between HDL and endogenous lipid metabolism. HDL originates in the liver or the intestine or from remnant lipoprotein products released during the hydrolysis of lipoproteins by plasma liporotein lipase.

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Le mie presentazioni Profilo Feed-back Uscire. HDL becomes larger as it accumulates more cholestery esters.

Dietary cholesterol and fatty acids are absorbed by enterocytes in the duodenum and proximal jejunum. As macrophages accumulate, they take up lipoproteins and actively accumulate lipid to become foam cells. Circulating chylomicrons are depleted of triglycerides by the action of lipoprotein lipase, in a reaction that is dependent on apoCII.

Apolipoprotein apo A-I may be shed from the particle in this process. Resident monocyte-macrophages bind to oxidized LDL via a scavenger receptor SR-Aresulting in the formation of lipid-laden foam cells C.

Copiare nel buffer di scambio. 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. Activated macrophages within the lesion secrete chemotactic products, including chemokines.

Oxidized LDL can directly injure endothelial cells and cause endothelial dysfunction D. 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. Expression of this transporter can also be stimulated by LXR activation. Statins competitively inhibit HGM CoA reductase, the enzyme that catalyzes a crucial step in cholesterol synthesis.

Pensiamo che vi sia piaciuta questa presentazione. LDL-R is recycled to the cell surface, whilethe lipoprotein particle is hydrolyzed into aminoacids and free cholestero. Several pleiotropic effects of HDL in the vasculature may underlie its ditestione.

Pubblicato Agnese Capone Modificato 4 anni fa.

The end result of these metabolic alterations is a decrease in plasma triglyceride levels and an increase in plasma HDL levels. Dissociation of co-repressors occurs as a consequence of a ligand-induced conformational change, and the activated heterodimer can then bind to the PPRE.

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