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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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. Copiare nel buffer lpiidi scambio.

Although inter-conversion of Digesrione subspecies is depicted as occurring in the arterial wall, it probably also occurs in the plasma. 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! 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 The endocytosed particles are transported to the lysosomes, and free d FC is then released into the cytosol.

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

Oxidized LDL promotes monocyte chemotaxis into the subendothelial space A and inhibits monocyte egress from that space B. Registrazione Hai dimenticato la passaword?

This decreased free fatty acid flux results in decrease epatic triglyceride synthesis and decrease VLD synthesis. Le mie presentazioni Profilo Feed-back Uscire. Infusion of apoA-I has been shown to attenuate atherosclerosis in animals and possibly in humans.

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.

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.

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Second, hepatic lipase can hydrolyze the triglyceride core, regenerating small HDL. The molecular mechanismo of niacin action is unknown, but niacin has been shown to decrease hormone-sensitive lipase activity in adipose tissue, leading assorbimejto decreased free fatty acid flux to the liver.

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 dek 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.

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

Cytosolic FC is kept in appropriate equilibrium with cholesterol ester CE through the action of two enzymes: In the absence of ligand, the heterodimer forms high-affinity complexes with nuclear co-repressor xigestione, such as nuclear receptor co-repressor N-CoRwhich prevent transcriptional activation by sequestration of the receptor complex from the promoter.

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

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

Using apoAI as a cofactor, plasma lecithin: 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.

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 lipids are then esterified and packed into chylomicrons in association with the apolipoproteins apoB48 and apoAI. As macrophages accumulate, they take up lipoproteins and actively accumulate lipid to become foam cells. Expression of this transporter can also be stimulated by LXR activation.

Note the many points of intersection between HDL and endogenous lipid metabolism.

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Several pleiotropic effects of HDL in the vasculature may underlie its anti-atherogenicity. Pensiamo che vi sia piaciuta questa presentazione. HDL originates in the liver or the intestine or from remnant lipoprotein products released during the hydrolysis of lipoproteins by plasma liporotein lipase.

LDL-R is recycled to the cell surface, whilethe lipoprotein particle is hydrolyzed into aminoacids and free cholestero.

Fibrates have several effects on lipid metabolism, all of whihc are thought to result from PPARalpha-mediated changes in gene transcription. The triglyceride core of VLDL is removed by the action of lipoprotein lipase on the endothelial cells of adipose and muscle tissue. Dietary cholesterol and fatty acids are digestioje by enterocytes in the duodenum and proximal jejunum. Sul progetto SlidePlayer Condizioni di utilizzo. Intracellular cholesterol has three regulatory effects on the cell.

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

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

The realtive triglycerdie rich HDL can then be eliminated by one of three mechanisms. Autorizzarsi attraverso i social network: LOD levels also decrease modestly because of a decrease in hepatic fatty acid and triglyceride synthesis not shown.

These mechanisms may assorbijento 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. Oxidized LDL can directly injure endothelial cells and cause endothelial dysfunction D.