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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Expression of this transporter can also be stimulated by LXR activation. Fibrates have several effects on lipid metabolism, all of whihc are thought to result from PPARalpha-mediated changes in gene transcription.

Autorizzarsi attraverso i social network: 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. Circulating chylomicrons are depleted of triglycerides by the action of lipoprotein lipase, in a reaction that is dependent on apoCII.

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

Activated macrophages within the lesion secrete chemotactic products, including chemokines. To use this website, you must agree to our Privacy Policyincluding cookie policy. 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.

Note the many points of intersection between HDL and endogenous lipid metabolism. Cytosolic FC is kept in appropriate equilibrium with cholesterol ester CE through the action of two enzymes: Pubblicato Agnese Capone Modificato 4 anni fa. Sul progetto SlidePlayer Condizioni di utilizzo. 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.

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. 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 Cigestione larger, less dense particles or HDL3 smaller, more dense ediwhich, 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.


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

Several pleiotropic effects of HDL in the vasculature may underlie its anti-atherogenicity. Second, hepatic lipase can hydrolyze the triglyceride core, regenerating small HDL. Alternatively, LDL can be oxidized and taken up by macrophages, in a digestinoe that depends on the scavenger receptor-A SR-A ; this reaction results in the formation of foam cells.

Le mie presentazioni Profilo Feed-back Uscire. LDL-R is recycled to the cell surface, whilethe lipoprotein particle is hydrolyzed into aminoacids and free cholestero.

Per scaricarla, consigliatela, per favore ai vostri amici su un qualsiasi social network. Feed-back Privacy Policy Feed-back. Lpidi liver takes up these remnants in an interactions mediated by apoE binding to the LDL receptor or to the LDL-related receptor not shown.

These lipids are then esterified and packed into chylomicrons in association with the assorbimentoo apoB48 and apoAI. This results in activation or suppression of transcription of a target gene. The realtive triglycerdie rich HDL can then be eliminated by one assorbimeno three mechanisms. The end result of these metabolic alterations is a decrease in plasma triglyceride levels and an increase in plasma HDL levels.

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. In the absence of ligand, the heterodimer forms high-affinity complexes with nuclear co-repressor proteins, such as nuclear receptor digestiond N-CoRwhich prevent transcriptional activation by sequestration of the receptor complex from the promoter.

HDL becomes larger as it assorbimemto more cholestery esters. 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.

The triglyceride core of VLDL is removed by the action of lipoprotein lipase on the endothelial cells of adipose and muscle tissue. Dissociation of lpidi occurs as a consequence of a ligand-induced conformational change, and the activated heterodimer can then bind to the PPRE.

To make this website work, we log user data and share it with processors. 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 Copiare nel buffer di scambio.


Registrazione Hai dimenticato la passaword? Fei, cholesterol inhibits the transcription of the gene encoding the LDL receptor, and thereby digestiine further uptake of cholesterol by the cell. The endocytosed particles are transported to the lysosomes, and free cholesterol FC is then released into the cytosol. Nascent HDL circulates in the plasma and receives free cholesterol from cholesterol laden cells,including macrophages, by assirbimento process that is depndent on the enzyme ATP-binding cassette transporter A!

Although inter-conversion of HDL subspecies is depicted as occurring in the arterial wall, it probably also occurs in the plasma. Pensiamo che vi sia piaciuta questa presentazione.

Using apoAI as a cofactor, plasma lecithin: 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 Dwi cholesterol levels. First, cholesterol decreases the activity of HGM CoA reductase, the rate-limiting enzyme in cholesterol synthesis.

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

On the basis of assorbimneto in genetically modified mice, E- and P-selectins have been implicated in the development of vascular lesions. Statins competitively inhibit HGM CoA reductase, the enzyme that catalyzes a crucial step in cholesterol synthesis.

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

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

As macrophages accumulate, they take up lipoproteins and actively accumulate lipid to become foam cells. Infusion of apoA-I has been shown to attenuate atherosclerosis in animals and possibly in humans.

In response to these chemokine gradients, cells migrate through the endothelium. The catabolism of HDL can also be inhibited by nicotinic acid through a mechanism that is largely unknown.