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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The decrease apoCIII, combined with incerased lipoprotein lipase expression in muscle vascular beds, leads to increased fatty acid uptake in muscle digestion and increased fatty acid oxidation. Resident monocyte-macrophages bind to oxidized LDL via a scavenger receptor SR-Aresulting in the formation of lipid-laden foam cells C. Autorizzarsi attraverso i social network: 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.
L’INTESTINO: assorbe colesterolo dal cibo o dalla bile IL FEGATO: – ppt scaricare
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. LDL-R is recycled to the cell surface, whilethe lipoprotein particle is hydrolyzed into aminoacids and free cholestero.
Third, cholesterol inhibits the transcription of the gene encoding the LDL receptor, and thereby decreases further uptake of cholesterol by the cell. Expression of this transporter can also be stimulated by LXR activation.
Oxidized LDL has a number of deleterious effects on vascular function. HDL metabolism in hypertriglyceridemic states: The endocytosed particles are transported to the lysosomes, and free cholesterol FC is then released into the cytosol. 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!
Second, hepatic lipase can hydrolyze the triglyceride core, regenerating small HDL. Oxidized LDL can also cause foam cell necrosis, with release of numerous proteolyitic enzymes that can damage the intima E. This decreased free fatty acid flux results in decrease epatic triglyceride synthesis and decrease VLD synthesis.
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. Sul progetto SlidePlayer Condizioni di utilizzo.
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. First, cholesterol decreases the activity of HGM CoA reductase, the rate-limiting enzyme in cholesterol synthesis.
Apolipoprotein apo A-I may be shed from the particle in this process. Elevated LDL is a major risk factor for the development lkpidi atherosclerosis.
On the basis of studies in genetically modified mice, E- and P-selectins have been implicated in the development of vascular lesions. Fibrates have been shown to increase the expression of apoA-I in human hepatocytes.
Registrazione Hai dimenticato la passaword? 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. Asorbimento 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. Per scaricarla, consigliatela, per favore ai vostri amici su un qualsiasi social network.
Dissociation of co-repressors occurs as a consequence of a ligand-induced conformational change, and the activated heterodimer can then bind to the PPRE. Oxidized LDL promotes monocyte chemotaxis into the subendothelial space A and inhibits monocyte egress from that space B.
The end result of these metabolic alterations is a decrease in plasma triglyceride levels and an lipido in plasma HDL levels. Infusion of apoA-I has been shown to attenuate atherosclerosis in animals and possibly in humans. The realtive triglycerdie rich HDL can then be eliminated by one of three mechanisms.
L’INTESTINO: assorbe colesterolo dal cibo o dalla bile IL FEGATO:
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. Note the many points of intersection between HDL and endogenous lipid metabolism. Le mie presentazioni Profilo Feed-back Uscire. Oxidized LDL can directly injure endothelial cells and cause endothelial dysfunction D. In the absence of assorbimetno, 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.
LOD levels also decrease modestly because of a decrease in hepatic fatty acid and triglyceride synthesis not shown. Fibrates have several effects on lipid metabolism, all of whihc are thought to result from PPARalpha-mediated changes in gene transcription.
HDL becomes larger as it accumulates more cholestery esters.