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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Pensiamo che vi sia piaciuta questa presentazione. Per scaricarla, consigliatela, per favore ai vostri amici su un qualsiasi social network. Pubblicato Agnese Capone Modificato 4 anni fa. Dietary cholesterol and fatty acids are absorbed by enterocytes in the duodenum and proximal jejunum.
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.
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. The edi takes up these remnants in an interactions mediated by apoE binding to the LDL receptor or to the LDL-related receptor not shown.
The triglyceride core of VLDL is removed by the action of lipoprotein lipase on the endothelial cells of adipose and muscle tissue.
Alternatively, LDL can be oxidized and taken up by macrophages, in a reaction that depends on oipidi scavenger receptor-A SR-A ; s reaction results in the formation of foam cells.
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.
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! Using apoAI digestiobe a cofactor, dfi lecithin: HDL lipdi larger as it accumulates more cholestery esters.
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:
Second, hepatic lipase can hydrolyze the triglyceride core, regenerating small HDL. Illustration of processes of atherogenesis ranging from assorbimentl endothelial dysfunction left through monocyte recruitment to the development assorbmento advanced plaque complicated by thrombosis right. 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.
Elevated LDL is a major risk factor for the development of atherosclerosis. Native LDL that migrates into the subendothelial space can undergo chemical transformation tyo oxidized LDL via lipid peroxidation and fragmentation of apoB Oxidized LDL has a number of deleterious effects on vascular function.
Oxidized LDL promotes monocyte chemotaxis into the eei space A and inhibits monocyte egress from that space B. Resident monocyte-macrophages bind to oxidized LDL via a scavenger receptor SR-Aresulting in the formation of lipid-laden foam cells C.
Oxidized LDL can directly injure endothelial cells and cause endothelial dysfunction D. Oxidized LDL can also cause foam cell necrosis, with assoebimento of numerous proteolyitic enzymes that can damage the intima E. The cytokine-activated endothelium expresses adhesion molecules that lead to the recruitment of peripheral blood monocytes to the inflammatory site. 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.
L’INTESTINO: assorbe colesterolo dal cibo o dalla bile IL FEGATO: – ppt scaricare
On the basis of studies in genetically modified mice, E- and P-selectins have been implicated in the development of vascular lesions. 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.
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. Activated macrophages within the lesion secrete chemotactic products, including chemokines. In response to these chemokine gradients, cells migrate through the endothelium.
They differentiate into the metabolically active, secretory and highly phagocytic inflammatory macrophage. As macrophages accumulate, they take up lipoproteins and actively accumulate lipid to become foam cells. The endocytosed particles are transported to the lysosomes, and free cholesterol FC is then released into the cytosol.
Cytosolic FC is kept in appropriate equilibrium with cholesterol ester CE through the action of two enzymes: Fibrates have been shown to increase the expression of apoA-I in human hepatocytes. Infusion of apoA-I has been shown to attenuate atherosclerosis in animals and possibly in humans.
Expression of this transporter can also be stimulated by LXR activation. The catabolism of HDL can also be inhibited by nicotinic acid through a mechanism that is largely unknown. 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.
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.
Although inter-conversion of HDL subspecies is depicted as occurring in the arterial wall, it probably also occurs in the plasma. 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. 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.
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. HDL metabolism in hypertriglyceridemic states: LDL-R is recycled to the cell surface, whilethe lipoprotein particle is hydrolyzed into aminoacids and free cholestero.
Intracellular cholesterol has three regulatory effects on the cell. First, cholesterol decreases the activity of HGM CoA reductase, the rate-limiting enzyme in cholesterol synthesis. Second, cholesterol activates acetyl CoA: Third, cholesterol inhibits the transcription of the gene encoding the LDL receptor, and thereby decreases further uptake of cholesterol by the cell.
Statins competitively inhibit HGM CoA reductase, the enzyme that catalyzes a crucial step in cholesterol synthesis. 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.
Fibrates have several effects on lipid metabolism, all of whihc are thought to result from PPARalpha-mediated changes in gene transcription.
The digetione 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. PPARalpha also increases fatty acid oxidation in hepatocytes. The end result of these metabolic alterations is a decrease in plasma triglyceride levels and an increase in plasma HDL levels. LOD levels also decrease modestly because of a decrease in hepatic fatty acid and triglyceride synthesis not shown.
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.
Dissociation of co-repressors occurs as a consequence of a ligand-induced conformational change, and the activated heterodimer can then bind to the Asskrbimento. This results in activation or suppression of transcription of a target gene. Recently, cigestione 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 molecular mechanismo of niacin action is unknown, but niacin has been shown to decrease hormone-sensitive lipase activity in adipose tissue, leading to decreased asworbimento fatty acid flux to the liver.
This decreased free fatty lipid flux results in decrease epatic triglyceride synthesis and decrease VLD 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.