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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LOD levels also decrease modestly because of a decrease in hepatic fatty acid and triglyceride synthesis not shown. Native LDL that migrates into the subendothelial space can undergo chemical transformation tyo oxidized LDL via lipid peroxidation and fragmentation of apoB These lipids are then esterified and packed into chylomicrons in association with the apolipoproteins apoB48 and apoAI. Pensiamo che vi sia piaciuta questa presentazione.
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.
As macrophages accumulate, they take up lipoproteins and actively accumulate lipid to become foam cells. 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 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.
L’INTESTINO: assorbe colesterolo dal cibo o dalla bile IL FEGATO: – ppt scaricare
On activation of monocytes by endothelial cell products such as chemokines, monocyte integrins achieve high-affinity interactions digestioje endothelial adhesion molecules, and cells arrest on the endothelial surface.
Note the many points of intersection between HDL and endogenous lipid metabolism. 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.
The endocytosed particles ddei transported to the lysosomes, and free cholesterol FC is then released into the cytosol.
Oxidized LDL has a number of deleterious effects on vascular function. Infusion of apoA-I has been shown to attenuate atherosclerosis in animals aasorbimento possibly in humans. Dietary cholesterol and fatty acids are absorbed by enterocytes in the duodenum and proximal jejunum.
Le mie presentazioni Profilo Feed-back Uscire. Expression of this transporter can also be stimulated by LXR activation. Oxidized LDL can directly injure endothelial cells and cause endothelial dysfunction D. The triglyceride core of VLDL is removed by the action of lipoprotein lipase on the endothelial cells of adipose and muscle tissue.
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. Oxidized LDL can also cause foam cell necrosis, with release of numerous proteolyitic enzymes assorbimebto can damage the intima E.
Oxidized LDL promotes monocyte chemotaxis into the subendothelial space A and inhibits monocyte egress from that space B.
The catabolism of HDL can also be inhibited by nicotinic acid through a mechanism that is largely unknown. 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.
Resident monocyte-macrophages bind to oxidized LDL via a scavenger receptor SR-Aresulting in the formation of lipid-laden foam cells C. HDL becomes larger as it accumulates more cholestery esters. Autorizzarsi digestioone i social network: In response to these chemokine gradients, cells migrate through the endothelium.
L’INTESTINO: assorbe colesterolo dal cibo o dalla bile IL FEGATO:
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. LDL-R is recycled to the cell surface, whilethe lipoprotein particle is hydrolyzed into asdorbimento and free cholestero.
Several pleiotropic effects of HDL in the vasculature may underlie its anti-atherogenicity. Although inter-conversion of HDL subspecies is depicted as occurring in the arterial wall, it probably also occurs in the plasma.
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. 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 dwi acyltransferase LCAT enzyme and develop into spherically shaped HDL2 larger, less dense particles or HDL3 smaller, more dense particleswhich, in turn, can oipidi as acceptors for ABCG1-mediated assofbimento efflux from macrophages, resulting in further cholesterol enrichment digestiond HDL, before returning to the circulation.
They differentiate into the metabolically active, secretory and highly phagocytic inflammatory macrophage.