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 the basis of studies in genetically modified mice, E- and P-selectins have been implicated in the development of vascular lesions. 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.

The realtive triglycerdie rich HDL can then be eliminated by one of three mechanisms. 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 Digestilne to the liver and excretion opf cholesterol in the bile.

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. Dietary cholesterol and fatty acids are absorbed by enterocytes in the duodenum and proximal jejunum. Sul progetto SlidePlayer Condizioni di utilizzo. HDL originates in the liver or the intestine or from remnant lipoprotein products released during the hydrolysis of lipoproteins by plasma liporotein lipase.

Oxidized LDL promotes monocyte chemotaxis into the subendothelial space A and inhibits monocyte egress from that space B. 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. Dissociation of co-repressors occurs as a consequence of a ligand-induced conformational change, and the activated heterodimer can then bind to the PPRE.

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Activated macrophages within the lesion secrete chemotactic products, including chemokines.

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

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.

The triglyceride core of VLDL is removed by the action of lipoprotein lipase on the endothelial cells of adipose and muscle tissue. The endocytosed particles are transported to the lysosomes, and free cholesterol FC is then released into the cytosol.

Le mie presentazioni Profilo Feed-back Uscire. Digestioje end result of these metabolic alterations is a decrease in plasma triglyceride levels and an increase in plasma HDL levels.

Using apoAI as a cofactor, plasma lecithin: 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. 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 They differentiate into the metabolically active, secretory and highly phagocytic inflammatory macrophage.

In response to these chemokine gradients, cells migrate through the endothelium.

Fibrates have several effects on lipid metabolism, all of whihc are thought to result from PPARalpha-mediated changes in gene transcription. Native LDL that migrates into the subendothelial space can undergo chemical transformation tyo oxidized LDL via lipid peroxidation and fragmentation of apoB Pensiamo che vi sia piaciuta questa presentazione.

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HDL becomes larger as it accumulates more cholestery esters. This decreased free fatty acid flux results in decrease epatic triglyceride synthesis and decrease VLD synthesis.

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

First, cholesterol decreases the activity of HGM CoA reductase, the rate-limiting enzyme in cholesterol synthesis. This results in activation or suppression of transcription of a target gene. LOD levels also decrease modestly because of a decrease in hepatic fatty acid and triglyceride synthesis not shown.

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

Cytosolic FC is kept in appropriate equilibrium with cholesterol ester CE through the action of two enzymes: PPARalpha also increases fatty acid oxidation in hepatocytes. Nascent HDL circulates in the plasma and receives free cholesterol from cholesterol laden cells,including macrophages, by a process that is digwstione on the enzyme ATP-binding cassette transporter A!

Second, cholesterol activates acetyl CoA: Alternatively, LDL can be oxidized and taken up by macrophages, assorbimenyo a reaction that depends on the scavenger receptor-A SR-A ; this reaction results in the formation of foam cells. The catabolism of HDL can also be inhibited by nicotinic acid through a mechanism that is largely unknown.

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.