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. The triglyceride core of VLDL is removed by the action of lipoprotein lipase on the lipidl cells of adipose and muscle tissue.

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

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 Registrazione Hai dimenticato la passaword?

Sul progetto SlidePlayer Condizioni di utilizzo. 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.

This results in activation or suppression of transcription of a target gene. Oxidized LDL promotes monocyte chemotaxis into the subendothelial space A and inhibits monocyte egress from that space B. 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 assorbimneto.


Oxidized LDL can directly injure endothelial cells and cause endothelial dysfunction D. Intracellular cholesterol has three regulatory effects on the cell.

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

Activated macrophages within the lesion secrete chemotactic products, including chemokines. Oxidized LDL has a number of deleterious effects on vascular function.

Third, cholesterol inhibits the transcription of the gene encoding the LDL receptor, and thereby decreases further uptake of cholesterol by the cell. Fibrates have several effects on lipid metabolism, all of whihc are thought dsi result from PPARalpha-mediated changes in gene transcription.

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. HDL originates in the liver or the intestine or from remnant lipoprotein products released during the hydrolysis of lipoproteins by plasma liporotein lipase.

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

This decreased free fatty acid flux results in decrease epatic triglyceride synthesis and decrease VLD synthesis. The catabolism of HDL can xssorbimento 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.

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. Resident monocyte-macrophages assoebimento to oxidized LDL via a scavenger receptor SR-Aresulting in the formation of lipid-laden foam cells C. Dietary cholesterol and fatty acids are absorbed by enterocytes in the duodenum and proximal jejunum.


In response to these chemokine gradients, cells migrate through the endothelium. Several mouse studies have implicated the 4 1-integrin also known as VLA-4 and its cognate ligand VCAM-1 in aassorbimento high-affinity interactions. 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.

Expression of this transporter can also be stimulated by LXR activation. Cytosolic FC is kept in appropriate equilibrium with cholesterol wssorbimento CE through the action of two enzymes: Several pleiotropic effects of HDL in the vasculature may underlie its anti-atherogenicity.

Oxidized LDL can also cause foam cell necrosis, with release of numerous proteolyitic enzymes that can damage the intima E. On entering the sub-endothelial space, lipid-free or lipid-poor apolipoprotein A-I diyestione 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.

The realtive triglycerdie rich HDL can then be eliminated by one of three mechanisms. 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.