DIGESTIONE E ASSORBIMENTO DEI LIPIDI PDF

August 2, 2019 posted by

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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PPARalpha also increases fatty acid oxidation in hepatocytes. The end result of these metabolic alterations is a decrease in lipidl triglyceride levels and an increase in plasma HDL levels. Pensiamo che vi sia piaciuta questa presentazione.

Fibrates have several effects on axsorbimento metabolism, all of whihc are thought to result from PPARalpha-mediated changes in gene transcription. 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.

On entering the sub-endothelial space, lipid-free or lipid-poor apolipoprotein A-I apoA-I can bind to the ABC asssorbimento A1 ABCA1 on the cell surface of macrophages in the arterial wall and promote efflux of free cholesterol and phospholipids from these cells. First, cholesterol decreases the activity of HGM CoA reductase, the rate-limiting enzyme in cholesterol synthesis. Autorizzarsi attraverso i social network: Nascent HDL circulates in the plasma and receives free cholesterol from cholesterol laden asslrbimento macrophages, by a process that is depndent on the enzyme ATP-binding cassette transporter A!

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

Note the many points of intersection between HDL and endogenous lipid metabolism. Oxidized LDL can directly injure endothelial cells and cause endothelial dysfunction D. Elevated LDL is a major risk factor for the development of atherosclerosis. The cytokine-activated endothelium expresses adhesion molecules that lead to the recruitment of peripheral blood monocytes to the inflammatory site.

As macrophages accumulate, they take up lipoproteins and actively accumulate lipid to become foam cells.

On the basis of studies in genetically modified mice, E- and P-selectins have been implicated in the development of vascular lesions. Oxidized LDL promotes monocyte chemotaxis into the subendothelial space A and inhibits monocyte egress from that space B. 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.

To use this website, you must agree to our Privacy Policyincluding cookie policy. Several pleiotropic effects of HDL in the vasculature may underlie its anti-atherogenicity. LDL-R is recycled to the cell surface, whilethe lipoprotein particle is hydrolyzed into aminoacids and free cholestero.

Oxidized LDL has a number of deleterious effects on vascular function. Dietary cholesterol and fatty acids are absorbed by enterocytes in the duodenum and proximal jejunum.

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. 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.

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Fibrates have been shown to increase the expression of apoA-I in human hepatocytes.

Le mie presentazioni Profilo Feed-back Uscire. This results in activation or suppression of transcription of a target gene.

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 free fatty acid flux ,ipidi the liver. To make this website work, we log user data and share it with processors.

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

LOD levels also decrease modestly because of a decrease in hepatic fatty acid and triglyceride synthesis not shown. Sul progetto SlidePlayer Condizioni di utilizzo.

Second, hepatic lipase can hydrolyze the triglyceride core, regenerating small HDL.

Registrazione Hai dimenticato la passaword? Statins competitively inhibit HGM CoA reductase, the enzyme that catalyzes a crucial step in cholesterol synthesis. The realtive triglycerdie rich HDL can then be eliminated by one of three mechanisms.