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Intracellular Fatty acids

The free fatty acid uptake by tissues is related directly to the plasma free fatty acid concentration, which in turn is determined by the rate of lipolysis in adipose tissue. After dissociation of the fatty acid-albumin complex at the plasma membrane, fatty acids bind to a membrane tty acid transport protein that acts as a transmembrane cotransporter with Na. On entering the cytosol, free fatty acids are bound by intracellular fatty acid-binding proteins. The role of these proteins in intracellular transport is thought to be similar to that of serum albumin in extracellular transport of long-chain fatty acids. [Pg.207]

Coe, N.R. and Bernlohr, D.A. (1998) Physiological properties and functions of intracellular fatty acid-binding proteins. Biochimica et Biophysica Acta 1391, 287-306. [Pg.333]

There are five intracellular retinoid binding proteins that show considerable sequence homology not only with each other, but also with a variety of other intracellular binding proteins for hydrophobic metabolites, including the intracellular fatty acid binding protein (Li and Norris, 1996 Noy, 2000 Vogel et al., 2001). [Pg.47]

Fatty acids C10 0 and longer have considerable detergent properties and are not found free within cells. Most cells contain small intracellular fatty acid-binding proteins (FABPs), which are thought to function in part to buffer the detergent effects of free fatty acids. In the commercial sense, soaps are the water-soluble sodium or potassium salts of fatty acids, which are made from fats and oils by treating them chemically with a strong base such as NaOH or KOH. [Pg.883]

If there is a connection between female sex hormone levels and VLDL secretion, injection of estrogen into a male rat should have the following effects There should be a timely and measurable increase in VLDL secretion. This process requires a concomitant increase in the synthesis of the components of VLDL, that is apoproteins, triacylglycerols, phospholipid, and cholesterol. FABP synthesis should increase in response to the increased intracellular fatty acid concentrations. [Pg.718]

Fig.1. Possible pathways for the intracellular movement of n-3 polyunsaturated fatty acid as it relates to the synthesis of 4,7,10,13,16,19-22 6. The pathway implies that when 24 6 (n-3) is produced in the endoplasmic reticulum, it preferentially moves to another cellular compartment rather than serving as a substrate for further chain elongation. It is not known whether fatty acids move between subcellular compartments as acyl-CoA or whether they are hydrolyzed followed by their reactivation at the subcellular site where they are to be metabolized. If 24 6 n-3 is to be metabolized by mitochondria, it must be transported across the outer (O.M.) and inner (I.M.) membranes into the mitochondrial matrix. This pathway has recently been shown to be of minor importance. The preferred, if not the exclusive pathway for 24 6 n-3 metabolism requires its movement to peroxisomes, where after one degradative cycle, the 22 6 n-3 preferentially moves back to the endoplasmic reticulum rather than serving as a substrate for continued (3-oxidation. Again it is not known in what form the 22 6 n-3 is transported, i.e., acyl-CoA or free fatty acid and how or whether these intracellular fatty acid movements require specific proteins. Fig.1. Possible pathways for the intracellular movement of n-3 polyunsaturated fatty acid as it relates to the synthesis of 4,7,10,13,16,19-22 6. The pathway implies that when 24 6 (n-3) is produced in the endoplasmic reticulum, it preferentially moves to another cellular compartment rather than serving as a substrate for further chain elongation. It is not known whether fatty acids move between subcellular compartments as acyl-CoA or whether they are hydrolyzed followed by their reactivation at the subcellular site where they are to be metabolized. If 24 6 n-3 is to be metabolized by mitochondria, it must be transported across the outer (O.M.) and inner (I.M.) membranes into the mitochondrial matrix. This pathway has recently been shown to be of minor importance. The preferred, if not the exclusive pathway for 24 6 n-3 metabolism requires its movement to peroxisomes, where after one degradative cycle, the 22 6 n-3 preferentially moves back to the endoplasmic reticulum rather than serving as a substrate for continued (3-oxidation. Again it is not known in what form the 22 6 n-3 is transported, i.e., acyl-CoA or free fatty acid and how or whether these intracellular fatty acid movements require specific proteins.
Matarese, V, Stone, R. L, Waggoner, D. W., and Bernlohr, D. A (1990) Intracellular fatty acid trafficking and the role of cytosoloc hpid-bmdmg proteins. Prog Lipid Res 28,245-272... [Pg.176]

Fig. 3.3. Possible roles of intracellular fatty acid-binding proteins (FABP) in fatty acid metabolism. Fatty acids are delivered to cells by extracellular fatty acid-binding proteins (albumin, lipocalins), by very low-density lipoproteins (VLDL) or by chylomicrons (ChM). After internalization, the FABP may bind the non-esterified fatty acid, and may facilitate their transport to appropriate subcellular sites where metabolism takes place. Fig. 3.3. Possible roles of intracellular fatty acid-binding proteins (FABP) in fatty acid metabolism. Fatty acids are delivered to cells by extracellular fatty acid-binding proteins (albumin, lipocalins), by very low-density lipoproteins (VLDL) or by chylomicrons (ChM). After internalization, the FABP may bind the non-esterified fatty acid, and may facilitate their transport to appropriate subcellular sites where metabolism takes place.

See other pages where Intracellular Fatty acids is mentioned: [Pg.495]    [Pg.497]    [Pg.340]    [Pg.270]    [Pg.96]    [Pg.401]    [Pg.48]    [Pg.655]    [Pg.495]    [Pg.497]    [Pg.888]    [Pg.146]    [Pg.476]    [Pg.122]    [Pg.400]    [Pg.286]    [Pg.21]    [Pg.284]    [Pg.298]    [Pg.1339]    [Pg.14]    [Pg.232]    [Pg.89]    [Pg.215]    [Pg.153]    [Pg.216]   
See also in sourсe #XX -- [ Pg.57 ]




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