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Fatty acids resources:

Fatty acids research abs 1 || Fatty acids research abs 2 || Fatty acids research abs 3 || Fatty acids research abs 4

J Neurosci. 2002 Oct 1;22(19):8429-37.
Arachidonic acid plays a role in rat vomeronasal signal transduction.

Spehr M, Hatt H, Wetzel CH.

Department of Cell Physiology, Ruhr-University Bochum, 44780 Bochum, Germany.

Sensory neurons of the vomeronasal organ (VNO) detect volatile chemicals that are released by conspecific animals and convey information about social and reproductive behavior. The signal transduction pathway in vomeronasal receptor neurons (VRNs) is not known in detail, but is believed to be distinct from that of the sensory neurons of the main olfactory system. Many of the identified olfactory transduction components are not expressed by VRNs. Using Ca2+ imaging and electrophysiological recordings, we investigated the signal transduction pathway of urine perception and the possible role of polyunsaturated fatty acids (PUFAs) as intracellular messengers in freshly dissociated rat VNO neurons. We found that application of urine induced a transient increase in intracellular Ca2+ that was dependent on the activity of phospholipase C and diacylglycerol (DAG) lipase. The Ca2+ transient was not dependent on depletion of intracellular Ca2+ stores but was dependent on the presence of extracellular Ca2+. Furthermore, the urine response was not sensitive to modulators of adenylate cyclase and inhibitors of inositol 1,4,5-trisphosphate receptors. Application of PUFAs (linolenic acid and arachidonic acid, synthesized in living cells from DAG) also elicited Ca2+ transients in fura 2 measurements and inward currents in whole-cell voltage-clamp recordings. Pharmacological inhibition of lipoxygenase and cyclooxygenase induced a transient increase in intracellular Ca2+, possibly by increasing the endogenous level of PUFAs, leading to activation of transduction channels. These data provide evidence for a role of PUFAs in rat vomeronasal signal transduction.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12351717&dopt=Abstract

Curr Opin Lipidol. 2002 Oct;13(5):471-81.
Lipoprotein lipase: the regulation of tissue specific expression and its role in lipid and energy metabolism.

Preiss-Landl K, Zimmermann R, Hammerle G, Zechner R.

Institute of Molecular Bioloogy, Biochemistry and Microbiology, Karl-Frasnzens-University, Graz, Heinrichstrasse 31a, A-8010 Graz, Austria.

PURPOSE OF REVIEW: The aim of this review is to summarize and discuss recent advances in the understanding of the physiological role of lipoprotein lipase in lipid and energy metabolism. RECENT FINDINGS: Studies on the transcriptional and the posttranscriptional level of lipoprotein lipase expression have provided new insights into the complex mechanisms that are involved in the regulation of the enzyme. Additionally a large body of evidence from both human studies and animal models suggests that the level of lipoprotein lipase expression in a given tissue is the rate limiting process for the uptake of triglyceride derived fatty acids. Imbalances in the partitioning of fatty acids among peripheral tissues have major metabolic consequences. For example, in mice both decreased lipoprotein lipase activities in adipose tissue and increased activity in muscle are associated with resistance to obesity; lack of lipoprotein lipase activity in macrophages is correlated with a decreased susceptibility to develop atherosclerotic lesions and overexpression of the enzyme in muscle is associated with increased blood glucose levels and insulin resistance. SUMMARY: Considering the central role of lipoprotein lipase in energy metabolism it is a reasonable goal to discover and develop new drugs that affect the tissue specific expression pattern of the enzyme.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12352010&dopt=Abstract [PubMed - in process]

Biosci Biotechnol Biochem. 2002 Aug;66(8):1723-6.
Solubility of saturated fatty acids in water at elevated temperatures.

Khuwijitjaru P, Adachi S, Matsuno R.

Division of Food Science and Biotechnology, Graduate School of Agriculture, Kyoto University, Japan.

The solubility in water of saturated fatty acids with even carbon numbers from 8 to 18 was measured in the temperature range of 60 to 230 degrees C and at a pressure of 5 or 15 MPa. The pressure had no significant effect on the solubility. The solubility of the fatty acids increased with increasing temperature. At temperatures higher than about 160 degrees C, the logarithm of the solubility in mole fraction was linearly related to the reciprocal of the absolute temperature for each fatty acid, indicating that the water containing solubilized fatty acid molecules formed a regular solution at the higher temperatures. The enthalpy of a solution of the fatty acids in water, which was evaluated from the linear relationship at the given temperatures, increased linearly with the carbon number of the fatty acid.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12353634&dopt=Abstract

J Nutr Sci Vitaminol (Tokyo). 1998 Dec;44(6):745-56.
Fatty acid composition and arachidonate metabolites in the livers of ethanol-treated rats fed an arachidonate-supplemented diet: effect of dietary fat.

Okita M, Sasagawa T, Suzuki K, Miyamoto A, Wakabayashi H, Watanabe A.

Department of Nutritional Science, Faculty of Health and Welfare Science, Okayama Prefectural University, Soja, Japan.

The effects of 1% arachidonic acid ethyl ester (AA) administration on the liver prostanoid metabolites and on serum and liver lipids in 3 g/kg ethanol-administered rats fed 10% lard or corn oil were studied. The rats were divided into 6 groups: lard-sucrose (Lard-Suc); lard-ethanol without AA (Lard-Et); lard-ethanol with AA (Lard-EtAA); corn oil-sucrose (Corn-Suc); corn oil-ethanol without AA (Corn-Et); and corn oil-ethanol with AA (Corn-EtAA). Liver triglyceride increased in Corn-EtAA compared with Corn-Et. Arachidonic acid (20: 4n-6) levels in liver phospholipid were significantly decreased in Corn-Et, but elevated in Lard-Et. The levels of 20:4n-6 were significantly increased with AA administration in both ethanol groups. Liver 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) in Corn-Suc (24.7 +/- 5.1 pg/mg protein) was markedly higher than in Lard-Suc (4.5 +/- 1.2 pg/mg protein), and the 6-keto-PGF1 alpha lowered significantly with the addition of ethanol (9.3 +/- 0.9 pg/mg protein), but it increased with AA administration (21.6 +/- 4.9 pg/mg protein). In Lard-EtAA, a significant increase in 6-keto-PGF1 alpha was observed compared with Lard-Suc. The liver leukotriene B4 (LTB4) level in Lard-Suc was significantly lower than that of Corn-Suc. In the corn oil group, ethanol feeding was associated with a significant increase in liver LTB4. AA administration to Corn-Et suppressed the elevated LTB4. Serum thiobarbituric acid-reactive substance (TBARS) concentrations in the corn oil group were higher than in the lard group, and these concentrations were not altered by AA administration. From these results, we concluded that the administration of AA in rats treated with ethanol increased 20:4n-6 in liver phospholipid and liver PGI2 levels, irrespective of dietary fat, and may protect against alcoholic liver injury. AA with a diet rich in linoleic acid (18:2n-6), however, may increase fat in the alcoholic liver.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10197306&dopt=Abstract

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