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		<title>Lipids in Health and Disease - Latest articles</title>
		<link>http://www.lipidworld.com</link>
		<description>The latest articles from Lipids in Health and Disease (ISSN 1476-511X) published by 
				
				BioMed Central
		</description>
        <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/"/>
        <items>
            <rdf:Seq>
            
				    <rdf:li rdf:resource="http://www.lipidworld.com/content/7/1/35"/>			    
            
				    <rdf:li rdf:resource="http://www.lipidworld.com/content/7/1/34"/>			    
            
				    <rdf:li rdf:resource="http://www.lipidworld.com/content/7/1/33"/>			    
            
				    <rdf:li rdf:resource="http://www.lipidworld.com/content/7/1/32"/>			    
            
				    <rdf:li rdf:resource="http://www.lipidworld.com/content/7/1/31"/>			    
            
				    <rdf:li rdf:resource="http://www.lipidworld.com/content/7/1/30"/>			    
            
				    <rdf:li rdf:resource="http://www.lipidworld.com/content/7/1/29"/>			    
            
				    <rdf:li rdf:resource="http://www.lipidworld.com/content/7/1/28"/>			    
            
				    <rdf:li rdf:resource="http://www.lipidworld.com/content/7/1/27"/>			    
            
				    <rdf:li rdf:resource="http://www.lipidworld.com/content/7/1/26"/>			    
            
            </rdf:Seq>
        </items>
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		<item rdf:about="http://www.lipidworld.com/content/7/1/35">
            
            <title>Cholesterol lowering effect of a soy drink enriched with plant sterols in a French population with moderate hypercholesterolemia</title>
			<description>Background:
Plant sterols are an established non-pharmacological means to reduce total and LDL blood cholesterol concentrations and are therefore recommended for cholesterol management by worldwide-renown health care institutions. Their efficacy has been proven in many types of foods with the majority of trials conducted in spreads or dairy products. As an alternative to dairy products, soy based foods are common throughout the world. Yet, there is little evidence supporting the efficacy of plant sterols in soy-based foods. The objective of this study was to investigate the effect of a soy drink enriched with plant sterols on blood lipid profiles in moderately hypercholesterolemic subjects.
Methods:
In a randomized, placebo-controlled double-blind mono-centric study, 50 subjects were assigned to 200 ml of soy drink either enriched with 2.6 g plant sterol esters (1.6 g/d free plant sterol equivalents) or without plant sterols (control) for 8 weeks. Subjects were instructed to maintain stable diet pattern and physical activity. Plasma concentrations of lipids were measured at initial visit, after 4 weeks and after 8 weeks. The primary measurement was the change in LDL cholesterol (LDL-C). Secondary measurements were changes in total cholesterol (TC), non-HDL cholesterol (non-HDL-C), HDL cholesterol (HDL-C) and triglycerides. 
Results:
Regular consumption of the soy drink enriched with plant sterols for 8 weeks significantly reduced LDL- C by 0.29 mmol/l or 7% compared to baseline (p&lt;0.05). TC and non-HDL-C concentrations decreased by 0.26 mmol/l and 0.31 mmol/l (each p&lt;0.05), respectively. Mean reductions in total, LDL and non-HDL cholesterol were significantly greater than in the placebo group (p&lt;0.05). HDL-C and triglycerides were not affected. Compliance was very high (>96%), and products were well tolerated.
Conclusion:
Daily consumption of a plant sterol-enriched soy drink significantly decreased total, non-HDL and LDL cholesterol and is therefore an interesting and convenient aid in managing mild to moderate hypercholesterolemia.</description>
			<link>http://www.lipidworld.com/content/7/1/35</link>
			
			 	<dc:creator>Christina Weidner, Michel Krempf, Jean-Marie Bard, Murielle Cazaubiel and Doris Bell</dc:creator>
			
			<dc:source>Lipids in Health and Disease 2008, 7:35</dc:source>
			<dc:date>2008-10-06</dc:date>
			<dc:identifier>doi:10.1186/1476-511X-7-35</dc:identifier>
			
			
							
					<prism:publicationName>Lipids in Health and Disease</prism:publicationName>
					
			
							
					<prism:issn>1476-511X</prism:issn>
					
			
							
					<prism:volume>7</prism:volume>
					
			
							
					<prism:startingPage>35</prism:startingPage>
					
			
							
					<prism:publicationDate>2008-10-06</prism:publicationDate>
					

            <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/"/>
        </item>
	
		<item rdf:about="http://www.lipidworld.com/content/7/1/34">
            
            <title>Conjugated linoleic acid content of human plasma</title>
			<description>Conjugated linoleic acid (CLA), a naturally occurring anticarcinogen found in dairy products, is an intermediary product of ruminal biohydrogenation of polyunsaturated fatty acids. Few data exist on the CLA content of the human blood plasma. The determination of a "normal" content could help in estimating if a person consumes satisfactory amounts of CLA with the diet and thus takes advantage of its potential beneficial effects on health. The purpose of this study was to compare the plasma CLA content of individuals not consuming dairy products (group 1, n = 12), individuals consuming normal amounts of dairy products (group 2, n = 77) and individuals consuming CLA supplement (group 3, n = 12). The only CLA isomer that presented higher percentage than the detection limit (0.03% of total fatty acids) was rumenic acid (cis9, trans11-octadecadienoic acid). An interesting finding is that compared to the other two groups, group 3 members show the highest average plasma content in rumenic acid, i.e. 0.20% of total fatty acids. The present study could be characterized as the first step in the direction of establishing a normal CLA content of human plasma. Based on these results, it could be suggested that the lower limit of the plasma CLA content is approximately 0.1% of total fatty acids.</description>
			<link>http://www.lipidworld.com/content/7/1/34</link>
			
			 	<dc:creator>Spiros N Zlatanos, Kostas Laskaridis and Angelos Sagredos</dc:creator>
			
			<dc:source>Lipids in Health and Disease 2008, 7:34</dc:source>
			<dc:date>2008-09-30</dc:date>
			<dc:identifier>doi:10.1186/1476-511X-7-34</dc:identifier>
			
			
							
					<prism:publicationName>Lipids in Health and Disease</prism:publicationName>
					
			
							
					<prism:issn>1476-511X</prism:issn>
					
			
							
					<prism:volume>7</prism:volume>
					
			
							
					<prism:startingPage>34</prism:startingPage>
					
			
							
					<prism:publicationDate>2008-09-30</prism:publicationDate>
					

            <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/"/>
        </item>
	
		<item rdf:about="http://www.lipidworld.com/content/7/1/33">
            
            <title>Genetic studies on the APOA1-C3-A5 gene cluster in Asian Indians with premature coronary artery disease</title>
			<description>Background:
The APOA1-C3-A5 gene cluster plays an important role in the regulation of lipids. Asian Indians have an increased tendency for abnormal lipid levels and high risk of Coronary Artery Disease (CAD). Therefore, the present study aimed to elucidate the relationship of four single nucleotide polymorphisms (SNPs) in the Apo11q cluster, namely the -75G>A, +83C>T SNPs in the APOA1 gene, the Sac1 SNP in the APOC3 gene and the S19W variant in the APOA5 gene to plasma lipids and CAD in 190 affected sibling pairs (ASPs) belonging to Asian Indian families with a strong CAD history.Methods &amp; resultsGenotyping and lipid assays were carried out using standard protocols. Plasma lipids showed a strong heritability (h2 48% &#8211; 70%; P &lt; 0.0001). A subset of 77 ASPs with positive sign of Logarithm of Odds (LOD) score showed significant linkage to CAD trait by multi-point analysis (LOD score 7.42, P &lt; 0.001) and to Sac1 (LOD score 4.49) and -75G>A (LOD score 2.77) SNPs by single-point analysis (P &lt; 0.001). There was significant proportion of mean allele sharing (pi) for the Sac1 (pi 0.59), -75G>A (pi 0.56) and +83C>T (pi 0.52) (P &lt; 0.001) SNPs, respectively. QTL analysis showed suggestive evidence of linkage of the Sac1 SNP to Total Cholesterol (TC), High Density Lipoprotein-cholesterol (HDL-C) and Apolipoprotein B (ApoB) with LOD scores of 1.42, 1.72 and 1.19, respectively (P &lt; 0.01). The Sac1 and -75G>A SNPs along with hypertension showed maximized correlations with TC, TG and Apo B by association analysis.
Conclusion:
The APOC3-Sac1 SNP is an important genetic variant that is associated with CAD through its interaction with plasma lipids and other standard risk factors among Asian Indians.</description>
			<link>http://www.lipidworld.com/content/7/1/33</link>
			
			 	<dc:creator>Jayashree Shanker, Ganapathy Perumal, Veena S Rao, Natesha B Khadrinarasimhiah, Shibu John, Sridhara Hebbagodi, Manjari Mukherjee and Vijay V Kakkar</dc:creator>
			
			<dc:source>Lipids in Health and Disease 2008, 7:33</dc:source>
			<dc:date>2008-09-19</dc:date>
			<dc:identifier>doi:10.1186/1476-511X-7-33</dc:identifier>
			
			
							
					<prism:publicationName>Lipids in Health and Disease</prism:publicationName>
					
			
							
					<prism:issn>1476-511X</prism:issn>
					
			
							
					<prism:volume>7</prism:volume>
					
			
							
					<prism:startingPage>33</prism:startingPage>
					
			
							
					<prism:publicationDate>2008-09-19</prism:publicationDate>
					

            <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/"/>
        </item>
	
		<item rdf:about="http://www.lipidworld.com/content/7/1/32">
            
            <title>s-ICAM-1 and s-VCAM-1 in healthy men are strongly associated with traits of the metabolic syndrome, becoming evident in the postprandial response to a lipid-rich meal</title>
			<description>Background:
The importance of the postprandial state for the early stages of atherogenesis is increasingly acknowledged. We conducted assessment of association between postprandial triglycerides, insulin and glucose after ingestion of a standardized lipid-rich test meal, and soluble cellular adhesion molecules (sCAM) in young healthy subjects.
Methods:
Metabolic parameters and sICAM-1, sVCAM-1 and E-selectin were measured before and hourly until 6 hours after ingestion of a lipid-rich meal in 30 healthy young men with fasting triglycerides &lt;150 mg/dl and normal fasting glucose levels. Subjects were classified as either normal responders (NR) (postprandial triglyceride maxima &lt; 260 mg/dl) or high responders (HR) (postprandial triglyceride maxima > 260 mg/dl). Levels of CAM were compared in HR and NR, and correlation with postprandial triglyceride, insulin and glucose response was assessed.
Results:
Fasting sICAM-1 and sVCAM-1 levels were significantly higher in HR as compared to NR (p = 0.046, p = 0.03). For sE-selectin there was such a trend (p = 0.05). There was a strong positive and independent correlation between sICAM-1 and postprandial insulin maxima (r = 0.70, p &lt; 0.001). sVCAM-1 showed significant correlation with postprandial triglycerides (AUC) (r = 0.37, p = 0.047). We found no correlation between sCAMs and fasting insulin or triglyceride concentrations.
Conclusion:
This independent association of postprandial triglycerides with sICAM-1 may indicate a particular impact of postprandial lipid metabolism on endothelial reaction.</description>
			<link>http://www.lipidworld.com/content/7/1/32</link>
			
			 	<dc:creator>Diana Rubin, Sandra Claas, Maria Pfeuffer, Michael Nothnagel, Ulrich R Foelsch and Juergen Schrezenmeir</dc:creator>
			
			<dc:source>Lipids in Health and Disease 2008, 7:32</dc:source>
			<dc:date>2008-09-01</dc:date>
			<dc:identifier>doi:10.1186/1476-511X-7-32</dc:identifier>
			
			
							
					<prism:publicationName>Lipids in Health and Disease</prism:publicationName>
					
			
							
					<prism:issn>1476-511X</prism:issn>
					
			
							
					<prism:volume>7</prism:volume>
					
			
							
					<prism:startingPage>32</prism:startingPage>
					
			
							
					<prism:publicationDate>2008-09-01</prism:publicationDate>
					

            <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/"/>
        </item>
	
		<item rdf:about="http://www.lipidworld.com/content/7/1/31">
            
            <title>Effects of butter naturally enriched with conjugated linoleic acid and vaccenic acid on blood lipids and LDL particle size in growing pigs</title>
			<description>Background:
Cow milk is a natural source of the cis 9, trans 11 isomer of conjugated linoleic acid (c9,t11-CLA) and trans vaccenic acid (VA). These fatty acids may be considered as functional foods, and the concentration in milk can be increased by e.g. sunflower oil supplementation to the dairy cow feed.The objective of this study was to compare the effects of regular butter with a special butter naturally enriched in c9,t11-CLA and VA on plasma lipids in female growing pigs. The experimental period lasted for three weeks and the two diets provided daily either 5.0 g c9,t11-CLA plus 15.1 g VA or 1.3 g c9,t11-CLA plus 3.6 g VA.
Results:
The serum concentrations of c9,t11-CLA, VA and alpha-linolenic acid were increased and myristic (14:0) and palmitic acid (16:0) were reduced in the pigs fed the CLA+VA-rich butter-diet compared to regular butter, but no differences in plasma concentrations of triacylglycerol, cholesterol, HDL-cholesterol, LDL-cholesterol, LDL particle size distribution or total cholesterol/HDL cholesterol were observed among the two dietary treatment groups.
Conclusion:
Growing pigs fed diets containing butter naturally enriched in about 20 g c9,t11-CLA plus VA daily for three weeks, had increased serum concentrations of alpha-linolenic acid and decreased myristic and palmitic acid compared to pigs fed regular butter, implying a potential benefit of the CLA+VA butter on serum fatty acid composition. Butter enriched in CLA+VA does not appear to have significant effect on the plasma lipoprotein profile in pigs.</description>
			<link>http://www.lipidworld.com/content/7/1/31</link>
			
			 	<dc:creator>Anna Haug, Per Sj&#248;gren, Nina H&#248;lland, Hanne M&#252;ller, Nils P Kjos, Ole Taugb&#248;l, Nina Fjerdingby, Anne S Biong, Eirik Selmer-Olsen and Odd M Harstad</dc:creator>
			
			<dc:source>Lipids in Health and Disease 2008, 7:31</dc:source>
			<dc:date>2008-08-29</dc:date>
			<dc:identifier>doi:10.1186/1476-511X-7-31</dc:identifier>
			
			
							
					<prism:publicationName>Lipids in Health and Disease</prism:publicationName>
					
			
							
					<prism:issn>1476-511X</prism:issn>
					
			
							
					<prism:volume>7</prism:volume>
					
			
							
					<prism:startingPage>31</prism:startingPage>
					
			
							
					<prism:publicationDate>2008-08-29</prism:publicationDate>
					

            <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/"/>
        </item>
	
		<item rdf:about="http://www.lipidworld.com/content/7/1/30">
            
            <title>Effects of Krill Oil on serum lipids of hyperlipidemic rats and human SW480 cells</title>
			<description>Background:
Cardiovascular disease (CVD) and colon cancer incidence are known to be closely related to dietary factors. This article evaluated effects of krill oil (KO) on serum lipids of hyperlipidemia rats and human colon cancer cells (SW480). Serum lipids of rats fed with high fat diet (HFD) and different doses of KO were measured by automatic analyzer. Effect of KO on viability of cells was determined by methyl thiazolyl tetrazolium (MTT) assay.
Results:
Except for higher dose group, body weights decreased significantly. Total cholesterol (TC), LDL-cholesterol (LDL-C) of all dose groups, Triglycerides (TG) of low and mid dose groups descended significantly, while there were no significant differences of HDL-cholesterol (HDL-C), compared with control group. Treatment of colon cancer cells with KO also resulted in time-dependent inhibition of cell growth.
Conclusion:
Our findings indicated that the consumption of KO may provide benefits to control serum lipid levels in certain diseases and inhibit growth of colon cancer cells. Therefore, KO may be a good candidate for development as a functional food and nutraceutical.</description>
			<link>http://www.lipidworld.com/content/7/1/30</link>
			
			 	<dc:creator>Jia-Jin Zhu, Jia-Hui Shi, Wen-Bin Qian, Zhen-Zhen Cai and Duo Li</dc:creator>
			
			<dc:source>Lipids in Health and Disease 2008, 7:30</dc:source>
			<dc:date>2008-08-29</dc:date>
			<dc:identifier>doi:10.1186/1476-511X-7-30</dc:identifier>
			
			
							
					<prism:publicationName>Lipids in Health and Disease</prism:publicationName>
					
			
							
					<prism:issn>1476-511X</prism:issn>
					
			
							
					<prism:volume>7</prism:volume>
					
			
							
					<prism:startingPage>30</prism:startingPage>
					
			
							
					<prism:publicationDate>2008-08-29</prism:publicationDate>
					

            <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/"/>
        </item>
	
		<item rdf:about="http://www.lipidworld.com/content/7/1/29">
            
            <title>Isoforms of Retinol binding protein 4 (RBP4) are increased in chronic diseases of the kidney but not of the liver</title>
			<description>Background:
The levels of retinol-binding protein 4 (RBP4) &#8211; the carrier protein for Vitamin A in plasma &#8211; are tightly regulated under healthy circumstances. The kidney, the main site of RBP4 catabolism, contributes to an elevation of RBP4 levels during chronic kidney disease (CKD) whereas during chronic liver disease (CLD) RBP4 levels decrease. Little is known about RBP4 isoforms including apo-RBP4, holo-RBP4 as well as RBP4 truncated at the C-terminus (RBP4-L and RBP4-LL) except that RBP4 isoforms have been reported to be increased in hemodialysis patients. Since it is not known whether CLD influence RBP4 isoforms, we investigated RBP4 levels, apo- and holo-RBP4 as well as RBP4-L and RBP4-LL in plasma of 36 patients suffering from CKD, in 55 CLD patients and in 50 control subjects. RBP4 was determined by ELISA and apo- and holo-RBP4 by native polyacrylamide gel electrophoresis (PAGE). RBP4-L and RBP4-LL were analyzed after immunoprecipitation by mass spectrometry (MALDI-TOF-MS).
Results:
RBP4 isoforms and levels were highly increased in CKD patients compared to controls (P &lt; 0.05) whereas in CLD patients RBP4 isoforms were not different from controls. In addition, in hepatic dysfunction RBP4 levels were decreased whereas the amount of isoforms was not affected.
Conclusion:
The occurrence of RBP4 isoforms is not influenced by liver function but seems to be strongly related to kidney function and may therefore be important in investigating kidney function and related disorders.</description>
			<link>http://www.lipidworld.com/content/7/1/29</link>
			
			 	<dc:creator>Simone K Frey, Britta Nagl, Andrea Henze, Jens Raila, Beate Schlosser, Thomas Berg, Martin Tepel, Walter Zidek, Martin O Weickert, Andreas FH Pfeiffer and Florian J Schweigert</dc:creator>
			
			<dc:source>Lipids in Health and Disease 2008, 7:29</dc:source>
			<dc:date>2008-08-27</dc:date>
			<dc:identifier>doi:10.1186/1476-511X-7-29</dc:identifier>
			
			
							
					<prism:publicationName>Lipids in Health and Disease</prism:publicationName>
					
			
							
					<prism:issn>1476-511X</prism:issn>
					
			
							
					<prism:volume>7</prism:volume>
					
			
							
					<prism:startingPage>29</prism:startingPage>
					
			
							
					<prism:publicationDate>2008-08-27</prism:publicationDate>
					

            <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/"/>
        </item>
	
		<item rdf:about="http://www.lipidworld.com/content/7/1/28">
            
            <title>Albuminuria and its correlates in an Iranian type 2 diabetic population</title>
			<description>ObjectiveTo study the prevalence and correlates of increased urinary albumin excretion (UAE) in an Iranian type 2 diabetic population.
Methods:
Over a one year period since October 2002, 400 consecutive type 2 diabetic patients referred to an outpatient diabetes clinic, were enrolled in a cross sectional study. Subjects had no history of renal impairment or overt proteinuria. Data concerning demographic characteristics and cardiovascular risk factors were recorded and height, weight and blood pressure were measured. Glucose, cholesterol, HDL-C, LDL-C, triglyceride, apoprotein B, lipoprotein a, creatinine, and HbA1c were measured in fasting blood samples. Overnight twelve-hour UAE were assessed by immunoturbidometry method. Regression analyses were employed to determine the correlates of UAE.
Results:
Out of 400 patients, 156 (40%) subjects had increased UAE (UAE &#8805; 30 mg/24 hour). The UAE was higher in males compared to females (145.5 vs. 72.1 mg/day; p &lt; 0.05); however, the age and HDL adjusted UAE levels were not significantly different between men and women (120.1 vs. and 87.9 mg/day; p = 0.37). Increased UAE was correlated with decreasing HDL-C and a longer duration of diabetes independent of other variables; increased UAE was correlated with HbA1c as well. Age, systolic and diastolic blood pressure, total cholesterol, LDL-C, triglyceride, apoprotein B, lipoprotein a, and GFR did not correlate with increased UAE.
Conclusion:
In this study, increased UAE was considerably frequent among type 2 diabetic patients without any significant history of renal dysfunction. Albuminuria was found to be associated with dyslipidemia (low HDL-C), long duration of diabetes, and uncontrolled glycemia revealed by higher HbA1c.</description>
			<link>http://www.lipidworld.com/content/7/1/28</link>
			
			 	<dc:creator>Manouchehr Nakhjavani, Alireza Esteghamati, Fatemeh Esfahanian, Naser Aghamohammadzadeh, Sepehr Hamidi, Alipasha Meysamie and Mehrshad Abbasi</dc:creator>
			
			<dc:source>Lipids in Health and Disease 2008, 7:28</dc:source>
			<dc:date>2008-08-10</dc:date>
			<dc:identifier>doi:10.1186/1476-511X-7-28</dc:identifier>
			
			
							
					<prism:publicationName>Lipids in Health and Disease</prism:publicationName>
					
			
							
					<prism:issn>1476-511X</prism:issn>
					
			
							
					<prism:volume>7</prism:volume>
					
			
							
					<prism:startingPage>28</prism:startingPage>
					
			
							
					<prism:publicationDate>2008-08-10</prism:publicationDate>
					

            <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/"/>
        </item>
	
		<item rdf:about="http://www.lipidworld.com/content/7/1/27">
            
            <title>The prevention of endothelial dysfunction through endothelial cell apoptosis inhibition in a hypercholesterolemic rabbit model: the effect of L-arginine supplementation</title>
			<description>Background:
The impact of L-arginine on atherogenesis and its ability to prevent endothelial dysfunction have been studied extensively during the past years. L-arginine is a substance for nitric oxide synthesis which involves in apoptosis. Hypercholesterolemia promotes endothelial dysfunction, and it is hypothesized that L-arginine prevents endothelial dysfunction through endothelial cells apoptosis inhibition. To test this hypothesis, thirty rabbits were assigned into two groups. The control group received 1% cholesterol diet for 4 weeks, and the L-arginine group received same diets plus 3% L-arginine in drinking water.
Results:
No significant differences were observed in cholesterol level between two groups, but the nitrite concentration in L-arginine group was significantly higher than other group (control group: 11.8 &#177; 1; L-arginine group: 14.7 &#177; 0.5 &#956;mol/l); (p &lt; 0.05). The aorta score of fatty streak in control group was 0.875 &#177; 0.35, but no fatty streak lesion was detected in L-arginine group (p &lt; 0.05). The number of intimal apoptotic cells/500 cells of aorta in two groups of experiment were statistically different (control group: 39.3 &#177; 7.6; L-arginine group: 21.5 &#177; 5.3) (p &lt; 0.05).
Conclusion:
The inhibition of endothelial cells apoptosis by L-arginine restores endothelial function in a model of hypercholesterolemia.</description>
			<link>http://www.lipidworld.com/content/7/1/27</link>
			
			 	<dc:creator>Mehdi Nematbakhsh, Shaghayegh Haghjooyjavanmard, Farzaneh Mahmoodi and Ali Reza Monajemi</dc:creator>
			
			<dc:source>Lipids in Health and Disease 2008, 7:27</dc:source>
			<dc:date>2008-08-02</dc:date>
			<dc:identifier>doi:10.1186/1476-511X-7-27</dc:identifier>
			
			
							
					<prism:publicationName>Lipids in Health and Disease</prism:publicationName>
					
			
							
					<prism:issn>1476-511X</prism:issn>
					
			
							
					<prism:volume>7</prism:volume>
					
			
							
					<prism:startingPage>27</prism:startingPage>
					
			
							
					<prism:publicationDate>2008-08-02</prism:publicationDate>
					

            <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/"/>
        </item>
	
		<item rdf:about="http://www.lipidworld.com/content/7/1/26">
            
            <title>Weight loss and brown adipose tissue reduction in rat model of sleep apnea</title>
			<description>Background -Obesity is related to obstructive sleep apnea-hypopnea syndrome (OSAHS), but its roles in OSAHS as cause or consequence are not fully clarified. Isocapnic intermittent hypoxia (IIH) is a model of OSAHS. We verified the effect of IIH on body weight and brown adipose tissue (BAT) of Wistar rats.
Methods:
Nine-month-old male breeders Wistar rats of two groups were studied: 8 rats submitted to IIH and 5 control rats submitted to sham IIH. The rats were weighed at the baseline and at the end of three weeks, after being placed in the IIH apparatus seven days per week, eight hours a day, in the lights on period, simulating an apnea index of 30/hour. After experimental period, the animals were weighed and measured as well as the BAT, abdominal, perirenal, and epididymal fat, the heart, and the gastrocnemius muscle.
Results:
Body weight of the hypoxia group decreased 17 &#177; 7 grams, significantly different from the variation observed in the control group (p = 0,001). The BAT was 15% lighter in the hypoxia group and reached marginally the alpha error probability (p = 0.054).
Conclusion:
Our preliminary results justify a larger study for a longer time in order to confirm the effect of isocapnic intermittent hypoxia on body weight and BAT.</description>
			<link>http://www.lipidworld.com/content/7/1/26</link>
			
			 	<dc:creator>Denis Martinez, Luiz FT Vasconcellos, Patricia G de Oliveira and Signor&#225; P Konrad</dc:creator>
			
			<dc:source>Lipids in Health and Disease 2008, 7:26</dc:source>
			<dc:date>2008-07-31</dc:date>
			<dc:identifier>doi:10.1186/1476-511X-7-26</dc:identifier>
			
			
							
					<prism:publicationName>Lipids in Health and Disease</prism:publicationName>
					
			
							
					<prism:issn>1476-511X</prism:issn>
					
			
							
					<prism:volume>7</prism:volume>
					
			
							
					<prism:startingPage>26</prism:startingPage>
					
			
							
					<prism:publicationDate>2008-07-31</prism:publicationDate>
					

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