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<pubDate>Sun, 27 Jul 2008 07:37:38 BST</pubDate>


	<title>CiteULike: omalbam's adiposity</title>
	<description>CiteULike: omalbam's adiposity</description>


	<link>http://www.citeulike.org/user/omalbam/tag/adiposity</link>
	<dc:publisher>CiteULike.org</dc:publisher>
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	<dc:rights>Copyright &#169; 2004-2008 citeulike.org</dc:rights>
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        <rdf:li rdf:resource="http://www.citeulike.org/user/omalbam/article/2624425"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/omalbam/article/2394905"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/omalbam/article/1478959"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/omalbam/article/1411430"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/omalbam/article/1803076"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/omalbam/article/159779"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/omalbam/article/2285975"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/omalbam/article/2063390"/>

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<item rdf:about="http://www.citeulike.org/user/omalbam/article/2624425">
    <title>Growth Hormone Decreases Visceral Fat and Improves Cardiovascular Risk Markers in Women with Hypopituitarism: a Randomized, Placebo-Controlled Study</title>
    <link>http://www.citeulike.org/user/omalbam/article/2624425</link>
    <description>&lt;i&gt;J Clin Endocrinol Metab (1 April 2008), jc.2007-2371.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Context: Data regarding gender-specific efficacy of growth hormone (GH) on critical endpoints are lacking. There are no randomized, placebo-controlled studies of physiologic GH therapy solely in women.Objective: To determine the effects of physiologic GH replacement on cardiovascular risk markers and body composition in women with GHD.Design: 6-month, randomized, placebo-controlled, double-blind studySetting: GCRCStudy Participants: 43 women with GHD due to hypopituitarismIntervention: Study participants were randomized to receive GH (goal mid-normal serum IGF-I) or placebo.Main Outcome Measures: Cardiovascular risk markers, including high sensitivity C-reactive protein, tissue plasminogen activator, and body composition, including visceral adipose tissue by cross-sectional computed tomography.Results: Mean daily GH dose was 0.67 mg. The mean IGF-I SD score increased from -2.5 +/- 0.3 to -1.4 +/- 0.9 (GH) (p&#60;0.0001 vs. placebo). High sensitivity C-reactive protein decreased by 38.2 +/- 9.6% (GH) vs. 18.2 +/- 6.0% (placebo) (p=0.03). Tissue plasminogen activator and total cholesterol decreased and high-density lipoprotein increased. Homeostasis model assessment: insulin resistance and other markers were unchanged. Body fat decreased [-5.1 +/- 2.0 (GH) vs. 1.9 +/- 1.0% (placebo), p=0.002], as did visceral adipose tissue [-9.0 +/- 5.9 (GH) vs. 4.3 +/- 2.7% (placebo), p=0.03]. Change in IGF-I level was inversely associated with % change in visceral adipose tissue (r= -0.61, p=0.002), total body fat (r= -0.69, p&#60;0.0001), and high sensitivity C-reactive protein (r= -0.51, p=0.003).Conclusions: Low-dose GH replacement in women with GHD decreased total and visceral adipose tissue, and improved cardiovascular markers with a relatively modest increase in IGF-I levels without worsening insulin resistance. 10.1210/jc.2007-2371</description>
    <dc:title>Growth Hormone Decreases Visceral Fat and Improves Cardiovascular Risk Markers in Women with Hypopituitarism: a Randomized, Placebo-Controlled Study</dc:title>

    <dc:creator>Catherine Beauregard</dc:creator>
    <dc:creator>Andrea Utz</dc:creator>
    <dc:creator>Amber Schaub</dc:creator>
    <dc:creator>Lisa Nachtigall</dc:creator>
    <dc:creator>Beverly Biller</dc:creator>
    <dc:creator>Karen Miller</dc:creator>
    <dc:creator>Anne Klibanski</dc:creator>
    <dc:identifier>doi:10.1210/jc.2007-2371</dc:identifier>
    <dc:source>J Clin Endocrinol Metab (1 April 2008), jc.2007-2371.</dc:source>
    <dc:date>2008-04-02T20:47:24-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>J Clin Endocrinol Metab</prism:publicationName>
    <prism:startingPage>jc.2007-2371</prism:startingPage>
    <prism:category>adiposity</prism:category>
    <prism:category>body-composition</prism:category>
    <prism:category>lipids</prism:category>
    <prism:category>r-gh</prism:category>
    <prism:category>therapy</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/omalbam/article/2394905">
    <title>The Association Between the FTO Gene and Fat Mass in Humans Develops by the Postnatal Age of Two Weeks.</title>
    <link>http://www.citeulike.org/user/omalbam/article/2394905</link>
    <description>&lt;i&gt;J Clin Endocrinol Metab (5 February 2008)&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Objective: Little is known about the genetic determinants of fat mass around birth. We hypothesized that the common rs9939609 single nucleotide polymorphism (SNP) in FTO is associated with fat mass and metabolic parameters in neonates. Design: Cross-sectional, hospital-based study. Patients: Two hundred and thirty-four full-term, healthy newborns [122 girls and 112 boys; gestational age (mean, range): 39.0 (37.0-42.0) w, birth weight: 3.2 (1.9-4.2) Kg]. Methods: Cord-blood insulin, IGF-I, IGFBP-1, adiponectin and visfatin, measured by specific immunoassays. Body composition, assessed by dual energy X-ray absorptiometry at approximately 13 d (range, 9-20 d). Genotyping of rs9939609 by retriction fragment length polymorphism analysis. Results: The rs9939609 SNP in FTO was not associated with birth weight; however it was associated with serum visfatin (p&#60;0.001), with weight and ponderal index at age 2 weeks (p&#60;0.05), and with total, truncal and abdominal fat (p&#60;0.05 to p=0.01), so that AA homozygotes had 37% higher plasma visfatin concentration and 17%, 20% and 17% higher total, truncal and abdominal fat mass, respectively, than T-carrier neonates. Conclusion: Our findings support a role of the common rs9939609 SNP in FTO gene in the early stages of fat accretion in humans, and disclose novel associations between this SNP and both serum visfatin and abdominal fat mass in neonates.</description>
    <dc:title>The Association Between the FTO Gene and Fat Mass in Humans Develops by the Postnatal Age of Two Weeks.</dc:title>

    <dc:creator>Abel López-Bermejo</dc:creator>
    <dc:creator>Clive J Petry</dc:creator>
    <dc:creator>Marta Díaz</dc:creator>
    <dc:creator>Giorgia Sebastiani</dc:creator>
    <dc:creator>Francis de Zegher</dc:creator>
    <dc:creator>David B Dunger</dc:creator>
    <dc:creator>Lourdes Ibáñez</dc:creator>
    <dc:identifier>doi:10.1210/jc.2007-2343</dc:identifier>
    <dc:source>J Clin Endocrinol Metab (5 February 2008)</dc:source>
    <dc:date>2008-02-18T16:12:09-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>J Clin Endocrinol Metab</prism:publicationName>
    <prism:issn>0021-972X</prism:issn>
    <prism:category>adiposity</prism:category>
    <prism:category>bmi</prism:category>
    <prism:category>molecular</prism:category>
    <prism:category>obesity</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/omalbam/article/1478959">
    <title>Clock genes are implicated in the human metabolic syndrome</title>
    <link>http://www.citeulike.org/user/omalbam/article/1478959</link>
    <description>&lt;i&gt;International Journal of Obesity, Vol. aop, No. current.&lt;/i&gt;</description>
    <dc:title>Clock genes are implicated in the human metabolic syndrome</dc:title>

    <dc:creator>P Gómez-Abellán</dc:creator>
    <dc:creator>JJ Hernández-Morante</dc:creator>
    <dc:creator>JA Luján</dc:creator>
    <dc:creator>JA Madrid</dc:creator>
    <dc:creator>M Garaulet</dc:creator>
    <dc:identifier>doi:10.1038/sj.ijo.0803689</dc:identifier>
    <dc:source>International Journal of Obesity, Vol. aop, No. current.</dc:source>
    <dc:date>2007-07-24T23:26:48-00:00</dc:date>
    <prism:publicationName>International Journal of Obesity</prism:publicationName>
    <prism:issn>0307-0565</prism:issn>
    <prism:volume>aop</prism:volume>
    <prism:number>current</prism:number>
    <prism:publisher>Nature Publishing Group</prism:publisher>
    <prism:category>adiposity</prism:category>
    <prism:category>metabolic-syndrome</prism:category>
    <prism:category>molecular</prism:category>
    <prism:category>physiology</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/omalbam/article/1411430">
    <title>Adipocyte prolactin: regulation of release and putative functions</title>
    <link>http://www.citeulike.org/user/omalbam/article/1411430</link>
    <description>&lt;i&gt;Diabetes, Obesity and Metabolism, Vol. 9, No. 4. (July 2007), pp. 464-476.&lt;/i&gt;</description>
    <dc:title>Adipocyte prolactin: regulation of release and putative functions</dc:title>

    <dc:creator>Brandebourg</dc:creator>
    <dc:creator></dc:creator>
    <dc:creator>Hugo</dc:creator>
    <dc:creator></dc:creator>
    <dc:creator>Ben-Jonathan</dc:creator>
    <dc:creator></dc:creator>
    <dc:identifier>doi:10.1111/j.1463-1326.2006.00671.x</dc:identifier>
    <dc:source>Diabetes, Obesity and Metabolism, Vol. 9, No. 4. (July 2007), pp. 464-476.</dc:source>
    <dc:date>2007-06-25T17:27:50-00:00</dc:date>
    <prism:publicationYear>2007</prism:publicationYear>
    <prism:publicationName>Diabetes, Obesity and Metabolism</prism:publicationName>
    <prism:issn>1462-8902</prism:issn>
    <prism:volume>9</prism:volume>
    <prism:number>4</prism:number>
    <prism:startingPage>464</prism:startingPage>
    <prism:endingPage>476</prism:endingPage>
    <prism:publisher>Blackwell Publishing</prism:publisher>
    <prism:category>adiposity</prism:category>
    <prism:category>obesity</prism:category>
    <prism:category>physiology</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/omalbam/article/1803076">
    <title>Dose-Dependent Effects of Testosterone on Regional Adipose Tissue Distribution in Healthy Young Men</title>
    <link>http://www.citeulike.org/user/omalbam/article/1803076</link>
    <description>&lt;i&gt;J Clin Endocrinol Metab, Vol. 89, No. 2. (1 February 2004), pp. 718-726.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Testosterone supplementation reduces total body adipose tissue (AT), but we do not know whether the effects are uniformly distributed throughout the body or are region specific, or whether they are dose related. We determined the effects of graded doses of testosterone on regional AT distribution in 54 healthy men (18-35 yr) in a 20-wk, randomized, double-blind study of combined treatment with GnRH agonist plus one of five doses (25, 50, 125, 300, or 600 mg/wk) of testosterone enanthate (TE). Total body, appendicular, and trunk AT and lean body mass were measured by dual-energy x-ray absorptiometry, and sc, intermuscular, and intraabdominal AT of the thigh and abdomen were measured by magnetic resonance imaging. Treatment regimens resulted in serum nadir testosterone concentrations ranging from subphysiological to supraphysiological levels. Dose-dependent changes in AT mass were negatively correlated with TE dose at all sites and were equally distributed between the trunk and appendices. The lowest dose was associated with gains in sc, intermuscular, and intraabdominal AT, with the greatest percent increase occurring in the sc stores. At the three highest TE doses, thigh intermuscular AT volume was significantly reduced, with a greater percent loss in intermuscular than sc depots, whereas intraabdominal AT stores remained unchanged. In conclusion, changes in testosterone concentrations in young men are associated with dose-dependent and region-specific changes in AT and lean body mass in the appendices and trunk. Lowering testosterone concentrations below baseline increases sc and deep AT stores in the appendices and abdomen, with a greater percent increase in sc depots. Conversely, elevating testosterone concentrations above baseline induces a greater loss of AT from the smaller, deeper intermuscular stores of the thigh. 10.1210/jc.2003-031492</description>
    <dc:title>Dose-Dependent Effects of Testosterone on Regional Adipose Tissue Distribution in Healthy Young Men</dc:title>

    <dc:creator>Linda Woodhouse</dc:creator>
    <dc:creator>Nidhi Gupta</dc:creator>
    <dc:creator>Meenakshi Bhasin</dc:creator>
    <dc:creator>Atam Singh</dc:creator>
    <dc:creator>Robert Ross</dc:creator>
    <dc:creator>Jeffrey Phillips</dc:creator>
    <dc:creator>Shalender Bhasin</dc:creator>
    <dc:identifier>doi:10.1210/jc.2003-031492</dc:identifier>
    <dc:source>J Clin Endocrinol Metab, Vol. 89, No. 2. (1 February 2004), pp. 718-726.</dc:source>
    <dc:date>2007-10-21T23:14:38-00:00</dc:date>
    <prism:publicationYear>2004</prism:publicationYear>
    <prism:publicationName>J Clin Endocrinol Metab</prism:publicationName>
    <prism:volume>89</prism:volume>
    <prism:number>2</prism:number>
    <prism:startingPage>718</prism:startingPage>
    <prism:endingPage>726</prism:endingPage>
    <prism:category>adiposity</prism:category>
    <prism:category>testosterone</prism:category>
    <prism:category>therapy</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/omalbam/article/159779">
    <title>Letrozole normalizes serum testosterone in severely obese men with hypogonadotropic hypogonadism</title>
    <link>http://www.citeulike.org/user/omalbam/article/159779</link>
    <description>&lt;i&gt;Diabetes, Obesity and Metabolism, Vol. 7, No. 3. (May 2005), pp. 211-215.&lt;/i&gt;</description>
    <dc:title>Letrozole normalizes serum testosterone in severely obese men with hypogonadotropic hypogonadism</dc:title>

    <dc:creator>H de Boer</dc:creator>
    <dc:creator>L Verschoor</dc:creator>
    <dc:creator>J Ruinemans-Koerts</dc:creator>
    <dc:creator>M Jansen</dc:creator>
    <dc:identifier>doi:10.1111/j.1463-1326.2004.00397.x</dc:identifier>
    <dc:source>Diabetes, Obesity and Metabolism, Vol. 7, No. 3. (May 2005), pp. 211-215.</dc:source>
    <dc:date>2005-04-13T12:04:45-00:00</dc:date>
    <prism:publicationYear>2005</prism:publicationYear>
    <prism:publicationName>Diabetes, Obesity and Metabolism</prism:publicationName>
    <prism:issn>1462-8902</prism:issn>
    <prism:volume>7</prism:volume>
    <prism:number>3</prism:number>
    <prism:startingPage>211</prism:startingPage>
    <prism:endingPage>215</prism:endingPage>
    <prism:publisher>Blackwell Publishing</prism:publisher>
    <prism:category>adiposity</prism:category>
    <prism:category>estrogen</prism:category>
    <prism:category>malegonadal</prism:category>
    <prism:category>obesity</prism:category>
    <prism:category>rct</prism:category>
    <prism:category>testosterone</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/omalbam/article/2285975">
    <title>Fatty acid desaturases in human adipose tissue: relationships between gene expression, desaturation indexes and insulin resistance</title>
    <link>http://www.citeulike.org/user/omalbam/article/2285975</link>
    <description>&lt;i&gt;Diabetologia, Vol. 51, No. 2. (1 February 2008), pp. 328-335.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Abstract Aims/hypothesis&#160;&#160;Fatty acid desaturases introduce double bonds into growing fatty acid chains. The key desaturases in humans are Δ5-desaturase (D5D), Δ6-desaturase (D6D) and stearoyl-CoA desaturase (SCD). Animal and human data implicate hepatic desaturase activities in insulin resistance, obesity and dyslipidaemia. However, the role of desaturase activity in adipose tissue is uncertain. We therefore evaluated relationships between adipose mRNA expression, estimated desaturase activities (fatty acid ratios) in adipose tissue and insulin resistance. Methods&#160;&#160;Subcutaneous adipose tissue mRNA expression of D5D (also known as FADS1), D6D (also known as FADS2) and SCD was determined in 75 individuals representative of the study population of 294 healthy 63-year-old men. Desaturation indexes (product/substrate fatty acid ratios) were generated from adipose tissue fatty acid composition in all individuals. Insulin resistance was defined as the upper quartile of the updated homeostasis model assessment (HOMA-2) index. Results&#160;&#160;The relevant desaturation indexes (16:1/16:0, 18:1/18:0, 20:4/20:3 and 18:3/18:2) reflected expression of SCD, but not of D5D or D6D in adipose tissue. Insulin-resistant individuals had a higher adipose tissue 18:1/18:0, but not 16:1/16:0 ratio than insulin-sensitive individuals. Individuals with a high adipose tissue 18:1/18:0 ratio were 4.4-fold (95% CI 1.8–11.8) more likely to be insulin resistant [threefold (95% CI 1.1–8.6) after adjustment for waist circumference and plasma triacylglycerol]. In a multiple regression model predicting HOMA-2, the independent effect of the 18:1/18:0 ratio was borderline (p = 0.086). Conclusions/interpretation&#160;&#160;Adipose tissue desaturation indexes of SCD reflect the expression of the gene encoding the enzyme in this tissue. Elevated SCD activity within adipose tissue is closely coupled to the development of insulin resistance.</description>
    <dc:title>Fatty acid desaturases in human adipose tissue: relationships between gene expression, desaturation indexes and insulin resistance</dc:title>

    <dc:creator>P Sjögren</dc:creator>
    <dc:creator>J Sierra-Johnson</dc:creator>
    <dc:creator>K Gertow</dc:creator>
    <dc:creator>M Rosell</dc:creator>
    <dc:creator>B Vessby</dc:creator>
    <dc:creator>U de Faire</dc:creator>
    <dc:creator>A Hamsten</dc:creator>
    <dc:creator>ML Hellenius</dc:creator>
    <dc:creator>R Fisher</dc:creator>
    <dc:identifier>doi:10.1007/s00125-007-0876-9</dc:identifier>
    <dc:source>Diabetologia, Vol. 51, No. 2. (1 February 2008), pp. 328-335.</dc:source>
    <dc:date>2008-01-24T20:57:17-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>Diabetologia</prism:publicationName>
    <prism:volume>51</prism:volume>
    <prism:number>2</prism:number>
    <prism:startingPage>328</prism:startingPage>
    <prism:endingPage>335</prism:endingPage>
    <prism:category>adiposity</prism:category>
    <prism:category>homa</prism:category>
    <prism:category>insulinresistance</prism:category>
    <prism:category>molecular</prism:category>
    <prism:category>obesity</prism:category>
    <prism:category>physiology</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/omalbam/article/2063390">
    <title>Testosterone Therapy Prevents Gain in Visceral Adipose Tissue and Loss of Skeletal Muscle in Non-obese Aging Men.</title>
    <link>http://www.citeulike.org/user/omalbam/article/2063390</link>
    <description>&lt;i&gt;J Clin Endocrinol Metab (16 October 2007)&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Background: Trials of testosterone therapy in aging men have demonstrated increases in fat free mass and skeletal muscle, and decreases in fat mass, but have not reported the impact of baseline body composition. Objective: To determine the effect, in non-obese aging men with symptoms of androgen deficiency and low-normal serum testosterone levels, of testosterone therapy on total and regional body composition, and hormonal and metabolic indices. Methods: 60 healthy but symptomatic, non-obese men aged &#62;/=55 years with TT levels &#60;15nM were randomized to transdermal testosterone patches or placebo for 12 months. Body composition, by DEXA (fat mass, fat free mass, skeletal muscle) and MRI (abdominal subcutaneous and visceral adipose tissue, thigh skeletal muscle and intermuscular fat) and hormonal and metabolic parameters were measured at Weeks 0 and 52. Results: Serum TT increased by 30% (P=0.01) LH decreased by 50% (P&#60;0.001). Relative to placebo, total body fat free mass (P=0.03) and skeletal muscle (P=0.008) were increased and thigh skeletal muscle loss was prevented (P=0.045) with testosterone therapy while visceral fat accumulation decreased (P=0.001) without change in total body or abdominal subcutaneous fat mass; change in visceral fat was correlated with change in TT levels (r(2)=0.36; P=0.014). There was a trend to increasing total and LDL cholesterol with placebo. Conclusion: Testosterone therapy, relative to placebo, selectively lessened visceral fat accumulation without change in total body fat mass, and increased total body fat free mass and total body and thigh skeletal muscle mass. Further studies are needed to determine the impact of these body compositional changes on markers of metabolic and cardiovascular risk.</description>
    <dc:title>Testosterone Therapy Prevents Gain in Visceral Adipose Tissue and Loss of Skeletal Muscle in Non-obese Aging Men.</dc:title>

    <dc:creator>C A Allan</dc:creator>
    <dc:creator>B J G Strauss</dc:creator>
    <dc:creator>H G Burger</dc:creator>
    <dc:creator>E A Forbes</dc:creator>
    <dc:creator>R I McLachlan</dc:creator>
    <dc:identifier>doi:10.1210/jc.2007-1291</dc:identifier>
    <dc:source>J Clin Endocrinol Metab (16 October 2007)</dc:source>
    <dc:date>2007-12-05T17:38:26-00:00</dc:date>
    <prism:publicationYear>2007</prism:publicationYear>
    <prism:publicationName>J Clin Endocrinol Metab</prism:publicationName>
    <prism:issn>0021-972X</prism:issn>
    <prism:category>adiposity</prism:category>
    <prism:category>testosterone</prism:category>
    <prism:category>therapy</prism:category>
</item>



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