<?xml version="1.0" encoding="UTF-8"?>

<rdf:RDF
   xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#"
   xmlns:rdfs="http://www.w3.org/2000/01/rdf-schema#"
   xmlns="http://purl.org/rss/1.0/"
   xmlns:dc="http://purl.org/dc/elements/1.1/"
   xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/"
   xmlns:dcterms="http://purl.org/dc/terms/"

>
<channel rdf:about="http://www.citeulike.org/about">
<pubDate>Sat, 26 Jul 2008 07:51:58 BST</pubDate>


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


	<link>http://www.citeulike.org/user/omalbam/tag/metabolism</link>
	<dc:publisher>CiteULike.org</dc:publisher>
	<dc:language>en-gb</dc:language>
	<dc:rights>Copyright &#169; 2004-2008 citeulike.org</dc:rights>
	<items>
    <rdf:Seq>
        <rdf:li rdf:resource="http://www.citeulike.org/user/omalbam/article/1453710"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/omalbam/article/2328068"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/omalbam/article/2323242"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/omalbam/article/1604513"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/omalbam/article/2294245"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/omalbam/article/2232701"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/omalbam/article/2214573"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/omalbam/article/2208598"/>

	</rdf:Seq>
	</items>
	</channel>


<item rdf:about="http://www.citeulike.org/user/omalbam/article/1453710">
    <title>Purine-rich foods, dairy and protein intake, and the risk of gout in men.</title>
    <link>http://www.citeulike.org/user/omalbam/article/1453710</link>
    <description>&lt;i&gt;N Engl J Med, Vol. 350, No. 11. (11 March 2004), pp. 1093-1103.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;BACKGROUND: Various purine-rich foods and high protein intake have long been thought to be risk factors for gout. Similarly, the possibility that the consumption of dairy products has a role in protecting against gout has been raised by metabolic studies. We prospectively investigated the association of these dietary factors with new cases of gout. METHODS: Over a 12-year period, we prospectively examined the relationship between purported dietary risk factors and new cases of gout among 47,150 men who had no history of gout at base line. We used a supplementary questionnaire to ascertain whether participants met the American College of Rheumatology survey criteria for gout. Diet was assessed every four years by means of a food-frequency questionnaire. RESULTS: During the 12 years of the study, we documented 730 confirmed new cases of gout. The multivariate relative risk of gout among men in the highest quintile of meat intake, as compared with those in the lowest quintile, was 1.41 (95 percent confidence interval, 1.07 to 1.86; P for trend = 0.02), and the corresponding relative risk associated with seafood intake was 1.51 (95 percent confidence interval, 1.17 to 1.95; P for trend = 0.02). In contrast, the incidence of gout decreased with increasing intake of dairy products; the multivariate relative risk among men in the highest quintile, as compared with those in the lowest quintile, was 0.56 (95 percent confidence interval, 0.42 to 0.74; P for trend &#60;0.001). The level of consumption of purine-rich vegetables and the total protein intake were not associated with an increased risk of gout. CONCLUSIONS: Higher levels of meat and seafood consumption are associated with an increased risk of gout, whereas a higher level of consumption of dairy products is associated with a decreased risk. Moderate intake of purine-rich vegetables or protein is not associated with an increased risk of gout.</description>
    <dc:title>Purine-rich foods, dairy and protein intake, and the risk of gout in men.</dc:title>

    <dc:creator>HK Choi</dc:creator>
    <dc:creator>K Atkinson</dc:creator>
    <dc:creator>EW Karlson</dc:creator>
    <dc:creator>W Willett</dc:creator>
    <dc:creator>G Curhan</dc:creator>
    <dc:identifier>doi:10.1056/NEJMoa035700</dc:identifier>
    <dc:source>N Engl J Med, Vol. 350, No. 11. (11 March 2004), pp. 1093-1103.</dc:source>
    <dc:date>2007-07-13T09:51:55-00:00</dc:date>
    <prism:publicationYear>2004</prism:publicationYear>
    <prism:publicationName>N Engl J Med</prism:publicationName>
    <prism:issn>1533-4406</prism:issn>
    <prism:volume>350</prism:volume>
    <prism:number>11</prism:number>
    <prism:startingPage>1093</prism:startingPage>
    <prism:endingPage>1103</prism:endingPage>
    <prism:category>diet</prism:category>
    <prism:category>metabolism</prism:category>
    <prism:category>risk</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/omalbam/article/2328068">
    <title>Soft drinks, fructose consumption, and the risk of gout in men: prospective cohort study</title>
    <link>http://www.citeulike.org/user/omalbam/article/2328068</link>
    <description>&lt;i&gt;BMJ (31 January 2008), bmj.39449.819271.BE.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Objective To examine the relation between intake of sugar sweetened soft drinks and fructose and the risk of incident gout in men. Design Prospective cohort over 12 years. Setting Health professionals follow-up study. Participants 46 393 men with no history of gout at baseline who provided information on intake of soft drinks and fructose through validated food frequency questionnaires. Main outcome measure Incident cases of gout meeting the American College of Rheumatology survey criteria for gout. Results During the 12 years of follow-up 755 confirmed incident cases of gout were reported. Increasing intake of sugar sweetened soft drinks was associated with an increasing risk of gout. Compared with consumption of less than one serving of sugar sweetened soft drinks a month the multivariate relative risk of gout for 5-6 servings a week was 1.29 (95% confidence interval 1.00 to 1.68), for one serving a day was 1.45 (1.02 to 2.08), and for two or more servings a day was 1.85 (1.08 to 3.16; P for trend=0.002). Diet soft drinks were not associated with risk of gout (P for trend=0.99). The multivariate relative risk of gout according to increasing fifths of fructose intake were 1.00, 1.29, 1.41, 1.84, and 2.02 (1.49 to 2.75; P for trend &#60;0.001). Other major contributors to fructose intake such as total fruit juice or fructose rich fruits (apples and oranges) were also associated with a higher risk of gout (P values for trend &#60;0.05). Conclusions Prospective data suggest that consumption of sugar sweetened soft drinks and fructose is strongly associated with an increased risk of gout in men. Furthermore, fructose rich fruits and fruit juices may also increase the risk. Diet soft drinks were not associated with the risk of gout. 10.1136/bmj.39449.819271.BE</description>
    <dc:title>Soft drinks, fructose consumption, and the risk of gout in men: prospective cohort study</dc:title>

    <dc:creator>Hyon Choi</dc:creator>
    <dc:creator>Gary Curhan</dc:creator>
    <dc:identifier>doi:10.1136/bmj.39449.819271.BE</dc:identifier>
    <dc:source>BMJ (31 January 2008), bmj.39449.819271.BE.</dc:source>
    <dc:date>2008-02-04T03:45:23-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>BMJ</prism:publicationName>
    <prism:startingPage>bmj.39449.819271.BE</prism:startingPage>
    <prism:category>diet</prism:category>
    <prism:category>foodsfunctional</prism:category>
    <prism:category>metabolism</prism:category>
    <prism:category>risk</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/omalbam/article/2323242">
    <title>Metabolic syndrome in men with prostate cancer undergoing long-term androgen-deprivation therapy.</title>
    <link>http://www.citeulike.org/user/omalbam/article/2323242</link>
    <description>&lt;i&gt;J Clin Oncol, Vol. 24, No. 24. (20 August 2006), pp. 3979-3983.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;PURPOSE: Prostate cancer (PCa) is one of the most common cancers in men. Men with recurrent or metastatic PCa are treated with androgen-deprivation therapy (ADT), resulting in profound hypogonadism. Because male hypogonadism is a risk factor for metabolic syndrome and men with PCa have high cardiovascular mortality, we evaluated the prevalence of metabolic syndrome in men undergoing long-term ADT. PATIENTS AND METHODS: This was a cross-sectional study. We evaluated 58 men, including 20 with PCa undergoing ADT for at least 12 months (ADT group), 18 age-matched men with nonmetastatic PCa who had received local treatment and were recently found to have an increasing prostate-specific antigen (non-ADT group), and 20 age-matched controls (control group). Men in the non-ADT and control groups were eugonadal. Metabolic syndrome was defined according to the Adult Treatment Panel III criteria. RESULTS: Mean age was similar among the groups. Men on ADT had significantly higher body mass index and lower total and free testosterone levels. The prevalence of metabolic syndrome was higher in the ADT group compared with the non-ADT (P &#60; .01) and control (P = .03) groups. Among the components of metabolic syndrome, men on ADT had a higher prevalence of abdominal obesity and hyperglycemia. Androgen-deprived men also had elevated triglycerides compared with controls (P = .02). The prevalence of hypertension and low high-density lipoprotein levels were similar. CONCLUSION: These data suggest that metabolic syndrome was present in more than 50% of the men undergoing long-term ADT, predisposing them to higher cardiovascular risk. Abdominal obesity and hyperglycemia were responsible for this higher prevalence. We recommend prospective studies to further delineate this association.</description>
    <dc:title>Metabolic syndrome in men with prostate cancer undergoing long-term androgen-deprivation therapy.</dc:title>

    <dc:creator>M Braga-Basaria</dc:creator>
    <dc:creator>AS Dobs</dc:creator>
    <dc:creator>DC Muller</dc:creator>
    <dc:creator>MA Carducci</dc:creator>
    <dc:creator>M John</dc:creator>
    <dc:creator>J Egan</dc:creator>
    <dc:creator>S Basaria</dc:creator>
    <dc:identifier>doi:10.1200/JCO.2006.05.9741</dc:identifier>
    <dc:source>J Clin Oncol, Vol. 24, No. 24. (20 August 2006), pp. 3979-3983.</dc:source>
    <dc:date>2008-02-02T15:59:21-00:00</dc:date>
    <prism:publicationYear>2006</prism:publicationYear>
    <prism:publicationName>J Clin Oncol</prism:publicationName>
    <prism:issn>1527-7755</prism:issn>
    <prism:volume>24</prism:volume>
    <prism:number>24</prism:number>
    <prism:startingPage>3979</prism:startingPage>
    <prism:endingPage>3983</prism:endingPage>
    <prism:category>androgen</prism:category>
    <prism:category>diagnosis</prism:category>
    <prism:category>malegonadal</prism:category>
    <prism:category>metabolic-syndrome</prism:category>
    <prism:category>metabolism</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/omalbam/article/1604513">
    <title>Effect of 6-month calorie restriction on biomarkers of longevity, metabolic adaptation, and oxidative stress in overweight individuals: a randomized controlled trial.</title>
    <link>http://www.citeulike.org/user/omalbam/article/1604513</link>
    <description>&lt;i&gt;JAMA, Vol. 295, No. 13. (5 April 2006), pp. 1539-1548.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;CONTEXT: Prolonged calorie restriction increases life span in rodents. Whether prolonged calorie restriction affects biomarkers of longevity or markers of oxidative stress, or reduces metabolic rate beyond that expected from reduced metabolic mass, has not been investigated in humans. OBJECTIVE: To examine the effects of 6 months of calorie restriction, with or without exercise, in overweight, nonobese (body mass index, 25 to &#60;30) men and women. DESIGN, SETTING, AND PARTICIPANTS: Randomized controlled trial of healthy, sedentary men and women (N = 48) conducted between March 2002 and August 2004 at a research center in Baton Rouge, La. INTERVENTION: Participants were randomized to 1 of 4 groups for 6 months: control (weight maintenance diet); calorie restriction (25% calorie restriction of baseline energy requirements); calorie restriction with exercise (12.5% calorie restriction plus 12.5% increase in energy expenditure by structured exercise); very low-calorie diet (890 kcal/d until 15% weight reduction, followed by a weight maintenance diet). MAIN OUTCOME MEASURES: Body composition; dehydroepiandrosterone sulfate (DHEAS), glucose, and insulin levels; protein carbonyls; DNA damage; 24-hour energy expenditure; and core body temperature. RESULTS: Mean (SEM) weight change at 6 months in the 4 groups was as follows: controls, -1.0% (1.1%); calorie restriction, -10.4% (0.9%); calorie restriction with exercise, -10.0% (0.8%); and very low-calorie diet, -13.9% (0.7%). At 6 months, fasting insulin levels were significantly reduced from baseline in the intervention groups (all P&#60;.01), whereas DHEAS and glucose levels were unchanged. Core body temperature was reduced in the calorie restriction and calorie restriction with exercise groups (both P&#60;.05). After adjustment for changes in body composition, sedentary 24-hour energy expenditure was unchanged in controls, but decreased in the calorie restriction (-135 kcal/d [42 kcal/d]), calorie restriction with exercise (-117 kcal/d [52 kcal/d]), and very low-calorie diet (-125 kcal/d [35 kcal/d]) groups (all P&#60;.008). These &#34;metabolic adaptations&#34; (~ 6% more than expected based on loss of metabolic mass) were statistically different from controls (P&#60;.05). Protein carbonyl concentrations were not changed from baseline to month 6 in any group, whereas DNA damage was also reduced from baseline in all intervention groups (P &#60;.005). CONCLUSIONS: Our findings suggest that 2 biomarkers of longevity (fasting insulin level and body temperature) are decreased by prolonged calorie restriction in humans and support the theory that metabolic rate is reduced beyond the level expected from reduced metabolic body mass. Studies of longer duration are required to determine if calorie restriction attenuates the aging process in humans. TRIAL REGISTRATION: ClinicalTrials.gov Identifier: NCT00099151.</description>
    <dc:title>Effect of 6-month calorie restriction on biomarkers of longevity, metabolic adaptation, and oxidative stress in overweight individuals: a randomized controlled trial.</dc:title>

    <dc:creator>LK Heilbronn</dc:creator>
    <dc:creator>L de Jonge</dc:creator>
    <dc:creator>MI Frisard</dc:creator>
    <dc:creator>JP DeLany</dc:creator>
    <dc:creator>DE Larson-Meyer</dc:creator>
    <dc:creator>J Rood</dc:creator>
    <dc:creator>T Nguyen</dc:creator>
    <dc:creator>CK Martin</dc:creator>
    <dc:creator>J Volaufova</dc:creator>
    <dc:creator>MM Most</dc:creator>
    <dc:creator>FL Greenway</dc:creator>
    <dc:creator>SR Smith</dc:creator>
    <dc:creator>WA Deutsch</dc:creator>
    <dc:creator>DA Williamson</dc:creator>
    <dc:creator>E Ravussin</dc:creator>
    <dc:creator></dc:creator>
    <dc:identifier>doi:10.1001/jama.295.13.1539</dc:identifier>
    <dc:source>JAMA, Vol. 295, No. 13. (5 April 2006), pp. 1539-1548.</dc:source>
    <dc:date>2007-08-29T10:03:01-00:00</dc:date>
    <prism:publicationYear>2006</prism:publicationYear>
    <prism:publicationName>JAMA</prism:publicationName>
    <prism:issn>1538-3598</prism:issn>
    <prism:volume>295</prism:volume>
    <prism:number>13</prism:number>
    <prism:startingPage>1539</prism:startingPage>
    <prism:endingPage>1548</prism:endingPage>
    <prism:category>aging</prism:category>
    <prism:category>diet</prism:category>
    <prism:category>insulinresistance</prism:category>
    <prism:category>metabolism</prism:category>
    <prism:category>obesity</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/omalbam/article/2294245">
    <title>SHBG gene promoter polymorphisms in men are associated with serum sex hormone-binding globulin, androgen and androgen metabolite levels, and hip bone mineral density.</title>
    <link>http://www.citeulike.org/user/omalbam/article/2294245</link>
    <description>&lt;i&gt;J Clin Endocrinol Metab, Vol. 91, No. 12. (December 2006), pp. 5029-5037.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;CONTEXT: SHBG regulates free sex steroid levels, which in turn regulate skeletal homeostasis. Twin studies have demonstrated that genetic factors largely account for interindividual variation in SHBG levels. Glucuronidated androgen metabolites have been proposed as markers of androgenic activity. OBJECTIVE: Our objective was to investigate whether polymorphisms in the SHBG gene promoter [(TAAAA)(n) microsatellite and rs1799941 single-nucleotide polymorphism] are associated with serum levels of SHBG, sex steroids, or bone mineral density (BMD) in men. DESIGN AND STUDY SUBJECTS: We conducted a population-based study of two cohorts of Swedish men: elderly men (MrOS Sweden; n congruent with 3000; average age, 75.4 yr) and young adult men (GOOD study; n = 1068; average age, 18.9 yr). MAIN OUTCOME MEASURES: We measured serum levels of SHBG, testosterone, estradiol, dihydrotestosterone, 5alpha-androstane-3alpha,17beta-diol glucuronides, androsterone glucuronide, and BMD determined by dual-energy x-ray absorptiometry. RESULTS: In both cohorts, (TAAAA)(n) and rs1799941 genotypes were associated with serum levels of SHBG (P &#60; 0.001), dihydrotestosterone (P &#60; 0.05), and 5alpha-androstane-3alpha,17beta-diol glucuronides (P &#60; 0.05). In the elderly men, they were also associated with testosterone and BMD at all hip bone sites. The genotype associated with high levels of SHBG was also associated with high BMD. Interestingly, male mice overexpressing human SHBG had increased cortical bone mineral content in the femur, suggesting that elevated SHBG levels may cause increased bone mass. CONCLUSIONS: Our findings demonstrate that polymorphisms in the SHBG promoter predict serum levels of SHBG, androgens, and glucuronidated androgen metabolites, and hip BMD in men.</description>
    <dc:title>SHBG gene promoter polymorphisms in men are associated with serum sex hormone-binding globulin, androgen and androgen metabolite levels, and hip bone mineral density.</dc:title>

    <dc:creator>AL Eriksson</dc:creator>
    <dc:creator>M Lorentzon</dc:creator>
    <dc:creator>D Mellström</dc:creator>
    <dc:creator>L Vandenput</dc:creator>
    <dc:creator>C Swanson</dc:creator>
    <dc:creator>N Andersson</dc:creator>
    <dc:creator>GL Hammond</dc:creator>
    <dc:creator>J Jakobsson</dc:creator>
    <dc:creator>A Rane</dc:creator>
    <dc:creator>ES Orwoll</dc:creator>
    <dc:creator>O Ljunggren</dc:creator>
    <dc:creator>O Johnell</dc:creator>
    <dc:creator>F Labrie</dc:creator>
    <dc:creator>SH Windahl</dc:creator>
    <dc:creator>C Ohlsson</dc:creator>
    <dc:identifier>doi:10.1210/jc.2006-0679</dc:identifier>
    <dc:source>J Clin Endocrinol Metab, Vol. 91, No. 12. (December 2006), pp. 5029-5037.</dc:source>
    <dc:date>2008-01-27T02:17:52-00:00</dc:date>
    <prism:publicationYear>2006</prism:publicationYear>
    <prism:publicationName>J Clin Endocrinol Metab</prism:publicationName>
    <prism:issn>0021-972X</prism:issn>
    <prism:volume>91</prism:volume>
    <prism:number>12</prism:number>
    <prism:startingPage>5029</prism:startingPage>
    <prism:endingPage>5037</prism:endingPage>
    <prism:category>androgen</prism:category>
    <prism:category>bmd</prism:category>
    <prism:category>malegonadal</prism:category>
    <prism:category>metabolism</prism:category>
    <prism:category>molecular</prism:category>
    <prism:category>shbg</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/omalbam/article/2232701">
    <title>The science behind dietary omega-3 fatty acids</title>
    <link>http://www.citeulike.org/user/omalbam/article/2232701</link>
    <description>&lt;i&gt;CMAJ, Vol. 178, No. 2. (15 January 2008), pp. 177-180.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;10.1503/cmaj.071356</description>
    <dc:title>The science behind dietary omega-3 fatty acids</dc:title>

    <dc:creator>Marc Surette</dc:creator>
    <dc:identifier>doi:10.1503/cmaj.071356</dc:identifier>
    <dc:source>CMAJ, Vol. 178, No. 2. (15 January 2008), pp. 177-180.</dc:source>
    <dc:date>2008-01-15T00:53:52-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>CMAJ</prism:publicationName>
    <prism:volume>178</prism:volume>
    <prism:number>2</prism:number>
    <prism:startingPage>177</prism:startingPage>
    <prism:endingPage>180</prism:endingPage>
    <prism:category>diet</prism:category>
    <prism:category>foodsfunctional</prism:category>
    <prism:category>metabolism</prism:category>
    <prism:category>physiology</prism:category>
    <prism:category>w3</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/omalbam/article/2214573">
    <title>Do Hand-Held Calorimeters Provide Reliable and Accurate Estimates of Resting Metabolic Rate?</title>
    <link>http://www.citeulike.org/user/omalbam/article/2214573</link>
    <description>&lt;i&gt;J Am Coll Nutr, Vol. 26, No. 6. (1 December 2007), pp. 625-629.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;This paper provides an overview of a new technique for indirect calorimetry and the assessment of resting metabolic rate. Information from the research literature includes findings on the reliability and validity of a new hand-held indirect calorimeter as well as use in clinical and field settings. Research findings to date are of mixed results. The MedGem instrument has provided more consistent results when compared to the Douglas bag method of measuring metabolic rate. The BodyGem instrument has been shown to be less accurate when compared to standard metabolic carts. Furthermore, when the Body Gem has been used with clinical patients or with under nourished individuals the results have not been acceptable. Overall, there is not a large enough body of evidence to definitively support the use of these hand-held devices for assessment of metabolic rate in a wide variety of clinical or research environments.</description>
    <dc:title>Do Hand-Held Calorimeters Provide Reliable and Accurate Estimates of Resting Metabolic Rate?</dc:title>

    <dc:creator>Marta Van Loan</dc:creator>
    <dc:source>J Am Coll Nutr, Vol. 26, No. 6. (1 December 2007), pp. 625-629.</dc:source>
    <dc:date>2008-01-10T14:26:04-00:00</dc:date>
    <prism:publicationYear>2007</prism:publicationYear>
    <prism:publicationName>J Am Coll Nutr</prism:publicationName>
    <prism:volume>26</prism:volume>
    <prism:number>6</prism:number>
    <prism:startingPage>625</prism:startingPage>
    <prism:endingPage>629</prism:endingPage>
    <prism:category>bmr</prism:category>
    <prism:category>lifestyle</prism:category>
    <prism:category>metabolism</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/omalbam/article/2208598">
    <title>Growth hormone treatment in adolescent males with idiopathic short stature: changes in body composition, protein, fat, and glucose metabolism.</title>
    <link>http://www.citeulike.org/user/omalbam/article/2208598</link>
    <description>&lt;i&gt;J Clin Endocrinol Metab, Vol. 92, No. 8. (August 2007), pp. 3033-3039.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;CONTEXT: Cross-sectional observations show an inverse relationship between pubertal increase in GH and insulin sensitivity, suggesting that pubertal insulin resistance may be mediated by GH. OBJECTIVE: Our objective was to assess longitudinally the effects of short-term GH supplementation in adolescent males with non-GH-deficient idiopathic short stature (ISS) on body composition, substrate metabolism, and insulin sensitivity. Children with ISS were studied to simulate the pubertal increase in GH secretion. PARTICIPANTS AND SETTING: Eight males with ISS (10.8-16.5 yr) were recruited from pediatric endocrinology clinics at an academic medical center. STUDY DESIGN: Participants were evaluated in the General Clinical Research Center before and after 4 months of GH supplementation (0.3 mg/kg.wk). Body composition was assessed with dual-energy x-ray absorptiometry. Whole-body glucose, protein, and fat turnover were measured using stable isotopes. In vivo insulin action was assessed during a 3-h hyperinsulinemic (40 mU/m(2).min) euglycemic clamp. RESULTS: GH supplementation led to 1) increase in hepatic glucose production and fasting insulin levels, 2) increase in lean body mass and decrease in fat mass, and 3) improvement in cardiovascular lipid risk profile. Plasma IGF-I levels correlated positively with insulin levels. CONCLUSIONS: Four months of GH supplementation in adolescent males with ISS is associated with significant body composition changes and hepatic insulin resistance.</description>
    <dc:title>Growth hormone treatment in adolescent males with idiopathic short stature: changes in body composition, protein, fat, and glucose metabolism.</dc:title>

    <dc:creator>TS Hannon</dc:creator>
    <dc:creator>K Danadian</dc:creator>
    <dc:creator>C Suprasongsin</dc:creator>
    <dc:creator>SA Arslanian</dc:creator>
    <dc:identifier>doi:10.1210/jc.2007-0308</dc:identifier>
    <dc:source>J Clin Endocrinol Metab, Vol. 92, No. 8. (August 2007), pp. 3033-3039.</dc:source>
    <dc:date>2008-01-08T19:17:20-00:00</dc:date>
    <prism:publicationYear>2007</prism:publicationYear>
    <prism:publicationName>J Clin Endocrinol Metab</prism:publicationName>
    <prism:issn>0021-972X</prism:issn>
    <prism:volume>92</prism:volume>
    <prism:number>8</prism:number>
    <prism:startingPage>3033</prism:startingPage>
    <prism:endingPage>3039</prism:endingPage>
    <prism:category>growth</prism:category>
    <prism:category>insulinresistance</prism:category>
    <prism:category>metabolism</prism:category>
    <prism:category>r-gh</prism:category>
</item>



</rdf:RDF>

