human
***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: Hyper and rogenism , a main clinical feature of polycystic ovary syndrome ( PCOS ) , is thought to result from enhanced ovarian and adrenal and rogen generation . To investigate the contribution of peripheral steroidogenesis , we used an oral challenge with dehydroepi and rosterone ( DHEA ) and analyzed its downstream conversion toward and rogens in eight women with PCOS ( age , 20 - 32 yr ; body mass index , 20 - 41 kg/m(2 ) ) and eight healthy women matched for age and body mass index . They underwent frequent serum sampling and urine collection for 8 h on three occasions : at baseline , and after 4 d of dexamethasone ( Dex ; 4 x 0.5 mg/d ) , followed by ingestion of 100 mg DHEA or placebo . Dex induced similar significant suppression of circulating steroids in both groups . The oral DHEA challenge led to similar significant increases in the area under the concentration-time curve ( 0 - 8 h after Dex )  of serum DHEA , DHEA sulfate , and rostenedione , and testosterone . However , after oral DHEA , PCOS women had significantly higher increases in serum 5 alpha-dihydrotestosterone ( P < 0.01 ) , its main metabolite and rostanediol glucuronide ( P < 0.05 ) , and the 5 alpha-reduced urinary and rogen metabolite and rosterone ( P < 0.05 ) . PCOS women also had significantly higher baseline excretion of 5 alpha-reduced glucocorticoid ( P < 0.01 ) and mineralocorticoid metabolites ( P < 0.05 ) . Taken together , these data indicate enhanced peripheral 5 alpha-reductase activity in PCOS . Thus , not only ovary and adrenal , but also liver and peripheral target tissues , significantly contribute to steroid alterations in PCOS Objective To develop a new polycystic ovary syndrome ( PCOS ) rat model suitable for exercise intervention . Method Thirty six rats were r and omly divided into three experimental groups :  PCOS rats with high-fat diet ( PF , n = 24 ) , PCOS rats with ordinary diet ( PO , n = 6 ) , and control rats with ordinary diet ( CO , n = 6 ) . Two kinds of PCOS rat model were made by adjustment diet structure and testosterone injection for 28 days . After a successful animal model , PF model rats were r and omly assigned to three groups : exercise with a continuation of high-fat diet ( PF-EF , n = 6 ) , sedentary with a continuation of high-fat diet ( PF-SF , n = 6 ) , exercise with an ordinary diet ( PF-EO , n = 6 ) . Fasting blood glucose ( FBG ) and insulin ( FINS ) , estrogen ( E2 ) , progesterone ( P ) , and testosterone ( T ) in serum were determined by RIA , and ovarian morphology was evaluated by Image-Pro plus 6.0 . Results Body weight , Lee index , FINS increased significantly in PF rat model . Serum levels of E2 and T were significantly higher in PF and PO than in CO . Ovary organ index and ovarian areas were significant lower in PF than in CO . After intervention for 2 weeks , the levels of 1 h postpr and ial blood glucose ( PBG1 ) , 2 h postpr and ial blood glucose ( PBG2 ) , FINS and the serum levels of T decreased significantly in PF-EF rats and PF-EO rats . The ratio of FBG/FINS was significant higher in PF-EO rats than in PF-SF rats . Ovarian morphology showed that the numbers of preantral follicles and atretic follicles decreased significantly , and the numbers of antral follicles and corpora lutea increased significantly in the rats of PF-EF and PF-EO . Conclusion By combination of high-fat diet and testosterone injection , the obese PCOS rat model is conformable with the lifestyle habits of fatty foods and insufficient exercise , and has metabolic and reproductive characteristics of human PCOS . This model can be applied to study exercise intervention Women with polycystic ovary syndrome ( PCOS ) are insulin resistant , have insulin secretory defects , and are at high risk for glucose intolerance . We performed this study to determine the prevalence of glucose intolerance and parameters associated with risk for this in PCOS women . Two-hundred and fifty-four PCOS women , aged 14 - 44 yr , were prospect ively evaluated at 2 centers , 1 urban and ethnically diverse ( n = 110 ) and 1 rural and ethnically homogeneous ( n = 144 ) . The rural PCOS women were compared to 80 control women of similar weight , ethnicity , and age . A 75-g oral glucose challenge was administered after a 3-day 300-g carbohydrate diet and an overnight fast with 0 and 2 h blood sample s for glucose levels .  Diabetes was categorized according to WHO criteria . The prevalence of glucose intolerance was 31.1 % impaired glucose intolerance ( IGT ) and 7.5 % diabetes . In nonobese PCOS women ( body mass index , < 27 kg/m2 ) , 10.3 % IGT and 1.5 % diabetes were found . The prevalence of glucose intolerance was significantly higher in PCOS vs. control women ( chi2 = 7.0 ; P = 0.01 ; odds ratio = 2.76 ; 95 % confidence interval = 1.23 - 6.57 ) . Variables most associated with postchallenge glucose levels were fasting glucose levels ( P < 0.0001 ) , PCOS status ( P = 0.002 ) , waist/hip ratio ( P = 0.01 ) , and body mass index ( P = 0.021 ) . The American Diabetes Association criteria applied to fasting glucose significantly underdiagnosed diabetes compared to the WHO criteria ( 3.2 % vs. 7.5 % ; chi2 = 4.7 ; P = 0.046 ; odds ratio = 2.48 ; 95 % confidence interval = 1.01 - 6.69 ) . We conclude that 1 ) PCOS women are at significantly increased risk for IGT and type 2 diabetes mellitus at all weights and at a young age ; 2 ) these prevalence rates are similar in 2 different population s of PCOS women , suggesting that PCOS may be a more important risk factor than ethnicity or race for glucose intolerance in young women ; and 3 ) the American Diabetes Association diabetes diagnostic criteria failed to detect a significant number of PCOS women with diabetes by postchallenge glucose values Objective : Increased peripheral metabolism of cortisol may explain compensatory ACTH-dependent adrenal steroidogenesis and hence hyper and rogenism in polycystic ovary syndrome ( PCOS ) . Previous studies have described an increased 5α-reduction of cortisol or impaired regeneration of cortisol by 11β-HSD1 in PCOS . However , these observations may be confounded by obesity . Moreover , the relationship between alterations in cortisol metabolism and the extent of adrenal and rogen hyper-secretion in response to ACTH has not been established . This study aim ed to examine the association between cortisol metabolism and ACTH-dependent adrenal hyper and rogenism in PCOS , independently of obesity . Design : We compared 90 PCOS women ( age 18–45 yr ) stratified by adrenal and rogen responses to ACTH1–24 and 45 controls matched for age and body weight . Methods : PCOS women were stratified as normal responders ( NR ) , intermediate responders ( IR ) , and high responders ( HR ) to 250 ug ACTH1–24 : NR ( no.=27 ) had and rostenedione and DHEA responses within 2 SD of the mean in controls ; IR ( no.=43 ) had DHEA responses > 2 SD above controls ; HR ( no.=20 ) had both and rostenedione and DHEA responses > 2 SD above controls . Results : All groups were similar for age , body weight , and body fat distribution . Basal testosterone , and rostenedione , and 5α-dihydrotestosterone plasma levels were similarly elevated among the 3 groups of PCOS compared with controls , whereas basal DHEA-S was higher in HR ( 2.8±1.2 μg/ml ) and IR ( 2.4±1.1 μg/ml ) than in NR ( 1.8±0.8 μg/ml ) and controls ( 1.7±0.6 μg/ml ) . The HR group had the lowest basal plasma cortisol levels ( 101±36 ng/ml vs IR 135±42 ng/ml , NR 144±48 ng/ml , and controls 165±48 ng/ml ; all p<0.01 ) , but the greatest cortisol response to ACTH1–24 ( Δ(60–0)cortisol 173±60 ng/ml vs IR 136±51 ng/ml , NR 114±50 ng/ml , and controls 127±50 ng/ml ; all p<0.01 ) , and the highest urinary excretion of total and 5β-reduced cortisol metabolites ( eg 5β-tetrahydrocortisol/cortisol ratio 25.2±15.3 vs IR 18.8±10.7 , NR 19.7±11.4 , and controls 17.2±13.7 ; all p<0.05 ) . There were no differences in urinary excretion of 5α-reduced cortisol metabolites or in 5α-dihydrotestosterone/testosterone ratio between groups . Conclusions : Adrenal and rogen excess in PCOS is associated with increased inactivation of cortisol by 5β-reductase that may lower cortisol blood levels and stimulate ACTH-dependent steroidogenesis 
    Output:
    
agent
***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: Hyper and rogenism , a main clinical feature of polycystic ovary syndrome ( PCOS ) , is thought to result from enhanced ovarian and adrenal and rogen generation . To investigate the contribution of peripheral steroidogenesis , we used an oral challenge with dehydroepi and rosterone ( DHEA ) and analyzed its downstream conversion toward and rogens in eight women with PCOS ( age , 20 - 32 yr ; body mass index , 20 - 41 kg/m(2 ) ) and eight healthy women matched for age and body mass index . They underwent frequent serum sampling and urine collection for 8 h on three occasions : at baseline , and after 4 d of dexamethasone ( Dex ; 4 x 0.5 mg/d ) , followed by ingestion of 100 mg DHEA or placebo . Dex induced similar significant suppression of circulating steroids in both groups . The oral DHEA challenge led to similar significant increases in the area under the concentration-time curve ( 0 - 8 h after Dex )  of serum DHEA , DHEA sulfate , and rostenedione , and testosterone . However , after oral DHEA , PCOS women had significantly higher increases in serum 5 alpha-dihydrotestosterone ( P < 0.01 ) , its main metabolite and rostanediol glucuronide ( P < 0.05 ) , and the 5 alpha-reduced urinary and rogen metabolite and rosterone ( P < 0.05 ) . PCOS women also had significantly higher baseline excretion of 5 alpha-reduced glucocorticoid ( P < 0.01 ) and mineralocorticoid metabolites ( P < 0.05 ) . Taken together , these data indicate enhanced peripheral 5 alpha-reductase activity in PCOS . Thus , not only ovary and adrenal , but also liver and peripheral target tissues , significantly contribute to steroid alterations in PCOS Objective To develop a new polycystic ovary syndrome ( PCOS ) rat model suitable for exercise intervention . Method Thirty six rats were r and omly divided into three experimental groups :  PCOS rats with high-fat diet ( PF , n = 24 ) , PCOS rats with ordinary diet ( PO , n = 6 ) , and control rats with ordinary diet ( CO , n = 6 ) . Two kinds of PCOS rat model were made by adjustment diet structure and testosterone injection for 28 days . After a successful animal model , PF model rats were r and omly assigned to three groups : exercise with a continuation of high-fat diet ( PF-EF , n = 6 ) , sedentary with a continuation of high-fat diet ( PF-SF , n = 6 ) , exercise with an ordinary diet ( PF-EO , n = 6 ) . Fasting blood glucose ( FBG ) and insulin ( FINS ) , estrogen ( E2 ) , progesterone ( P ) , and testosterone ( T ) in serum were determined by RIA , and ovarian morphology was evaluated by Image-Pro plus 6.0 . Results Body weight , Lee index , FINS increased significantly in PF rat model . Serum levels of E2 and T were significantly higher in PF and PO than in CO . Ovary organ index and ovarian areas were significant lower in PF than in CO . After intervention for 2 weeks , the levels of 1 h postpr and ial blood glucose ( PBG1 ) , 2 h postpr and ial blood glucose ( PBG2 ) , FINS and the serum levels of T decreased significantly in PF-EF rats and PF-EO rats . The ratio of FBG/FINS was significant higher in PF-EO rats than in PF-SF rats . Ovarian morphology showed that the numbers of preantral follicles and atretic follicles decreased significantly , and the numbers of antral follicles and corpora lutea increased significantly in the rats of PF-EF and PF-EO . Conclusion By combination of high-fat diet and testosterone injection , the obese PCOS rat model is conformable with the lifestyle habits of fatty foods and insufficient exercise , and has metabolic and reproductive characteristics of human PCOS . This model can be applied to study exercise intervention Women with polycystic ovary syndrome ( PCOS ) are insulin resistant , have insulin secretory defects , and are at high risk for glucose intolerance . We performed this study to determine the prevalence of glucose intolerance and parameters associated with risk for this in PCOS women . Two-hundred and fifty-four PCOS women , aged 14 - 44 yr , were prospect ively evaluated at 2 centers , 1 urban and ethnically diverse ( n = 110 ) and 1 rural and ethnically homogeneous ( n = 144 ) . The rural PCOS women were compared to 80 control women of similar weight , ethnicity , and age . A 75-g oral glucose challenge was administered after a 3-day 300-g carbohydrate diet and an overnight fast with 0 and 2 h blood sample s for glucose levels .  Diabetes was categorized according to WHO criteria . The prevalence of glucose intolerance was 31.1 % impaired glucose intolerance ( IGT ) and 7.5 % diabetes . In nonobese PCOS women ( body mass index , < 27 kg/m2 ) , 10.3 % IGT and 1.5 % diabetes were found . The prevalence of glucose intolerance was significantly higher in PCOS vs. control women ( chi2 = 7.0 ; P = 0.01 ; odds ratio = 2.76 ; 95 % confidence interval = 1.23 - 6.57 ) . Variables most associated with postchallenge glucose levels were fasting glucose levels ( P < 0.0001 ) , PCOS status ( P = 0.002 ) , waist/hip ratio ( P = 0.01 ) , and body mass index ( P = 0.021 ) . The American Diabetes Association criteria applied to fasting glucose significantly underdiagnosed diabetes compared to the WHO criteria ( 3.2 % vs. 7.5 % ; chi2 = 4.7 ; P = 0.046 ; odds ratio = 2.48 ; 95 % confidence interval = 1.01 - 6.69 ) . We conclude that 1 ) PCOS women are at significantly increased risk for IGT and type 2 diabetes mellitus at all weights and at a young age ; 2 ) these prevalence rates are similar in 2 different population s of PCOS women , suggesting that PCOS may be a more important risk factor than ethnicity or race for glucose intolerance in young women ; and 3 ) the American Diabetes Association diabetes diagnostic criteria failed to detect a significant number of PCOS women with diabetes by postchallenge glucose values Objective : Increased peripheral metabolism of cortisol may explain compensatory ACTH-dependent adrenal steroidogenesis and hence hyper and rogenism in polycystic ovary syndrome ( PCOS ) . Previous studies have described an increased 5α-reduction of cortisol or impaired regeneration of cortisol by 11β-HSD1 in PCOS . However , these observations may be confounded by obesity . Moreover , the relationship between alterations in cortisol metabolism and the extent of adrenal and rogen hyper-secretion in response to ACTH has not been established . This study aim ed to examine the association between cortisol metabolism and ACTH-dependent adrenal hyper and rogenism in PCOS , independently of obesity . Design : We compared 90 PCOS women ( age 18–45 yr ) stratified by adrenal and rogen responses to ACTH1–24 and 45 controls matched for age and body weight . Methods : PCOS women were stratified as normal responders ( NR ) , intermediate responders ( IR ) , and high responders ( HR ) to 250 ug ACTH1–24 : NR ( no.=27 ) had and rostenedione and DHEA responses within 2 SD of the mean in controls ; IR ( no.=43 ) had DHEA responses > 2 SD above controls ; HR ( no.=20 ) had both and rostenedione and DHEA responses > 2 SD above controls . Results : All groups were similar for age , body weight , and body fat distribution . Basal testosterone , and rostenedione , and 5α-dihydrotestosterone plasma levels were similarly elevated among the 3 groups of PCOS compared with controls , whereas basal DHEA-S was higher in HR ( 2.8±1.2 μg/ml ) and IR ( 2.4±1.1 μg/ml ) than in NR ( 1.8±0.8 μg/ml ) and controls ( 1.7±0.6 μg/ml ) . The HR group had the lowest basal plasma cortisol levels ( 101±36 ng/ml vs IR 135±42 ng/ml , NR 144±48 ng/ml , and controls 165±48 ng/ml ; all p<0.01 ) , but the greatest cortisol response to ACTH1–24 ( Δ(60–0)cortisol 173±60 ng/ml vs IR 136±51 ng/ml , NR 114±50 ng/ml , and controls 127±50 ng/ml ; all p<0.01 ) , and the highest urinary excretion of total and 5β-reduced cortisol metabolites ( eg 5β-tetrahydrocortisol/cortisol ratio 25.2±15.3 vs IR 18.8±10.7 , NR 19.7±11.4 , and controls 17.2±13.7 ; all p<0.05 ) . There were no differences in urinary excretion of 5α-reduced cortisol metabolites or in 5α-dihydrotestosterone/testosterone ratio between groups . Conclusions : Adrenal and rogen excess in PCOS is associated with increased inactivation of cortisol by 5β-reductase that may lower cortisol blood levels and stimulate ACTH-dependent steroidogenesis 
    Output:
    