Age, Body Mass Index, and Waist-to-Hip Ratio Related Changes in Insulin Secretion and Insulin Sensitivity in Women with Polycystic Ovary Syndrome: Minimal Model Analyses
Insulin resistance is believed to be an integral component of the polycystic ovary syndrome (PCOS). Beta (ß) cell dysfunction is also found in PCOS. In the study, we determined the influence of age, body mass index (BMI), and waist-to-hip ratio (WHR) on insulin response to oral glucose load (OGTT) a...
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| Published in | International journal of endocrinology Vol. 2022; pp. 1 - 11 |
|---|---|
| Main Authors | , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Egypt
Hindawi
18.05.2022
John Wiley & Sons, Inc Wiley |
| Subjects | |
| Online Access | Get full text |
| ISSN | 1687-8337 1687-8345 |
| DOI | 10.1155/2022/6630498 |
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| Abstract | Insulin resistance is believed to be an integral component of the polycystic ovary syndrome (PCOS). Beta (ß) cell dysfunction is also found in PCOS. In the study, we determined the influence of age, body mass index (BMI), and waist-to-hip ratio (WHR) on insulin response to oral glucose load (OGTT) and on insulin sensitivity (Si) and ß-cell function in young women with PCOS. One hundred fourteen patients with PCOS and 41 controls with normal basal plasma glucose were studied. A 75-g OGTT was performed to determine glucose tolerance and insulin response. Insulin sensitivity and ß-cell function were studied using a modified frequently sampled IV glucose tolerance test (FISGTT) to determine the acute insulin response (AIRG), as well as Si by minimal model analysis. Si was decreased in PCOS women (2.49 0.18 vs. 3.41 ± 0.36, p<0.05), but no difference in AIRG existed between the PCOS and control group (75.1 ± 4.6 vs. 63.4 ± 4.6, p<0.05). BMI and WHR correlated negatively with Si (r = −0.43; r = −0.289, p<0.001, respectively), but not with AIRG (r = 0.116; r = −0.02, p>0.05, respectively). Increasing age correlated negatively with AIRG (r = −0.285, p<0.001). There was a significant interaction between disease (PCOS), BMI, and WHR on Si as well as between age and PCOS on AIRG. Thus, patients below the age of 25 with PCOS showed enhanced AIRG (89.5 ± 7.1 vs. 65.1 ± 6.7, p<0.05) and decreased Si (2.43 ± 0.25 vs. 4.52 ± 0.62, p<0.05) compared to age-matched controls. In conclusion, these data suggest that not all patients with PCOS have basal and stimulated hyperinsulinemia, insulin resistance, and impaired glucose tolerance. Based on these data in young PCOS subjects, the development of insulin resistance and T2DM may be prevented with appropriate treatment strategies. |
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| AbstractList | Insulin resistance is believed to be an integral component of the polycystic ovary syndrome (PCOS). Beta (ß) cell dysfunction is also found in PCOS. In the study, we determined the influence of age, body mass index (BMI), and waist-to-hip ratio (WHR) on insulin response to oral glucose load (OGTT) and on insulin sensitivity (Si) and ß-cell function in young women with PCOS. One hundred fourteen patients with PCOS and 41 controls with normal basal plasma glucose were studied. A 75-g OGTT was performed to determine glucose tolerance and insulin response. Insulin sensitivity and ß-cell function were studied using a modified frequently sampled IV glucose tolerance test (FISGTT) to determine the acute insulin response (AIR[sub.G]), as well as S[sub.i] by minimal model analysis. S[sub.i] was decreased in PCOS women (2.49 0.18 vs. 3.41±0.36, p<0.05), but no difference in AIR[sub.G] existed between the PCOS and control group (75.1±4.6 vs. 63.4±4.6, p<0.05). BMI and WHR correlated negatively with S[sub.i] (r=-0.43; r=-0.289, p<0.001, respectively), but not with AIR[sub.G] (r=0.116; r=-0.02, p>0.05, respectively). Increasing age correlated negatively with AIR[sub.G] (r=-0.285, p<0.001). There was a significant interaction between disease (PCOS), BMI, and WHR on S[sub.i] as well as between age and PCOS on AIR[sub.G]. Thus, patients below the age of 25 with PCOS showed enhanced AIR[sub.G] (89.5±7.1 vs. 65.1±6.7, p<0.05) and decreased S[sub.i] (2.43±0.25 vs. 4.52±0.62, p<0.05) compared to age-matched controls. In conclusion, these data suggest that not all patients with PCOS have basal and stimulated hyperinsulinemia, insulin resistance, and impaired glucose tolerance. Based on these data in young PCOS subjects, the development of insulin resistance and T2DM may be prevented with appropriate treatment strategies. Insulin resistance is believed to be an integral component of the polycystic ovary syndrome (PCOS). Beta (ß) cell dysfunction is also found in PCOS. In the study, we determined the influence of age, body mass index (BMI), and waist-to-hip ratio (WHR) on insulin response to oral glucose load (OGTT) and on insulin sensitivity (Si) and ß-cell function in young women with PCOS. One hundred fourteen patients with PCOS and 41 controls with normal basal plasma glucose were studied. A 75-g OGTT was performed to determine glucose tolerance and insulin response. Insulin sensitivity and ß-cell function were studied using a modified frequently sampled IV glucose tolerance test (FISGTT) to determine the acute insulin response (AIRG), as well as Si by minimal model analysis. Si was decreased in PCOS women (2.49 0.18 vs. 3.41 ± 0.36, p<0.05), but no difference in AIRG existed between the PCOS and control group (75.1 ± 4.6 vs. 63.4 ± 4.6, p<0.05). BMI and WHR correlated negatively with Si (r = −0.43; r = −0.289, p<0.001, respectively), but not with AIRG (r = 0.116; r = −0.02, p>0.05, respectively). Increasing age correlated negatively with AIRG (r = −0.285, p<0.001). There was a significant interaction between disease (PCOS), BMI, and WHR on Si as well as between age and PCOS on AIRG. Thus, patients below the age of 25 with PCOS showed enhanced AIRG (89.5 ± 7.1 vs. 65.1 ± 6.7, p<0.05) and decreased Si (2.43 ± 0.25 vs. 4.52 ± 0.62, p<0.05) compared to age-matched controls. In conclusion, these data suggest that not all patients with PCOS have basal and stimulated hyperinsulinemia, insulin resistance, and impaired glucose tolerance. Based on these data in young PCOS subjects, the development of insulin resistance and T2DM may be prevented with appropriate treatment strategies. Insulin resistance is believed to be an integral component of the polycystic ovary syndrome (PCOS). Beta (ß) cell dysfunction is also found in PCOS. In the study, we determined the influence of age, body mass index (BMI), and waist-to-hip ratio (WHR) on insulin response to oral glucose load (OGTT) and on insulin sensitivity (Si) and ß-cell function in young women with PCOS. One hundred fourteen patients with PCOS and 41 controls with normal basal plasma glucose were studied. A 75-g OGTT was performed to determine glucose tolerance and insulin response. Insulin sensitivity and ß-cell function were studied using a modified frequently sampled IV glucose tolerance test (FISGTT) to determine the acute insulin response (AIRG), as well as Si by minimal model analysis. Si was decreased in PCOS women (2.49 0.18 vs. 3.41 ± 0.36, p < 0.05 ), but no difference in AIRG existed between the PCOS and control group (75.1 ± 4.6 vs. 63.4 ± 4.6, p < 0.05 ). BMI and WHR correlated negatively with Si (r = −0.43; r = −0.289, p < 0.001 , respectively), but not with AIRG (r = 0.116; r = −0.02, p > 0.05 , respectively). Increasing age correlated negatively with AIRG (r = −0.285, p < 0.001 ). There was a significant interaction between disease (PCOS), BMI, and WHR on Si as well as between age and PCOS on AIRG. Thus, patients below the age of 25 with PCOS showed enhanced AIRG (89.5 ± 7.1 vs. 65.1 ± 6.7, p < 0.05 ) and decreased Si (2.43 ± 0.25 vs. 4.52 ± 0.62, p < 0.05 ) compared to age-matched controls. In conclusion, these data suggest that not all patients with PCOS have basal and stimulated hyperinsulinemia, insulin resistance, and impaired glucose tolerance. Based on these data in young PCOS subjects, the development of insulin resistance and T2DM may be prevented with appropriate treatment strategies. Insulin resistance is believed to be an integral component of the polycystic ovary syndrome (PCOS). Beta ( ß ) cell dysfunction is also found in PCOS. In the study, we determined the influence of age, body mass index (BMI), and waist-to-hip ratio (WHR) on insulin response to oral glucose load (OGTT) and on insulin sensitivity (Si) and ß -cell function in young women with PCOS. One hundred fourteen patients with PCOS and 41 controls with normal basal plasma glucose were studied. A 75-g OGTT was performed to determine glucose tolerance and insulin response. Insulin sensitivity and ß -cell function were studied using a modified frequently sampled IV glucose tolerance test (FISGTT) to determine the acute insulin response (AIR G ), as well as S i by minimal model analysis. S i was decreased in PCOS women (2.49 0.18 vs. 3.41 ± 0.36, p < 0.05), but no difference in AIR G existed between the PCOS and control group (75.1 ± 4.6 vs. 63.4 ± 4.6, p < 0.05). BMI and WHR correlated negatively with S i ( r = −0.43; r = −0.289, p < 0.001, respectively), but not with AIR G ( r = 0.116; r = −0.02, p > 0.05, respectively). Increasing age correlated negatively with AIR G ( r = −0.285, p < 0.001). There was a significant interaction between disease (PCOS), BMI, and WHR on S i as well as between age and PCOS on AIR G . Thus, patients below the age of 25 with PCOS showed enhanced AIR G (89.5 ± 7.1 vs. 65.1 ± 6.7, p < 0.05) and decreased S i (2.43 ± 0.25 vs. 4.52 ± 0.62, p < 0.05) compared to age-matched controls. In conclusion, these data suggest that not all patients with PCOS have basal and stimulated hyperinsulinemia, insulin resistance, and impaired glucose tolerance. Based on these data in young PCOS subjects, the development of insulin resistance and T2DM may be prevented with appropriate treatment strategies. Insulin resistance is believed to be an integral component of the polycystic ovary syndrome (PCOS). Beta (ß) cell dysfunction is also found in PCOS. In the study, we determined the influence of age, body mass index (BMI), and waist-to-hip ratio (WHR) on insulin response to oral glucose load (OGTT) and on insulin sensitivity (Si) and ß-cell function in young women with PCOS. One hundred fourteen patients with PCOS and 41 controls with normal basal plasma glucose were studied. A 75-g OGTT was performed to determine glucose tolerance and insulin response. Insulin sensitivity and ß-cell function were studied using a modified frequently sampled IV glucose tolerance test (FISGTT) to determine the acute insulin response (AIRG), as well as Si by minimal model analysis. Si was decreased in PCOS women (2.49 0.18 vs. 3.41 ± 0.36, p < 0.05), but no difference in AIRG existed between the PCOS and control group (75.1 ± 4.6 vs. 63.4 ± 4.6, p < 0.05). BMI and WHR correlated negatively with Si (r = -0.43; r = -0.289, p < 0.001, respectively), but not with AIRG (r = 0.116; r = -0.02, p > 0.05, respectively). Increasing age correlated negatively with AIRG (r = -0.285, p < 0.001). There was a significant interaction between disease (PCOS), BMI, and WHR on Si as well as between age and PCOS on AIRG. Thus, patients below the age of 25 with PCOS showed enhanced AIRG (89.5 ± 7.1 vs. 65.1 ± 6.7, p < 0.05) and decreased Si (2.43 ± 0.25 vs. 4.52 ± 0.62, p < 0.05) compared to age-matched controls. In conclusion, these data suggest that not all patients with PCOS have basal and stimulated hyperinsulinemia, insulin resistance, and impaired glucose tolerance. Based on these data in young PCOS subjects, the development of insulin resistance and T2DM may be prevented with appropriate treatment strategies.Insulin resistance is believed to be an integral component of the polycystic ovary syndrome (PCOS). Beta (ß) cell dysfunction is also found in PCOS. In the study, we determined the influence of age, body mass index (BMI), and waist-to-hip ratio (WHR) on insulin response to oral glucose load (OGTT) and on insulin sensitivity (Si) and ß-cell function in young women with PCOS. One hundred fourteen patients with PCOS and 41 controls with normal basal plasma glucose were studied. A 75-g OGTT was performed to determine glucose tolerance and insulin response. Insulin sensitivity and ß-cell function were studied using a modified frequently sampled IV glucose tolerance test (FISGTT) to determine the acute insulin response (AIRG), as well as Si by minimal model analysis. Si was decreased in PCOS women (2.49 0.18 vs. 3.41 ± 0.36, p < 0.05), but no difference in AIRG existed between the PCOS and control group (75.1 ± 4.6 vs. 63.4 ± 4.6, p < 0.05). BMI and WHR correlated negatively with Si (r = -0.43; r = -0.289, p < 0.001, respectively), but not with AIRG (r = 0.116; r = -0.02, p > 0.05, respectively). Increasing age correlated negatively with AIRG (r = -0.285, p < 0.001). There was a significant interaction between disease (PCOS), BMI, and WHR on Si as well as between age and PCOS on AIRG. Thus, patients below the age of 25 with PCOS showed enhanced AIRG (89.5 ± 7.1 vs. 65.1 ± 6.7, p < 0.05) and decreased Si (2.43 ± 0.25 vs. 4.52 ± 0.62, p < 0.05) compared to age-matched controls. In conclusion, these data suggest that not all patients with PCOS have basal and stimulated hyperinsulinemia, insulin resistance, and impaired glucose tolerance. Based on these data in young PCOS subjects, the development of insulin resistance and T2DM may be prevented with appropriate treatment strategies. Insulin resistance is believed to be an integral component of the polycystic ovary syndrome (PCOS). Beta ( ) cell dysfunction is also found in PCOS. In the study, we determined the influence of age, body mass index (BMI), and waist-to-hip ratio (WHR) on insulin response to oral glucose load (OGTT) and on insulin sensitivity (Si) and -cell function in young women with PCOS. One hundred fourteen patients with PCOS and 41 controls with normal basal plasma glucose were studied. A 75-g OGTT was performed to determine glucose tolerance and insulin response. Insulin sensitivity and -cell function were studied using a modified frequently sampled IV glucose tolerance test (FISGTT) to determine the acute insulin response (AIR ), as well as S by minimal model analysis. S was decreased in PCOS women (2.49 0.18 vs. 3.41 ± 0.36, < 0.05), but no difference in AIR existed between the PCOS and control group (75.1 ± 4.6 vs. 63.4 ± 4.6, < 0.05). BMI and WHR correlated negatively with S ( = -0.43; = -0.289, < 0.001, respectively), but not with AIR ( = 0.116; = -0.02, > 0.05, respectively). Increasing age correlated negatively with AIR ( = -0.285, < 0.001). There was a significant interaction between disease (PCOS), BMI, and WHR on S as well as between age and PCOS on AIR . Thus, patients below the age of 25 with PCOS showed enhanced AIR (89.5 ± 7.1 vs. 65.1 ± 6.7, < 0.05) and decreased S (2.43 ± 0.25 vs. 4.52 ± 0.62, < 0.05) compared to age-matched controls. In conclusion, these data suggest that not all patients with PCOS have basal and stimulated hyperinsulinemia, insulin resistance, and impaired glucose tolerance. Based on these data in young PCOS subjects, the development of insulin resistance and T2DM may be prevented with appropriate treatment strategies. |
| Audience | Academic |
| Author | Šumarac-Dumanović, Mirjana Micić, Dragan Žarković, Miloš Stamenković-Pejković, Danica Mandić-Marković, Vesna Dumanović, Janko Jeremić, Danka |
| AuthorAffiliation | 4 Department of Medical Sciences, Serbian Academy of Sciences and Arts, Belgrade, Serbia 1 School of Medicine, University of Belgrade, Belgrade, Serbia 3 Obstetrics and Gynaecology Clinic Narodni Front, Belgrade, Serbia 2 Clinic for Endocrinology, Diabetes and Diseases of Metabolism, Clinical Center of Serbia, Belgrade, Serbia |
| AuthorAffiliation_xml | – name: 2 Clinic for Endocrinology, Diabetes and Diseases of Metabolism, Clinical Center of Serbia, Belgrade, Serbia – name: 4 Department of Medical Sciences, Serbian Academy of Sciences and Arts, Belgrade, Serbia – name: 1 School of Medicine, University of Belgrade, Belgrade, Serbia – name: 3 Obstetrics and Gynaecology Clinic Narodni Front, Belgrade, Serbia |
| Author_xml | – sequence: 1 givenname: Mirjana orcidid: 0000-0002-6216-6650 surname: Šumarac-Dumanović fullname: Šumarac-Dumanović, Mirjana organization: School of MedicineUniversity of BelgradeBelgradeSerbiabg.ac.rs – sequence: 2 givenname: Danica orcidid: 0000-0002-3990-0212 surname: Stamenković-Pejković fullname: Stamenković-Pejković, Danica organization: School of MedicineUniversity of BelgradeBelgradeSerbiabg.ac.rs – sequence: 3 givenname: Danka orcidid: 0000-0003-1826-1439 surname: Jeremić fullname: Jeremić, Danka organization: Clinic for Endocrinology, Diabetes and Diseases of MetabolismClinical Center of SerbiaBelgradeSerbiakcs.ac.rs – sequence: 4 givenname: Janko orcidid: 0000-0002-7301-859X surname: Dumanović fullname: Dumanović, Janko organization: Obstetrics and Gynaecology Clinic Narodni FrontBelgradeSerbia – sequence: 5 givenname: Vesna orcidid: 0000-0002-0005-8443 surname: Mandić-Marković fullname: Mandić-Marković, Vesna organization: School of MedicineUniversity of BelgradeBelgradeSerbiabg.ac.rs – sequence: 6 givenname: Miloš orcidid: 0000-0001-9977-5970 surname: Žarković fullname: Žarković, Miloš organization: School of MedicineUniversity of BelgradeBelgradeSerbiabg.ac.rs – sequence: 7 givenname: Dragan orcidid: 0000-0003-0018-2169 surname: Micić fullname: Micić, Dragan organization: Department of Medical SciencesSerbian Academy of Sciences and ArtsBelgradeSerbiasanu.ac.rs |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/35646110$$D View this record in MEDLINE/PubMed |
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| Copyright | Copyright © 2022 Mirjana Šumarac-Dumanović et al. COPYRIGHT 2022 John Wiley & Sons, Inc. Copyright © 2022 Mirjana Šumarac-Dumanović et al. This work is licensed under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. Copyright © 2022 Mirjana Šumarac-Dumanović et al. 2022 |
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| References_xml | – ident: 44 doi: 10.1210/jcem.86.2.7202 – ident: 34 doi: 10.1016/s0015-0282(01)02843-6 – volume: 727 start-page: 1 year: 1985 ident: 10 article-title: Diabetes mellitus publication-title: World Health Organization Technical Report Series – start-page: 111 volume-title: Seminars in Reproductive Endocrinology year: 1997 ident: 4 article-title: Role of hyperinsulinemia in the pathogenesis of the polycystic ovary syndrome, and its clinical implications – ident: 11 doi: 10.1152/ajpendo.1979.236.6.e667 – ident: 24 doi: 10.1210/jc.81.3.942 – ident: 33 doi: 10.1210/jcem-57-2-356 – ident: 31 doi: 10.1210/jc.86.5.2027 – ident: 3 doi: 10.1210/jc.2010-0202 – ident: 49 doi: 10.1677/joe.0.1740001 – ident: 15 doi: 10.1046/j.1365-2265.2000.00884.x – ident: 16 doi: 10.1016/0026-0495(94)90118-x – ident: 41 doi: 10.1210/jcem.87.4.8398 – ident: 13 doi: 10.1046/j.1365-2362.32.s3.5.x – ident: 23 doi: 10.1093/humrep/dew243 – ident: 1 doi: 10.1056/nejm199509283331307 – ident: 27 doi: 10.1172/jci10761 – ident: 9 doi: 10.1210/er.2011-1034 – ident: 29 doi: 10.1210/jc.80.9.2586 – ident: 21 doi: 10.1093/humrep/des463 – ident: 26 doi: 10.1210/jc.78.5.1052 – ident: 48 doi: 10.1080/1464727002000198771 – ident: 22 doi: 10.1093/humrep/dex308 – ident: 46 doi: 10.1093/humrep/17.8.1950 – ident: 5 doi: 10.1210/jc.76.5.1241 – ident: 19 doi: 10.1186/1741-7015-8-41 – ident: 43 doi: 10.1016/j.fertnstert.2011.11.036 – ident: 40 doi: 10.1016/s0895-4356(98)00035-3 – ident: 30 doi: 10.1016/s0950-351x(96)80085-1 – ident: 6 doi: 10.1210/jc.84.1.165 – ident: 42 doi: 10.1093/humrep/17.4.853 – ident: 47 doi: 10.1053/beem.2002.0203 – ident: 35 doi: 10.1210/jcem.87.3.8305 – ident: 17 doi: 10.1016/s0015-0282(02)03111-4 – ident: 25 doi: 10.1210/jc.77.6.1636 – volume: 14 start-page: 1353 year: 2001 ident: 37 article-title: Cardiovascular risk in adolescent and young adult obese females with polycystic ovary syndrome (PCOS) publication-title: Journal of Pediatric Endocrinology & Metabolism – ident: 8 doi: 10.1210/jc.86.1.66 – ident: 38 doi: 10.1080/1464727002000198781 – ident: 18 doi: 10.1016/j.fertnstert.2004.11.070 – ident: 28 doi: 10.1210/clinem/dgaa095 – ident: 12 doi: 10.1016/0169-2607(86)90106-9 – ident: 45 doi: 10.1517/14656566.3.8.1177 – volume: 54 start-page: 97 issue: 2 year: 2002 ident: 36 article-title: Polycystic ovary syndrome long term sequelae and management publication-title: Minerva Ginecologica – ident: 20 doi: 10.1210/jc.2004-1973 – ident: 39 doi: 10.1016/s0015-0282(01)02963-6 – volume: 19 start-page: 41 year: 2004 ident: 2 article-title: Revised 2003 consensus on diagnostic criteria and long-term health risks related to polycystic ovary syndrome (PCOS) publication-title: Human Reproduction doi: 10.1093/humrep/deh098 – ident: 32 doi: 10.1146/annurev.med.52.1.401 – volume-title: Leaps: Regression Subset Selection. R package version 3.1 year: 2020 ident: 14 – ident: 7 doi: 10.1530/eje.0.1450749 |
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| Snippet | Insulin resistance is believed to be an integral component of the polycystic ovary syndrome (PCOS). Beta (ß) cell dysfunction is also found in PCOS. In the... Insulin resistance is believed to be an integral component of the polycystic ovary syndrome (PCOS). Beta ( ) cell dysfunction is also found in PCOS. In the... Insulin resistance is believed to be an integral component of the polycystic ovary syndrome (PCOS). Beta ( ß ) cell dysfunction is also found in PCOS. In the... |
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| SubjectTerms | Analysis Body mass index Dextrose Endocrinology Glucose Glucose tolerance tests Insulin Insulin resistance Investigations Polycystic ovary syndrome Stein-Leventhal syndrome Type 2 diabetes |
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| Title | Age, Body Mass Index, and Waist-to-Hip Ratio Related Changes in Insulin Secretion and Insulin Sensitivity in Women with Polycystic Ovary Syndrome: Minimal Model Analyses |
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