Determinants of impaired fasting glucose versus glucose intolerance in polycystic ovary syndrome

Siddika E Karakas, Kyoungmi Kim, Antoni J. Duleba

Research output: Contribution to journalArticle

22 Citations (Scopus)

Abstract

OBJECTIVE - To determine insulin resistance and response in patients with polycystic ovary syndrome (PCOS) and normal glucose tolerance (NGT), impaired fasting glucose (IFG), impaired glucose tolerance, and combined glucose intolerance (CGI). RESEARCH DESIGN AND METHODS - In this cross-sectional study, 143 patients with PCOS (diagnosed on the basis of National Institutes of Health criteria) underwent oral glucose tolerance testing (OGTT), and 68 patients also had frequently sampled intravenous glucose tolerance tests. Changes in plasma glucose, insulin, cardiovascular risk factors, and androgens were measured. RESULTS - Compared with patients with NGT, those with both IFG and CGI were signifi-cantly insulin resistant (homeostasis model assessment 3.3 ± 0.2 vs. 6.1 ± 0.9 and 6.4 ± 0.5, P < 0.0001) and hyperinsulinemic (insulin area under the curve for 120 min 973 ± 69 vs. 1,470 ± 197 and 1,461 ± 172 pmol/l, P < 0.0001). Insulin response was delayed in patients with CGI but not in those with IFG (2-h OGTT, insulin 1,001 ± 40 vs. 583 ± 45 pmol/l, P < 0.0001). Compared with the NGT group, the CGI group had a lower disposition index (1,615± 236 vs. 987 ± 296, P < 0.0234) and adiponectin level (11.1 ± 1.1 vs. 6.2 ± 0.8 ng/ml, P < 0.0096). Compared with the insulin-resistant tertile of the NGT group, those with IFG had a reduced insulinogenic index (421 ± 130 vs. 268 ± 68, P < 0.05). Compared with the insulin-sensitive tertile of the NGT group, the resistant tertile had higher triglyceride and high-sensitivity C-reactive protein (hs-CRP) and lower HDL cholesterol and sex hormone-binding globulin (SHBG). In the entire population, insulin resistance correlated directly with triglyceride, hs-CRP, and the free androgen index and inversely with SHBG. CONCLUSIONS - Patients with PCOS develop IFG and CGI despite having significant hyperinsulinemia. Patients with IFG and CGI exhibit similar insulin resistance but very different insulin response patterns. Increases in cardiac risk factors and free androgen level precede overt glucose intolerance.

Original languageEnglish (US)
Pages (from-to)887-893
Number of pages7
JournalDiabetes Care
Volume33
Issue number4
DOIs
StatePublished - Apr 2010

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Glucose Intolerance
Polycystic Ovary Syndrome
Fasting
Glucose
Insulin
Glucose Tolerance Test
Androgens
Insulin Resistance
Sex Hormone-Binding Globulin
C-Reactive Protein
Triglycerides
Adiponectin
National Institutes of Health (U.S.)
Hyperinsulinism
HDL Cholesterol
Area Under Curve
Homeostasis
Research Design
Cross-Sectional Studies

ASJC Scopus subject areas

  • Internal Medicine
  • Endocrinology, Diabetes and Metabolism
  • Advanced and Specialized Nursing

Cite this

Determinants of impaired fasting glucose versus glucose intolerance in polycystic ovary syndrome. / Karakas, Siddika E; Kim, Kyoungmi; Duleba, Antoni J.

In: Diabetes Care, Vol. 33, No. 4, 04.2010, p. 887-893.

Research output: Contribution to journalArticle

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abstract = "OBJECTIVE - To determine insulin resistance and response in patients with polycystic ovary syndrome (PCOS) and normal glucose tolerance (NGT), impaired fasting glucose (IFG), impaired glucose tolerance, and combined glucose intolerance (CGI). RESEARCH DESIGN AND METHODS - In this cross-sectional study, 143 patients with PCOS (diagnosed on the basis of National Institutes of Health criteria) underwent oral glucose tolerance testing (OGTT), and 68 patients also had frequently sampled intravenous glucose tolerance tests. Changes in plasma glucose, insulin, cardiovascular risk factors, and androgens were measured. RESULTS - Compared with patients with NGT, those with both IFG and CGI were signifi-cantly insulin resistant (homeostasis model assessment 3.3 ± 0.2 vs. 6.1 ± 0.9 and 6.4 ± 0.5, P < 0.0001) and hyperinsulinemic (insulin area under the curve for 120 min 973 ± 69 vs. 1,470 ± 197 and 1,461 ± 172 pmol/l, P < 0.0001). Insulin response was delayed in patients with CGI but not in those with IFG (2-h OGTT, insulin 1,001 ± 40 vs. 583 ± 45 pmol/l, P < 0.0001). Compared with the NGT group, the CGI group had a lower disposition index (1,615± 236 vs. 987 ± 296, P < 0.0234) and adiponectin level (11.1 ± 1.1 vs. 6.2 ± 0.8 ng/ml, P < 0.0096). Compared with the insulin-resistant tertile of the NGT group, those with IFG had a reduced insulinogenic index (421 ± 130 vs. 268 ± 68, P < 0.05). Compared with the insulin-sensitive tertile of the NGT group, the resistant tertile had higher triglyceride and high-sensitivity C-reactive protein (hs-CRP) and lower HDL cholesterol and sex hormone-binding globulin (SHBG). In the entire population, insulin resistance correlated directly with triglyceride, hs-CRP, and the free androgen index and inversely with SHBG. CONCLUSIONS - Patients with PCOS develop IFG and CGI despite having significant hyperinsulinemia. Patients with IFG and CGI exhibit similar insulin resistance but very different insulin response patterns. Increases in cardiac risk factors and free androgen level precede overt glucose intolerance.",
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N2 - OBJECTIVE - To determine insulin resistance and response in patients with polycystic ovary syndrome (PCOS) and normal glucose tolerance (NGT), impaired fasting glucose (IFG), impaired glucose tolerance, and combined glucose intolerance (CGI). RESEARCH DESIGN AND METHODS - In this cross-sectional study, 143 patients with PCOS (diagnosed on the basis of National Institutes of Health criteria) underwent oral glucose tolerance testing (OGTT), and 68 patients also had frequently sampled intravenous glucose tolerance tests. Changes in plasma glucose, insulin, cardiovascular risk factors, and androgens were measured. RESULTS - Compared with patients with NGT, those with both IFG and CGI were signifi-cantly insulin resistant (homeostasis model assessment 3.3 ± 0.2 vs. 6.1 ± 0.9 and 6.4 ± 0.5, P < 0.0001) and hyperinsulinemic (insulin area under the curve for 120 min 973 ± 69 vs. 1,470 ± 197 and 1,461 ± 172 pmol/l, P < 0.0001). Insulin response was delayed in patients with CGI but not in those with IFG (2-h OGTT, insulin 1,001 ± 40 vs. 583 ± 45 pmol/l, P < 0.0001). Compared with the NGT group, the CGI group had a lower disposition index (1,615± 236 vs. 987 ± 296, P < 0.0234) and adiponectin level (11.1 ± 1.1 vs. 6.2 ± 0.8 ng/ml, P < 0.0096). Compared with the insulin-resistant tertile of the NGT group, those with IFG had a reduced insulinogenic index (421 ± 130 vs. 268 ± 68, P < 0.05). Compared with the insulin-sensitive tertile of the NGT group, the resistant tertile had higher triglyceride and high-sensitivity C-reactive protein (hs-CRP) and lower HDL cholesterol and sex hormone-binding globulin (SHBG). In the entire population, insulin resistance correlated directly with triglyceride, hs-CRP, and the free androgen index and inversely with SHBG. CONCLUSIONS - Patients with PCOS develop IFG and CGI despite having significant hyperinsulinemia. Patients with IFG and CGI exhibit similar insulin resistance but very different insulin response patterns. Increases in cardiac risk factors and free androgen level precede overt glucose intolerance.

AB - OBJECTIVE - To determine insulin resistance and response in patients with polycystic ovary syndrome (PCOS) and normal glucose tolerance (NGT), impaired fasting glucose (IFG), impaired glucose tolerance, and combined glucose intolerance (CGI). RESEARCH DESIGN AND METHODS - In this cross-sectional study, 143 patients with PCOS (diagnosed on the basis of National Institutes of Health criteria) underwent oral glucose tolerance testing (OGTT), and 68 patients also had frequently sampled intravenous glucose tolerance tests. Changes in plasma glucose, insulin, cardiovascular risk factors, and androgens were measured. RESULTS - Compared with patients with NGT, those with both IFG and CGI were signifi-cantly insulin resistant (homeostasis model assessment 3.3 ± 0.2 vs. 6.1 ± 0.9 and 6.4 ± 0.5, P < 0.0001) and hyperinsulinemic (insulin area under the curve for 120 min 973 ± 69 vs. 1,470 ± 197 and 1,461 ± 172 pmol/l, P < 0.0001). Insulin response was delayed in patients with CGI but not in those with IFG (2-h OGTT, insulin 1,001 ± 40 vs. 583 ± 45 pmol/l, P < 0.0001). Compared with the NGT group, the CGI group had a lower disposition index (1,615± 236 vs. 987 ± 296, P < 0.0234) and adiponectin level (11.1 ± 1.1 vs. 6.2 ± 0.8 ng/ml, P < 0.0096). Compared with the insulin-resistant tertile of the NGT group, those with IFG had a reduced insulinogenic index (421 ± 130 vs. 268 ± 68, P < 0.05). Compared with the insulin-sensitive tertile of the NGT group, the resistant tertile had higher triglyceride and high-sensitivity C-reactive protein (hs-CRP) and lower HDL cholesterol and sex hormone-binding globulin (SHBG). In the entire population, insulin resistance correlated directly with triglyceride, hs-CRP, and the free androgen index and inversely with SHBG. CONCLUSIONS - Patients with PCOS develop IFG and CGI despite having significant hyperinsulinemia. Patients with IFG and CGI exhibit similar insulin resistance but very different insulin response patterns. Increases in cardiac risk factors and free androgen level precede overt glucose intolerance.

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