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Original Studies |
Department of Obstetrics and Gynecology, Pennsylvania State University College of Medicine (R.S.L.), Hershey Pennsylvania 17033; the Diabetes Research Laboratory, Simon Fraser University School of Kinesiology (D.F.), Burnaby, British Columbia, Canada V5A 1S6; and the Division of Women’s Health, Brigham and Women’s Hospital (A.D.), Boston, Massachusetts 02115.
Address all correspondence and requests for reprints to: Andrea Dunaif, M.D., Division of Women’s Health, Brigham and Women’s Hospital, PBB-Admin-5, 75 Francis Street, Boston, Massachusetts 02115.
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Abstract |
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Introduction |
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Initial studies have shown that agents that ameliorate insulin resistance and reduce circulating insulin levels, such as troglitazone (7, 8) or metformin (9, 10), may provide a new therapeutic modality in PCOS. Thus, identifying the subset of PCOS women who are the most insulin resistant with a simple test may become more relevant as therapeutic interventions that improve insulin sensitivity in PCOS women are identified. We sought, therefore, to assess whether there was a simple fasting measure of insulin resistance in PCOS women that correlated well with more involved dynamic tests of insulin action.
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Subjects and Methods |
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We studied 40 PCOS and 15 control women. All were non-Hispanic white women from the south central Pennsylvania area. This study was approved by the institutional review board of the Milton S. Hershey Medical Center (Hershey, PA), and all subjects gave written informed consent. The women had a body mass index greater than 26 kg/m2 and were between 18–40 yr of age. All women were in good health, euthyroid, and, for at least 1 month before each study, were not taking any medication (except for oral contraceptive agents, which were stopped for 3 months before the study) known to affect sex hormone or carbohydrate metabolism. The diagnosis of PCOS was made by the finding of an elevation of either total testosterone or biologically available testosterone levels associated with chronic oligomenorrhea (6 or fewer menses/yr). Nonclassical 21-hydroxylase deficiency, hyperprolactinemia, and androgen-secreting tumors were excluded by appropriate tests before the diagnosis of PCOS was made. Control women were matched for age, weight, and ethnicity to the women with PCOS. They did not engage in regular aerobic activity, nor did they have a history of diabetes mellitus or hypertension. There was no history of diabetes mellitus in the first degree relatives of the control women. Control women had regular menses every 27–32 days and were not hirsute. Androgen levels in control women were determined without regard to cycle day.
Study protocol
All studies were performed after a 3-day 300-g carbohydrate diet and an overnight fast. Each woman was allowed to rest for 0.5 h after insertion of an iv catheter before the oral glucose tolerance test (OGTT). A 75-g oral glucose load was administered, and blood was obtained for glucose and insulin determinations at 0, 30, 60, 90, and 120 min through the catheter. In two PCOS women we were unable to obtain a sample at 30 min during the OGTT because of technical problems with access. Glucose tolerance was assessed by WHO criteria (11). Forty-three percent of the PCOS women (17 of 40) were glucose intolerant, and all of the control women had normal glucose tolerance.
Insulin action was determined by a frequently sampled iv glucose tolerance test (FSIGT) (12, 13, 14). These tests were performed without regard to the phase of the menstrual cycle to assess whether it would still be possible to detect insulin resistance with this simplified study design (14). The FSIGTs were performed after a standard overnight fast of 10 h on a separate day after the OGTT. Women had two iv catheters inserted, one in each arm, and then were allowed to rest for 30 min. At 0 min, 0.3 g/kg glucose was injected over 1 min, and at 20 min, 500 mg tolbutamide (Upjohn Co., Kalamazoo, MI) were injected over 20 s. Blood samples were drawn at -15, -10, -5, -1, 0, 2, 3, 4, 5, 8, 10, 12, 14, 16, 19, 22, 23, 24, 25, 27, 30, 40, 50, 60, 70, 90, 100, 120, 140, 160, and 180 min. The insulin sensitivity index (SI) and glucose effectiveness (SG; MINMOD computer program version NUDEMM1, R. Bergman, Los Angeles, CA) as well as the acute insulin response to glucose (AIRg) and the disposition index (the product of SI x AIRg) were calculated as previously reported (14).
Assays
A single fasting blood sample obtained at 0 min of the OGTT was used for the androgen assays. Assays for testosterone, biologically available, and dehyroepiandrosterone sulfate were performed as previously reported (7). Glucose was measured by the glucose oxidase technique with a Beckman Glucose Analyzer 2 (Fullerton, CA), and insulin levels were measured using Diagnostic Products Corp. kits (Los Angeles, CA) as previously reported (7). The cross-reactivity with proinsulin at the midcurve of the assay is approximately 40%.
Definition of insulin resistance
SI values from the age-, weight-, and ethnicity-matched control group were used to define the normal distribution; the tenth percentile for SI was less than 1.12 x 10-4 min-1/(µU/mL). We have previously found that this sample size is adequate to define the variance in this normal population (14). Insulin resistance was then defined in PCOS women as an SI value less than this.
Data analysis
Continuous data were compared between the two groups (PCOS and controls) using unpaired t tests. The integrated area under the curve (AUC) analysis for glucose and insulin was determined according to the formula of Tai et al. (15). Regression analysis was performed using SI as the dependent variable and OGTT fasting and stimulated glucose and insulin levels as independent parameters. Stepwise regression analysis was performed with SI as the dependent variable and fasting glucose and insulin levels, AUC for glucose and insulin, and fasting G:I ratio. Data were analyzed using StatView 4.5 for the Macintosh (Abacus Concepts, Berkeley, CA). Receiver operator curves (ROCs) were created by calculating the sensitivity and specificity of fixed cut-off points of the various parameters examined. Values are reported as the mean ± SD. P < 0.05 was considered statistically significant.
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Results |
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. By design, there
were no significant differences between the two groups in age or
weight. Waist/hip girth ratios were significantly higher in the PCOS
women than in the control women (0.84 ± 0.08 vs.
0.78 ± 0.05; P < 0.05). PCOS women also had
significantly higher levels of circulating testosterone (86.2 ±
34.5 vs. 33.4 ± 9.7 ng/dL; P <
0.0001), biologically available testosterone (31.2 ± 12.5
vs. 8.3 ± 3.8 ng/dL; P < 0.0001), and
dehyroepiandrosterone sulfate (2472 ± 1570 vs.
1501 ± 553 ng/mL; P < 0.001). Fasting glucose
levels did not differ, but PCOS women had significantly higher fasting
insulin levels than control women (27.0 ± 18.1 vs.
13.3 ± 10.1 µU/mL; P < 0.001). SI
was significantly lower in PCOS than in control women [1.81 ±
1.82 vs. 4.37 ± 2.60 x 10-4
min-1/(µU/mL); P < 0.0001].
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), followed by the fasting G:I
ratio (F = 42.0; P < 0.0001; Fig. 1). There was a weaker, but significant,
correlation between the fasting G:I ratio with the AIRg in PCOS (r
= 0.43; F = 8.7; P < 0.01) and the disposition
index (r = 0.43; F = 8.9; P < 0.01), but no
correlation with glucose effectiveness (r = 0.01; F = 0.24;
P = NS). Stepwise regression analysis with
SI as the dependent variable and fasting glucose and
insulin levels, AUC for glucose and insulin, and a fasting G:I ratio
showed that only the fasting G:I ratio was significantly predictive of
SI in the model (F to remove value = 38.1;
P < 0.001).
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). We examined the
sensitivity and specificity of various cut-off values for predicting
insulin resistance to create ROC curves for OGTT glucose and insulin
levels and G:I ratios (Fig. 2).
Sensitivity is plotted against 1 - specificity (or the false
positive rate). The ideal screening test is one that approaches or
reaches the upper left corner of the graph (100% sensitivity and 100%
specificity). A test that approximates a coin flip is the diagonal from
the lower left to the upper right corner of the graph. This is best
illustrated in Fig. 2A by the fasting glucose level, which comes
closest to this diagonal and has corresponding poor sensitivity and
specificity at the selected cut-off point (Table 3). The cut-off point
for each of the screening tests that has the best combination of
sensitivity and specificity is located at the "knee" of the graph
and is labeled for each parameter (Fig. 2, A–G).
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) provided the best single fasting
measure of insulin action and was comparable to glucose-stimulated
parameters (Fig. 2B). A fasting G:I ratio (cut-off value, <4.5)
provided the best combination of sensitivity (95%) and specificity
(84%) as well as the best positive predictive value (87%) and
negative predictive value (94%) as a screening test for predicting
insulin resistance in PCOS (Table 3). This was similar for the lower
limits of the 95% confidence intervals for the fasting G:I ratio. The
next best single predictor of insulin resistance was the fasting
insulin level. The glucose-stimulated parameters obtained from the
OGTT, although sensitive, displayed less specificity than the fasting
insulin and/or the fasting G:I ratio (Table 3). |
Discussion |
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Insulin resistance and the resulting hyperinsulinemia contribute to the reproductive abnormalities of PCOS women (2, 18). Lowering circulating insulin levels by a variety of mechanisms has resulted in decreased androgen levels in PCOS women. As little as a 7% decrease in body weight has significantly improved hyperandrogenism (19). The short term use of agents that lower insulin secretion, such as diazoxide or somatostatin, produces similar effects (20, 21). Therapy with metformin, which acts primarily by suppressing hepatic gluconeogenesis, when accompanied by a reduction in circulating insulin levels, can decrease androgen levels in PCOS (9, 10, 22). In two small studies, the administration of troglitazone, an agent that directly reduces target tissue insulin resistance and, accordingly, circulating insulin levels, also resulted in a decrease in circulating androgen levels in PCOS women (7, 8). A baseline fasting G:I ratio has been shown to have good correlation with the clinical efficacy of troglitazone on hyperglycemia in Japanese patients with type 2 diabetes (23).
We have chosen the lower decile of insulin sensitivity from an age-, weight-, and ethnicity-matched control group to define insulin resistance. If we had selected a less stringent criterion that reflects the prevalence of insulin resistance in the larger population (24), such as a value below the 25th percentile of the control population, 80% of PCOS women would have been designated insulin resistant. For the purposes of evaluating the usefulness of the fasting G:I ratio as well as other OGTT parameters as screening tests for insulin action, we used the more stringent criterion of the lowest decile of insulin sensitivity as the cut-off point. Other groups have defined insulin resistance as a measure of insulin action in the lower decile of insulin sensitivity in lean subjects (25). By using obese women to define the normal range of insulin sensitivity, we were assessing insulin resistance that was beyond that due to obesity per se.
A brief report by Parra and colleagues suggested that a fasting G:I ratio might be a useful measurement for predicting glucose-stimulated hyperinsulinemia in PCOS women (26). We have shown for the first time that the fasting G:I ratio is a sensitive and specific marker of insulin sensitivity in PCOS. SI as determined by FSIGT has been shown to be highly correlated with insulin action determined by the euglycemic glucose clamp technique in many insulin-resistant states, including PCOS (27, 28). We have also controlled for the effects of age, weight, and ethnicity in PCOS women on insulin sensitivity by using an appropriate control group (4, 29, 30, 31).
We chose ROC curve analysis to graphically portray the trade-off involved in improving a test’s sensitivity at a cost of lower specificity and to select the best cut-off value. The fasting G:I ratio offered the best single cut-off measure (including sensitivity, specificity, positive predictive value, negative predictive value, and 95% confidence intervals), had a better correlation with SI by simple regression than fasting insulin level, and was a better fasting predictor of SI by our stepwise regression model. We do not have an adequate sample size to assess statistically whether the fasting G:I ratio is superior to a fasting insulin level by comparison of ROC AUC analysis. A power analysis based on our preliminary findings suggests that we would need 4 times as many PCOS women in the insulin-resistant group to detect a difference in the sensitivity of the two measures.
Our results indicate that a fasting G:I ratio is an easily obtainable, safe, highly sensitive, and specific measure of insulin sensitivity in obese non-Hispanic white PCOS women. The predictive power of both a positive and a negative test is excellent. Further studies will be needed to validate this measure in other populations. We suggest that the fasting G:I ratio may be a useful test for identifying PCOS women with insulin resistance. These women may be more likely to benefit from therapies that lower circulating insulin levels.
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Acknowledgments |
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Footnotes |
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Received March 4, 1998.
Revised May 6, 1998.
Accepted May 8, 1998.
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References |
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activity and serum free testosterone
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R. S. Legro, E. Myers, and for the Reproductive Medicine Network Surrogate end-points or primary outcomes in clinical trials in women with polycystic ovary syndrome? Hum. Reprod., August 1, 2004; 19(8): 1697 - 1704. [Abstract] [Full Text] [PDF]
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M. Misra, K. K. Miller, C. Almazan, K. Ramaswamy, A. Aggarwal, D. B. Herzog, G. Neubauer, J. Breu, and A. Klibanski Hormonal and Body Composition Predictors of Soluble Leptin Receptor, Leptin, and Free Leptin Index in Adolescent Girls with Anorexia Nervosa and Controls and Relation to Insulin Sensitivity J. Clin. Endocrinol. Metab., July 1, 2004; 89(7): 3486 - 3495. [Abstract] [Full Text] [PDF]
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 H-W. Yen, A.J. Jakimiuk, I. Munir, and D.A. Magoffin Selective alterations in insulin receptor substrates-1, -2 and -4 in theca but not granulosa cells from polycystic ovaries Mol. Hum. Reprod., July 1, 2004; 10(7): 473 - 479. [Abstract] [Full Text] [PDF]
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M. A. Ganie, M. L. Khurana, M. Eunice, M. Gulati, S. N. Dwivedi, and A. C. Ammini Comparison of Efficacy of Spironolactone with Metformin in the Management of Polycystic Ovary Syndrome: An Open-Labeled Study J. Clin. Endocrinol. Metab., June 1, 2004; 89(6): 2756 - 2762. [Abstract] [Full Text] [PDF]
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J. Tesarik, A. Hazout, and C. Mendoza Enhancement of embryo developmental potential by a single administration of GnRH agonist at the time of implantation Hum. Reprod., May 1, 2004; 19(5): 1176 - 1180. [Abstract] [Full Text] [PDF]
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C.J. Glueck, N. Goldenberg, P. Wang, M. Loftspring, and A. Sherman Metformin during pregnancy reduces insulin, insulin resistance, insulin secretion, weight, testosterone and development of gestational diabetes: prospective longitudinal assessment of women with polycystic ovary syndrome from preconception throughout pregnancy Hum. Reprod., March 1, 2004; 19(3): 510 - 521. [Abstract] [Full Text] [PDF]
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H. M. Domene, S. V. Bengolea, A. S. Martinez, M. G. Ropelato, P. Pennisi, P. Scaglia, J. J. Heinrich, and H. G. Jasper Deficiency of the Circulating Insulin-like Growth Factor System Associated with Inactivation of the Acid-Labile Subunit Gene N. Engl. J. Med., February 5, 2004; 350(6): 570 - 577. [Full Text] [PDF]
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P. Cousin, L. Calemard-Michel, H. Lejeune, G. Raverot, N. Yessaad, A. Emptoz-Bonneton, Y. Morel, and M. Pugeat Influence of SHBG Gene Pentanucleotide TAAAA Repeat and D327N Polymorphism on Serum Sex Hormone-Binding Globulin Concentration in Hirsute Women J. Clin. Endocrinol. Metab., February 1, 2004; 89(2): 917 - 924. [Abstract] [Full Text] [PDF]
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M.H.A. van Hooff, F.J. Voorhorst, M.B.H. Kaptein, R.A. Hirasing, C. Koppenaal, and J. Schoemaker Predictive value of menstrual cycle pattern, body mass index, hormone levels and polycystic ovaries at age 15 years for oligo-amenorrhoea at age 18 years Hum. Reprod., February 1, 2004; 19(2): 383 - 392. [Abstract] [Full Text] [PDF]
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L. S. Conwell, S. G. Trost, W. J. Brown, and J. A. Batch Indexes of Insulin Resistance and Secretion in Obese Children and Adolescents: A validation study Diabetes Care, February 1, 2004; 27(2): 314 - 319. [Abstract] [Full Text] [PDF]
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 M. T. Sheehan Polycystic Ovarian Syndrome: Diagnosis and Management Clin. Med. Res., February 1, 2004; 2(1): 13 - 27. [Abstract] [Full Text] [PDF]
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 C. L. Rock, S. W. Flatt, C. A. Thomson, M. L. Stefanick, V. A. Newman, L. Jones, L. Natarajan, J. P. Pierce, R. J. Chang, and J. L. Witztum Plasma Triacylglycerol and HDL Cholesterol Concentrations Confirm Self-Reported Changes in Carbohydrate and Fat Intakes in Women in a Diet Intervention Trial J. Nutr., February 1, 2004; 134(2): 342 - 347. [Abstract] [Full Text] [PDF]
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F. Orio, S. Palomba, F. Zullo, A. Colao, and G. Lombardi Are serum adiponectin levels really reduced in obese women with polycystic ovary syndrome? Hum. Reprod., January 1, 2004; 19(1): 215 - 215. [Full Text] [PDF]
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I. Munir, H.-W. Yen, D. H. Geller, D. Torbati, R. M. Bierden, S. R. Weitsman, S. K. Agarwal, and D. A. Magoffin Insulin Augmentation of 17{alpha}-Hydroxylase Activity Is Mediated by Phosphatidyl Inositol 3-Kinase But Not Extracellular Signal-Regulated Kinase-1/2 in Human Ovarian Theca Cells Endocrinology, January 1, 2004; 145(1): 175 - 183. [Abstract] [Full Text] [PDF]
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F. Orio Jr., G. Matarese, S. Di Biase, S. Palomba, D. Labella, V. Sanna, S. Savastano, F. Zullo, A. Colao, and G. Lombardi Exon 6 and 2 Peroxisome Proliferator-Activated Receptor-{gamma} Polymorphisms in Polycystic Ovary Syndrome J. Clin. Endocrinol. Metab., December 1, 2003; 88(12): 5887 - 5892. [Abstract] [Full Text] [PDF]
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 J. Sheeder, S. H. Travers, and C. Stevens-Simon Is This Patient Insulin Resistant? How Much Does It Matter? Clinical Pediatrics, November 1, 2003; 42(9): 835 - 839. [PDF]
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 V. De Leo, A. la Marca, and F. Petraglia Insulin-Lowering Agents in the Management of Polycystic Ovary Syndrome Endocr. Rev., October 1, 2003; 24(5): 633 - 667. [Abstract] [Full Text] [PDF]
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M. E. Silfen, M. R. Denburg, A. M. Manibo, R. A. Lobo, R. Jaffe, M. Ferin, L. S. Levine, and S. E. Oberfield Early Endocrine, Metabolic, and Sonographic Characteristics of Polycystic Ovary Syndrome (PCOS): Comparison between Nonobese and Obese Adolescents J. Clin. Endocrinol. Metab., October 1, 2003; 88(10): 4682 - 4688. [Abstract] [Full Text] [PDF]
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D. Panidis, A. Kourtis, D. Farmakiotis, T. Mouslech, D. Rousso, and G. Koliakos Serum adiponectin levels in women with polycystic ovary syndrome Hum. Reprod., September 1, 2003; 18(9): 1790 - 1796. [Abstract] [Full Text] [PDF]
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P.-H. Ducluzeau, P. Cousin, E. Malvoisin, H. Bornet, H. Vidal, M. Laville, and M. Pugeat Glucose-to-Insulin Ratio Rather than Sex Hormone-Binding Globulin and Adiponectin Levels Is the Best Predictor of Insulin Resistance in Nonobese Women with Polycystic Ovary Syndrome J. Clin. Endocrinol. Metab., August 1, 2003; 88(8): 3626 - 3631. [Abstract] [Full Text] [PDF]
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H. Yokoyama, M. Emoto, S. Fujiwara, K. Motoyama, T. Morioka, M. Komatsu, H. Tahara, T. Shoji, Y. Okuno, and Y. Nishizawa Quantitative Insulin Sensitivity Check Index and the Reciprocal Index of Homeostasis Model Assessment in Normal Range Weight and Moderately Obese Type 2 Diabetic Patients Diabetes Care, August 1, 2003; 26(8): 2426 - 2432. [Abstract] [Full Text] [PDF]
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 K-L. C. Jen, A. Buison, M. Pellizzon, F. Ordiz Jr., L. Santa Ana, and J. Brown Differential Effects of Fatty Acids and Exercise on Body Weight Regulation and Metabolism in Female Wistar Rats Experimental Biology and Medicine, July 1, 2003; 228(7): 843 - 849. [Abstract] [Full Text] [PDF]
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R. S. Legro Polycystic Ovary Syndrome and Cardiovascular Disease: A Premature Association? Endocr. Rev., June 1, 2003; 24(3): 302 - 312. [Abstract] [Full Text] [PDF]
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J. Tesarik Effects of LH on oocyte yield and developmental competence Hum. Reprod., June 1, 2003; 18(6): 1358 - 1360. [Full Text] [PDF]
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 A. S. M Ahmed Polycystic ovaries: the role of insulin Perspectives in Public Health, June 1, 2003; 123(2): 78 - 79. [PDF]
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M. Schachter, A. Raziel, S. Friedler, D. Strassburger, O. Bern, and R. Ron-El Insulin resistance in patients with polycystic ovary syndrome is associated with elevated plasma homocysteine Hum. Reprod., April 1, 2003; 18(4): 721 - 727. [Abstract] [Full Text] [PDF]
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G. Guercio, M. A. Rivarola, E. Chaler, M. Maceiras, and A. Belgorosky Relationship between the Growth Hormone/Insulin-Like Growth Factor-I Axis, Insulin Sensitivity, and Adrenal Androgens in Normal Prepubertal and Pubertal Girls J. Clin. Endocrinol. Metab., March 1, 2003; 88(3): 1389 - 1393. [Abstract] [Full Text] [PDF]
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F. Orio Jr., S. Palomba, S. Di Biase, A. Colao, L. Tauchmanova, S. Savastano, D. Labella, T. Russo, F. Zullo, and G. Lombardi Homocysteine Levels and C677T Polymorphism of Methylenetetrahydrofolate Reductase in Women with Polycystic Ovary Syndrome J. Clin. Endocrinol. Metab., February 1, 2003; 88(2): 673 - 679. [Abstract] [Full Text] [PDF]
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S. S. George, K. George, C. Irwin, V. Job, R. Selvakumar, V. Jeyaseelan, and M.S. Seshadri Sequential treatment of metformin and clomiphene citrate in clomiphene-resistant women with polycystic ovary syndrome: a randomized, controlled trial Hum. Reprod., February 1, 2003; 18(2): 299 - 304. [Abstract] [Full Text] [PDF]
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J.G. Dolfing, K.E. Tucker, C.M. Lem, J. Uittenbogaart, J.C. Verzijl, and D.H. Schweitzer Low 11-deoxycortisol to cortisol conversion reflects extra-adrenal factors in the majority of women with normo-gonadotrophic normo-estrogenic infertility Hum. Reprod., February 1, 2003; 18(2): 333 - 337. [Abstract] [Full Text] [PDF]
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S. Taponen, H. Martikainen, M.-R. Jarvelin, J. Laitinen, A. Pouta, A.-L. Hartikainen, U. Sovio, M. I. McCarthy, S. Franks, and A. Ruokonen Hormonal Profile of Women with Self-Reported Symptoms of Oligomenorrhea and/or Hirsutism: Northern Finland Birth Cohort 1966 Study J. Clin. Endocrinol. Metab., January 1, 2003; 88(1): 141 - 147. [Abstract] [Full Text] [PDF]
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R. D'Alfonso, M. A. Marini, L. Frittitta, R. Sorge, S. Frontoni, O. Porzio, L. M. Mariani, D. Lauro, S. Gambardella, V. Trischitta, et al. Polymorphisms of the Insulin Receptor Subtrate-2 in Patients with Type 2 Diabetes J. Clin. Endocrinol. Metab., January 1, 2003; 88(1): 317 - 322. [Abstract] [Full Text] [PDF]
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 M. Urbanek, Y. Du, K. Silander, F. S. Collins, C. M. Steppan, J. F. Strauss III, A. Dunaif, R. S. Spielman, and R. S. Legro Variation in Resistin Gene Promoter Not Associated With Polycystic Ovary Syndrome Diabetes, January 1, 2003; 52(1): 214 - 217. [Abstract] [Full Text] [PDF]
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U. Pagotto, A. Gambineri, V. Vicennati, M. L. Heiman, M. Tschop, and R. Pasquali Plasma Ghrelin, Obesity, and the Polycystic Ovary Syndrome: Correlation with Insulin Resistance and Androgen Levels J. Clin. Endocrinol. Metab., December 1, 2002; 87(12): 5625 - 5629. [Abstract] [Full Text] [PDF]
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 R. Murray Recognizing the Signs of Metabolic Syndrome and Polycystic Ovary Syndrome in a Caucasian Adolescent Girl: Differentiating Type 2 From Type 1 Diabetes Diabetes Spectr, October 1, 2002; 15(4): 227 - 231. [Full Text] [PDF]
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R. Homburg What is polycystic ovarian syndrome?: A proposal for a consensus on the definition and diagnosis of polycystic ovarian syndrome Hum. Reprod., October 1, 2002; 17(10): 2495 - 2499. [Abstract] [Full Text] [PDF]
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R. Azziz Polycystic Ovary Syndrome, Insulin Resistance, and Molecular Defects of Insulin Signaling J. Clin. Endocrinol. Metab., September 1, 2002; 87(9): 4085 - 4087. [Full Text] [PDF]
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K. Elter, G. Imir, and F. Durmusoglu Clinical, endocrine and metabolic effects of metformin added to ethinyl estradiol-cyproterone acetate in non-obese women with polycystic ovarian syndrome: a randomized controlled study Hum. Reprod., July 1, 2002; 17(7): 1729 - 1737. [Abstract] [Full Text] [PDF]
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J. Vrbikova, B. Bendlova, M. Hill, M. Vankova, K. Vondra, and L. Starka Insulin Sensitivity and {beta}-Cell Function in Women With Polycystic Ovary Syndrome Diabetes Care, July 1, 2002; 25(7): 1217 - 1222. [Abstract] [Full Text] [PDF]
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S. B. Seminara and W. F. Crowley Jr. Genetic Approaches to Unraveling Reproductive Disorders: Examples of Bedside to Bench Research in the Genomic Era Endocr. Rev., June 1, 2002; 23(3): 382 - 392. [Abstract] [Full Text] [PDF]
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R. S. Legro, R. Bentley-Lewis, D. Driscoll, S. C. Wang, and A. Dunaif Insulin Resistance in the Sisters of Women with Polycystic Ovary Syndrome: Association with Hyperandrogenemia Rather Than Menstrual Irregularity J. Clin. Endocrinol. Metab., May 1, 2002; 87(5): 2128 - 2133. [Abstract] [Full Text] [PDF]
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V. Jayagopal, E. S. Kilpatrick, S. Holding, P. E. Jennings, and S. L. Atkin The Biological Variation of Insulin Resistance in Polycystic Ovarian Syndrome J. Clin. Endocrinol. Metab., April 1, 2002; 87(4): 1560 - 1562. [Abstract] [Full Text] [PDF]
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M. R. Palmert, C. M. Gordon, A. I. Kartashov, R. S. Legro, S. J. Emans, and A. Dunaif Screening for Abnormal Glucose Tolerance in Adolescents with Polycystic Ovary Syndrome J. Clin. Endocrinol. Metab., March 1, 2002; 87(3): 1017 - 1023. [Abstract] [Full Text] [PDF]
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D. A. Dumesic, R. D. Schramm, E. Peterson, A. M. Paprocki, R. Zhou, and D. H. Abbott Impaired Developmental Competence of Oocytes in Adult Prenatally Androgenized Female Rhesus Monkeys Undergoing Gonadotropin Stimulation for in Vitro Fertilization J. Clin. Endocrinol. Metab., March 1, 2002; 87(3): 1111 - 1119. [Abstract] [Full Text] [PDF]
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G. Guercio, M. A. Rivarola, E. Chaler, M. Maceiras, and A. Belgorosky Relationship between the GH/IGF-I Axis, Insulin Sensitivity, and Adrenal Androgens in Normal Prepubertal and Pubertal Boys J. Clin. Endocrinol. Metab., March 1, 2002; 87(3): 1162 - 1169. [Abstract] [Full Text] [PDF]
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M. E. Silfen, A. M. Manibo, M. Ferin, D. J. McMahon, L. S. Levine, and S. E. Oberfield Elevated Free IGF-I Levels in Prepubertal Hispanic Girls with Premature Adrenarche: Relationship with Hyperandrogenism and Insulin Sensitivity J. Clin. Endocrinol. Metab., January 1, 2002; 87(1): 398 - 403. [Abstract] [Full Text] [PDF]
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R. M. Koivunen, L. C. Morin-Papunen, A. Ruokonen, J. S. Tapanainen, and H. K. Martikainen Ovarian steroidogenic response to human chorionic gonadotrophin in obese women with polycystic ovary syndrome: effect of metformin Hum. Reprod., December 1, 2001; 16(12): 2546 - 2551. [Abstract] [Full Text] [PDF]
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J. J. Meier, K. Hucking, J. J. Holst, C. F. Deacon, W. H. Schmiegel, and M. A. Nauck Reduced Insulinotropic Effect of Gastric Inhibitory Polypeptide in First-Degree Relatives of Patients With Type 2 Diabetes Diabetes, November 1, 2001; 50(11): 2497 - 2504. [Abstract] [Full Text] [PDF]
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M. J. Quon Limitations of the Fasting Glucose to Insulin Ratio as an Index of Insulin Sensitivity J. Clin. Endocrinol. Metab., October 1, 2001; 86(10): 4615 - 4617. [Full Text] [PDF]
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A. P. Goldstone, E. L. Thomas, A. E. Brynes, J. D. Bell, G. Frost, N. Saeed, J. V. Hajnal, J. K. Howard, A. Holland, and S. R. Bloom Visceral Adipose Tissue and Metabolic Complications of Obesity Are Reduced in Prader-Willi Syndrome Female Adults: Evidence for Novel Influences on Body Fat Distribution J. Clin. Endocrinol. Metab., September 1, 2001; 86(9): 4330 - 4338. [Abstract] [Full Text] [PDF]
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P.M. Spritzer, M. Poy, D. Wiltgen, L.S. Mylius, and E. Capp Leptin concentrations in hirsute women with polycystic ovary syndrome or idiopathic hirsutism: influence on LH and relationship with hormonal, metabolic, and anthropometric measurements Hum. Reprod., July 1, 2001; 16(7): 1340 - 1346. [Abstract] [Full Text] [PDF]
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M. E. Silfen, A. M. Manibo, D. J. McMahon, L. S. Levine, A. R. Murphy, and S. E. Oberfield Comparison of Simple Measures of Insulin Sensitivity in Young Girls with Premature Adrenarche: The Fasting Glucose to Insulin Ratio May Be a Simple and Useful Measure J. Clin. Endocrinol. Metab., June 1, 2001; 86(6): 2863 - 2868. [Abstract] [Full Text] [PDF]
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