TY - JOUR
T1 - Influence of basal androgen levels in euandrogenic women on glucose homeostasis
AU - Grainger, D.
AU - DeFronzo, R.
AU - Thornton, K.
AU - Sherwin, R.
AU - Rossi, G.
AU - Diamond, M. P.
AU - Connoly-Diamond, M.
N1 - Funding Information:
Received June 1, 1992; revised and accepted August 12, 1992. * Supported by grant RR-OOI25 from the Yale General Clinical Research Center, New Haven, Connecticut. t Department of Obstetrics and Gynecology. :j: Present address: Department of Obstetrics and Gynecology, University of Kansas School of Medicine-Wichita, Wichita, Kansas. § Present address: Department of Obstetrics and Gynecology, University of Connecticut Health Center, Farmington, Connecticut. II Present address: Department of Obstetrics and Gynecology, Vanderbilt University Medical Center, Nashville, Tennessee.
PY - 1992
Y1 - 1992
N2 - Objective: To evaluate possible relationships between insulin action and the normal variations of serum androgens in euandrogenic women. Design: Prospective evaluation of insulin action in normal nonobese women using hyperglycemic and euglycemic hyperinsulinemic clamp techniques, correlating insulin action to serum testosterone (T), free T, androstenedione (A), and dehydroepiandrosterone sulfate (DHEAS). Statistical analysis used Spearman's rank correlation. Setting: Yale University Clinical Research Center. Participants: Nonobese females with normal oral glucose tolerance tests, on no medications known to affect glucose metabolism, having the following range of serum androgen levels: T, 0.69 to 3.12 nmol/L; free T, 0.17 to 1.25 nmol/L; A, 2.48 to 11.31 nmol/L; DHEAS, 0.68 to 10.61 μmol/L. Total number of patients studied: hyperglycemic clamps, n = 58; euglycemic hyperinsulinemic clamps, n = 43. Interventions: None. Main Outcome Measures: Pancreatic insulin secretion in response to hyperglycemia and insulin action as assessed by insulin-mediated glucose utilization using the euglycemic, hyperinsulinemic clamp technique. Results: We identified no significant correlation between serum androgens and either glucose uptake or insulin- mediated glucose utilization. Glucose-stimulated insulin release was negatively correlated with serum T and free T throughout the normal range of these hormones. Conclusion: We conclude that, within the normal range, variations of serum androgens are not correlated with changes in the response to insulin. It seems unlikely, therefore, that modest increases of serum androgens within the normal range are responsible for inducing insulin resistance.
AB - Objective: To evaluate possible relationships between insulin action and the normal variations of serum androgens in euandrogenic women. Design: Prospective evaluation of insulin action in normal nonobese women using hyperglycemic and euglycemic hyperinsulinemic clamp techniques, correlating insulin action to serum testosterone (T), free T, androstenedione (A), and dehydroepiandrosterone sulfate (DHEAS). Statistical analysis used Spearman's rank correlation. Setting: Yale University Clinical Research Center. Participants: Nonobese females with normal oral glucose tolerance tests, on no medications known to affect glucose metabolism, having the following range of serum androgen levels: T, 0.69 to 3.12 nmol/L; free T, 0.17 to 1.25 nmol/L; A, 2.48 to 11.31 nmol/L; DHEAS, 0.68 to 10.61 μmol/L. Total number of patients studied: hyperglycemic clamps, n = 58; euglycemic hyperinsulinemic clamps, n = 43. Interventions: None. Main Outcome Measures: Pancreatic insulin secretion in response to hyperglycemia and insulin action as assessed by insulin-mediated glucose utilization using the euglycemic, hyperinsulinemic clamp technique. Results: We identified no significant correlation between serum androgens and either glucose uptake or insulin- mediated glucose utilization. Glucose-stimulated insulin release was negatively correlated with serum T and free T throughout the normal range of these hormones. Conclusion: We conclude that, within the normal range, variations of serum androgens are not correlated with changes in the response to insulin. It seems unlikely, therefore, that modest increases of serum androgens within the normal range are responsible for inducing insulin resistance.
KW - Insulin resistance
KW - hyperandrogenism
KW - polycystic ovarian syndrome
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U2 - 10.1016/s0015-0282(16)55553-8
DO - 10.1016/s0015-0282(16)55553-8
M3 - Article
C2 - 1459257
AN - SCOPUS:0026620877
SN - 0015-0282
VL - 58
SP - 1113
EP - 1118
JO - Fertility and sterility
JF - Fertility and sterility
IS - 6
ER -