TY - JOUR
T1 - β-Cell dysfunction independent of obesity and glucose intolerance in the polycystic ovary syndrome
AU - Dunaif, Andrea
AU - Finegood, Diane T.
PY - 1996
Y1 - 1996
N2 - Several distinct groups of subjects at high risk to develop noninsulin- dependent diabetes mellitus (NIDDM) have been found to have insulin secretory defects when β-cell function is assessed in the context of peripheral insulin sensitivity. We investigated this with a modified frequently sampled iv glucose tolerance test to determine acute insulin responses to glucose (AIRg) as well as insulin action by minimal model analysis in 28 women with polycystic ovary syndrome (PCOS; 15 obese and 13 nonobese) and 29 age- and weight-matched normal women (14 obese and 15 nonobese). No subject, PCOS or control, had fasting hyperglycemia, but seven PCOS women (six obese and one nonobese) had impaired glucose tolerance or NIDDM. The PCOS women had significantly decreased insulin sensitivity compared to the normal women (P ≤ 0.001), and the obese women were less sensitive than the nonobese women (P ≤ 0.001). The empiric measure of insulin release, AIRg, was significantly increased by obesity (P ≤ 0.01), but not by PCOS. However, the disposition index (insulin sensitivity x AIRg) was significantly decreased by both PCOS (≤0.005) and obesity (≤0.005), suggesting that AIRg was inadequate for the degree of insulin resistance. When the PCOS women with impaired glucose tolerance or NIDDM were removed from the analysis, all of the reported PCOS- related changes in insulin action and secretion remained significant. We conclude that both obese and nonobese PCOS women have β-cell dysfunction as well as insulin resistance. However, this was not associated with glucose intolerance in the majority of PCOS women.
AB - Several distinct groups of subjects at high risk to develop noninsulin- dependent diabetes mellitus (NIDDM) have been found to have insulin secretory defects when β-cell function is assessed in the context of peripheral insulin sensitivity. We investigated this with a modified frequently sampled iv glucose tolerance test to determine acute insulin responses to glucose (AIRg) as well as insulin action by minimal model analysis in 28 women with polycystic ovary syndrome (PCOS; 15 obese and 13 nonobese) and 29 age- and weight-matched normal women (14 obese and 15 nonobese). No subject, PCOS or control, had fasting hyperglycemia, but seven PCOS women (six obese and one nonobese) had impaired glucose tolerance or NIDDM. The PCOS women had significantly decreased insulin sensitivity compared to the normal women (P ≤ 0.001), and the obese women were less sensitive than the nonobese women (P ≤ 0.001). The empiric measure of insulin release, AIRg, was significantly increased by obesity (P ≤ 0.01), but not by PCOS. However, the disposition index (insulin sensitivity x AIRg) was significantly decreased by both PCOS (≤0.005) and obesity (≤0.005), suggesting that AIRg was inadequate for the degree of insulin resistance. When the PCOS women with impaired glucose tolerance or NIDDM were removed from the analysis, all of the reported PCOS- related changes in insulin action and secretion remained significant. We conclude that both obese and nonobese PCOS women have β-cell dysfunction as well as insulin resistance. However, this was not associated with glucose intolerance in the majority of PCOS women.
UR - http://www.scopus.com/inward/record.url?scp=0029880488&partnerID=8YFLogxK
U2 - 10.1210/jc.81.3.942
DO - 10.1210/jc.81.3.942
M3 - Article
C2 - 8772555
AN - SCOPUS:0029880488
SN - 0021-972X
VL - 81
SP - 942
EP - 947
JO - Journal of Clinical Endocrinology and Metabolism
JF - Journal of Clinical Endocrinology and Metabolism
IS - 3
ER -