Endocrine Abstracts

Aim: To examine the secretion of insulin and glucagon in PCOS in the context of insulin sensitivity.

Patients and methods: 13 healthy women (BMI 21.8(2.2) kg/m²), 21 PCOS without family history of DM2 (FH-); BMI 24.3 (4.4) kg/m² and 16 PCOS with the 1st degree relative affected by DM2 (FH+); BMI 26.7 (4.2) kg/m². Euglyceamic hyperinsulinaemic clamp (1mIU kg⁻¹.min⁻¹; with the determination of insulin sensitivity index (ISI)) and arginine secretion test to measure insulin (AIR) and glucagon (AGR) secretion after arginine bolus at fasting glycaemia (AIRf and AGRf) and at hyperglycaemia (AGRf and AGRg). Kruskal-Wallis ANOVA followed by Kruskal-Wallis multiple comparisons and Spearman correlations adjusted to a constant BMI were used for data evaluation.

Results: PCOS had higher basal insulin (P=0.004) and higher HOMA-R than C (P=0.002). Higher basal glucagon (P=0.005) and higher glucagon secretion at hyperglycemia (AGRg; P=0.05) in PCOS than in C was seen. PCOS FH+ had higher insulin secretion at fasting glycaemia (P=0.05) with no difference at hyperglycemia. Insulin sensitivity index (ISI, ISI _LBM) was lower in PCOS FH+ (P=0.002) than in C or PCOS FH-.Concerning beta cell function, disposition indices calculated from ISI and slope I or from AIRg were lower in PCOS FH+ than in PCOS FH- or C (P=0.05 for both). Basal glucagon correlated significantly with lean body mass (r=−0.322, P=0.03), basal insulin (r=0.308; P=0.05) and AGRg (r=0.31; P=0.04), with T (r=0.479; P=0.001), DHEAS (r=0.335; P=0.028) and with SHBG (r=−0.356; P=0.015). AGRg correlated with T (r=0.32; P=0.03), DHEAS (r=0.40; P=0.008), DHEA (r=0.36; P=0.02) and with SHBG (r=−0.28; P=0.06).

Conclusions: Higher basal glucagon levels are present in PCOS irrespective of obesity and family history of DM 2. Insulin resistance and beta cell secretory dysfunction are detectable only in PCOS with the family history of DM 2.

Supported by grant IGA MHCR 8759-3.