Endocrine Abstracts

In population studies, premature cardiovascular disease is associated with cortisol dysregulation. Recently, recurrent hypoglycaemia in individuals with type 1 diabetes (T1D) was reported to be associated with increase carotid intima–media thickness. Hypoglycaemia is a potent activator of the hypothalamo-pituitary–adrenal axis (HPA axis) with eventual release of cortisol. We hypothesized that individuals with T1D who experience recurrent hypoglycaemia might demonstrate abnormal cortisol diurnal rhythms.

Data are presented on 100 subjects (N=74 T1D, N=26 non-diabetic, with each group matched for BMI, age, and sex) who participated in an on-going study examining the association between increased blood glucose variability and 24 h cortisol profiles as assessed by salivary cortisol. Each subject underwent a period of 6–7 days continuous glucose monitoring to assess glucose variability and in addition provided seven spit samples spaced through the day, to measure the free unbound cortisol.

T1D with high exposure to hypoglycaemia (low blood glucose Index (LBGI) >5) showed a non-significant trend to a greater cortisol AUC compared to control subjects (median AUC of control vs high LBGI was 9054 vs 10 350 with P=0.0871). There is also a non-significant reduction (1.2 vs 1.5 with P=0.38) in the slope of the cortisol decline, in those with high exposure to hypoglycaemia compared to controls. The AUC (g) measure was used to look at the morning cortisol rise. Those with high exposure to hypoglycaemia, also had a non-significant trend in lower AUC(g) as compared to the control group (47 vs 57 with P=0.39).

This study is still recruiting, however, these preliminary results suggest that increased glucose variability with a greater exposure to hypoglycaemia in T1D is associated with cortisol dysregulation which may in turn increase propensity to other conditions associated with hypercortisolaemia such as insulin resistance, cardiovascular morbidity, and psychological disturbances.