Women with Turner Syndrome (TS) have an increased risk of diabetes mellitus (DM), both types 1 and 2, and obesity is a common problem. This study aimed to characterise the relationship between markers of obesity and metabolic factors which might predispose to DM.
Anthropometric and fasting metabolic assessments were performed in 56 non-diabetic women with TS and 24 control women (mean±SD age 31.6±7.2 vs 35.6±7.1 years, p=0.051, and height 1.48±0.06 vs 1.60±0.06 metres, p<0.001, for TS and controls respectively). All measurements were taken during the oestrogen-only phase of cyclical oestrogen replacement therapy or in the follicular phase of menstruating women.
The women with TS were more obese in terms of BMI and waist-hip ratio (26.6±5.7 vs 23.8±3.1 kg/m2,p=0.041, and 0.83±0.05 vs 0.77±0.05,p<0.001 respectively). Glucose concentrations were slightly lower in the TS women (4.7±0.5 vs 4.9±0.3 mmol/l,p=0.020), but insulin concentrations were also lower (5.0±2.9 vs 7.4±4.4 mU/l,p=0.007).
With regard to markers of insulin resistance, triglyceride concentrations were higher in the TS women (1.1±0.8 vs 0.8±0.3mmol/l,p=0.002), but there was no difference in HDL concentrations (1.9±0.6 vs 1.9±0.2mmol/l,p=0.769). Blood pressure was higher in women with TS (diastolic 77±11 vs 68±6mmHg,p=0.001, and systolic 122±14 vs 112±8mmHg,p=0.003).
With regard to markers of adipocyte function, CRP was higher in women with TS (3.3±1.6 vs 0.6±0.6mg/l,p<0.001), but leptin did not differ between the two groups (14.2±15.5 vs 15.5±10.1ng/ml,p=0.109).
Some features of the metabolic syndrome are evident in women with TS, such as increased BMI, waist-hip ratio, triglycerides, blood pressure and CRP, but not others, such as hyperinsulinaemia, glucose intolerance, low HDL and hyperleptinaemia. The raised CRP and HDL concentrations could be related to oral oestrogen replacement.
In conclusion, insulin resistance does not appear to be the predominant cause of diabetes in women with TS, suggesting that they may have a unique metabolic defect.
22 - 24 Mar 2004
British Endocrine Societies