Body composition is distinctly altered in Turner syndrome: relations to glucose metabolism, circulating adipokines, and endothelial adhesion molecules

Abstract

Background: Body composition in Turner syndrome (TS) is altered with final height of TS decreased; anthropometry and bone mass distinctly changed. Aim: To describe total and regional distribution of fat and muscle mass in TS and the relation to measures of glucose metabolism, sex hormones, IGFs, and markers of inflammation and vascular function. Material and methods: Fifty-four women with TS (mean age, 42.5G9.7 years) and an age-matched group of controls (nZ55) were examined by dual-energy X-ray absorptiometry scans with determination of regional body composition and estimation of visceral fat and skeletal muscle mass. We determined maximal oxygen uptake and assessed physical activity using a questionnaire. We measured serum adiponectin, ghrelin, IGF-I, IGF-binding protein-3 (IGFBP-3), estradiol, testosterone, sex hormone-binding globulin (SHBG), insulin, glucose, cytokines, vascular cell adhesion molecule-I, and intercellular cell adhesion molecule-I. Insulin sensitivity was estimated. Multiple linear regression models were used to examine the relationships between variables. Results: TS had lower total lean body mass (LBM), while body mass index (BMI) and total fat mass (FM) were increased. We found increased visceral FM, and decreased trunk LBM, appendicular LBM, and skeletal muscle mass. VO 2max and physical activity were significantly lower in TS, as were most hormone levels, except increased leptin. In multiple linear regression models, status (i.e. TS or control) was a consistent contributing variable. Conclusion: Profound changes are present in body composition in TS, with increased FM, and decreased skeletal muscle mass. Circulating hormones, VO 2max , and insulin sensitivity influence body composition. The accumulation of visceral fat would predict a higher risk of development of the insulin resistance syndrome.

Long-term hormone replacement therapy preserves bone mineral density in Turner syndrome

“…We also observed a tight coupling between changes in markers of bone formation and resorption, contrary to what we observed in the initial baseline study from the present cohort (4), where we found bone formation markers to be comparable or only marginally elevated in comparison with controls, while bone resorption markers were 35-70% elevated (4). In the present population, it is difficult to determine whether inadequate sex HRT or the relative secondary hyperparathyroidism is the cause of the enhanced resorption, or if it is a consequence of other metabolic changes, such as low serum testosterone (18,37) and low bioavailable IGF1 (38,39), or the genetic defect per se. The observed positive correlation between plasma PTH and total OC and renal NTX/creatinine corroborates a biological effect of PTH on bone in Turner patients.…”

“…Regardless of BMD, end-point studies have documented increased fracture frequency in girls and women with TS (11)(12)(13). It is not entirely clear whether a primary bone defect exists in TS (4,14), perhaps due to skeletal dysmorphogenesis (15) caused by haploinsufficiency of the short stature homeoboxcontaining gene (SHOX) (16,17) or rather endocrine or metabolic defects exists (18), resulting in estrogen deficiency and other endocrine deficiencies (4).…”

A specific bioelectrical impedance equation to predict body composition in Turner's syndrome

“…nography (18), DXA (19,20), BIA (21,22) and magnetic resonance imaging (23). If, on the one hand they produce high-quality information on the other some of these instruments are relatively expensive and have little mobility (24).…”

Endocrine diseases, perspectives and care in Turner syndrome

“…However, proinflamatory cytokines, interleukin-6, interleukin-8 and tumor necrosis factor α may be partly responsible for that (29,30). Su and cols.…”