Body composition is distinctly altered in Turner syndrome: relations to glucose metabolism, circulating adipokines, and endothelial adhesion molecules.
BACKGROUND
Body composition in Turner syndrome (TS) is altered with final height of TS decreased; anthropometry and bone mass distinctly changed.


OBJECTIVE
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.


METHODS
Fifty-four women with TS (mean age, 42.5 +/- 9.7 years) and an age-matched group of controls (n = 55) 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. VO2max 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.


CONCLUSIONS
Profound changes are present in body composition in TS, with increased FM, and decreased skeletal muscle mass. Circulating hormones, VO2max, and insulin sensitivity influence body composition. The accumulation of visceral fat would predict a higher risk of development of the insulin resistance syndrome.
Gravholt
Claus Højbjerg
CH
Medical Research Laboratories, Medical department M (Endocrinology and Diabetes), Aarhus Sygehus NBG, Denmark. ch.gravholt@dadlnet.dk
Hjerrild
Britta Eilersen
BE
Mosekilde
Leif
L
Hansen
Troels Krarup
TK
Rasmussen
Lars Melholt
LM
Frystyk
Jan
J
Flyvbjerg
Allan
A
Christiansen
Jens Sandahl
JS
D017667:Adipocytes / Q000378:metabolism; D000328:Adult; D000368:Aged; D000886:Anthropometry; D015415:Biomarkers / Q000097:blood; D001786:Blood Glucose / Q000032:analysis; D001823:Body Composition; D050260:Carbohydrate Metabolism; D015815:Cell Adhesion Molecules / Q000097:blood* / Q000378:metabolism; D016207:Cytokines / Q000097:blood* / Q000378:metabolism; D042783:Endothelial Cells / Q000378:metabolism; D005260:Female; D005947:Glucose / Q000378:metabolism*; D012739:Gonadal Steroid Hormones / Q000097:blood; D006706:Homeostasis; D006801:Humans; D007333:Insulin Resistance; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood; D007621:Karyotyping; D008875:Middle Aged; D009043:Motor Activity; D013002:Somatomedins / Q000032:analysis; D014424:Turner Syndrome / Q000097:blood* / Q000150:complications*; D019010:Vascular Cell Adhesion Molecule-1 / Q000097:blood
D015415:Biomarkers; D001786:Blood Glucose; D015815:Cell Adhesion Molecules; D016207:Cytokines; D012739:Gonadal Steroid Hormones; D013002:Somatomedins; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1; D005947:Glucose