Effect of sex hormone treatment on circulating adiponectin and subforms in Turner and Klinefelter syndrome.

BACKGROUND: Sex hormones have been shown to influence levels of adiponectin. Furthermore, testosterone has been shown to alter the subform distribution of adiponectin, whereas the effects of oestradiol are equivocal. We investigated the impact of sex hormone replacement therapy (HRT) on circulating adiponectin and its subforms, fasting lipids and measures of insulin sensitivity in Turner syndrome (TS) and Klinefelter syndrome (KS) respectively. MATERIALS AND METHODS: We compared eight young TS patients on and off 2 months of HRT vs. eight age- and body mass index (BMI) matched healthy females as well as 19 untreated KS patients vs. 20 testosterone treated KS patients vs. 20 age and BMI matched healthy males. Total adiponectin and adiponectin subforms separated by fast protein liquid chromatography were measured using an in-house assay. In addition, fasting levels of insulin, glucose and homeostasis model assessment estimates were determined. RESULTS: In TS, total adiponectin levels were 10.5 +/- 3.1 (mean +/- SD) vs. 12.8 +/- 3.5 mg L(-1) (P = 0.02) and high molecular weight (HMW) adiponectin 5.8 +/- 2.7 and 6.8 +/- 1.9 mg L(-1) (P = 0.02) on and off HRT respectively. Irrespective of HRT, total adiponectin and HMW adiponectin were similar to control values. In KS, total adiponectin levels were 6.5 (3.0-24.2) (median and range) and 9.3 (4.3-14.3) mg L(-1) (P = NS) and HMW adiponectin was 2.5 (0.5-16.0) and 4.6 (1.3-8.6) mg L(-1) (P = NS) with and without testosterone treatment respectively, and similar to controls. CONCLUSION: Short time HRT suppressed HMW and total adiponectin levels in TS patients. Testosterone treatment in KS patients had no effect on these parameters. In both groups of patients either adiponectin or the HMW subform seems to play no greater role in reflecting or mediating insulin sensitivity. Our data indicates that in patients with TS and KS, sex hormones have different effects on circulating adiponectin and its HMW subform than previously reported in other sex hormone deficient patients and healthy subjects.

The effects of altered exercise distribution on lymphocyte subpopulations.

The effects of exercise distribution on lymphocyte count, lymphocyte subpopulations and plasma cortisol concentration in peripheral blood were assessed in 19 healthy subjects. The subjects were randomly divided into group A (n = 10) or group B (n = 9) according to exercise distribution. Both groups underwent a 10-week programme involving 5 x 2-week blocks: baseline (B), training period 1 (TP1), stabilisation 1 (S1), training period 2 (TP2), and stabilisation 2 (S2). During B, S1 and S2 normal training was undertaken. During TP1 and TP2 the subjects increased the amount of training by 50% in week 1 and by 100% in week 2. During TP1 subjects in group A exercised 6 days.week-1, while during TP2 these subjects exercised on 3 alternate days.week-1, but doubled the duration of each training session. The subjects in group B reversed this training order. Blood was collected 36-42 h following exercise period B, and at the end of periods TP1, S1, TP2 and S2, and also 12-18 h following completion of exercise at the end of TP1 and TP2. There were no significant differences (P > 0.05) between the 6 day.week-1 programme and the 3 alternate day.week-1 programme in total lymphocyte count, CD3+, CD4+, CD8+, CD16+, or CD19+ cells, the CD4:CD8 ratio, HLA-DR+ (activated) T cells or plasma cortisol concentrations. Following both TP1 and TP2 there was a nonsignificant decrease in lymphocyte subpopulations. However following both S1 and S2 (baseline training) there was a significant increase in total lymphocyte count, CD3+, CD4+ and CD8+ lymphocytes. The S2 variables statistically significant from B were: total lymphocyte count (P < 0.01), CD3+ T-cells and percentage of circulating lymphocytes (P < 0.01), CD4+ cells (P < or = 0.0001), CD8+ cells (P < 0.05), and HLA-DR+ (activated) T-cells (P < 0.05). The results indicated that provided the amount of exercise is constant for a given period, then exercise distribution is not a critical variable in the alteration of lymphocyte subpopulations that may occur in response to overload training. However 2 weeks of overload training followed by 2 weeks of active recovery (baseline) training may induce an increase in the lymphocyte count.