Medicine (Austin & Northern Health) - Theses
Permanent URI for this collection
Search Results
1 - 1 of 1
-
ItemControl of musculoskeletal function and body composition by androgens in males( 2014)Context: Testosterone is the main male sex hormone and is important for normal male development and reproductive health. Testosterone also has actions on non-reproductive tissues including bone, fat and muscle, although the understanding of these actions is incomplete. The effects of testosterone withdrawal (in men about to commence androgen deprivation therapy (ADT) for prostate cancer) and testosterone replacement (in men about to commence testosterone replacement therapy (TRT) for classical androgen deficiency) on bone microarchitecture, bone mineral density (BMD), body composition, abdominal fat distribution, insulin resistance and metabolic profile were studied using rigorous, identical methodology. Objective and Patients: We prospectively investigated changes in bone microarchitecture in 26 men (70.6 ± 6.8 years) with non-metastatic prostate cancer during the first year of ADT and 10 men (52.0 ± 17.6 years) with classical androgen deficiency during the first year of TRT using the new technique high resolution peripheral quantitative computed tomography (HR-pQCT). BMD and body composition were studied using dual energy x-ray absorptiometry and subcutaneous and visceral abdominal fat were quantitated from abdominal computed tomography images using Slice-O-Matic software. Results: After 12 months ADT, total volumetric bone density decreased by 5.2 ± 5.4% at the distal radius and 4.2 ± 2.7% at the distal tibia (both p <0.001). This was due to a decrease in cortical volumetric BMD (by 11.3 ± 8.6% radius and 6.0 ± 4.2% tibia, all p<0.001) and trabecular density (by 3.5 ± 6.0% radius and 1.5 ± 2.3% tibia, all p<0.01), after correcting for trabecularisation of cortical bone. Trabecular density decreased due to a decrease in trabecular number at both sites (p<0.05). Total testosterone (TT), not estradiol (E2), was independently associated with total and corrected cortical volumetric BMD at the tibia. 12 months ADT increased visceral abdominal fat area from 160.81 ± 61.68 to 195.94 ± 69.71 cm2 (p<0.01) and subcutaneous abdominal fat area from 240.74 ± 107.54 to 271.27 ± 92.83 cm2 (p<0.01). Fat mass increased by 3.4 kg (24100 ± 9240 to 27500 ± 8702g; p<0.001) and lean body mass decreased by 1.9 kg (52500 ± 7105 to 50600 ± 7150g; p<0.001). Insulin resistance (HOMA-IR) increased after 12 months of ADT (2.50 ± 1.12 to 2.79 ± 1.31, p<0.05) but there was no change in fasting glucose or glycated haemoglobin levels. TT was inversely associated with visceral fat area independently of E2, but not vice versa. Visceral fat area, not TT or E2, was independently associated with insulin resistance. After 12 months of TRT, trabecular density increased at the radius, but there were no other significant changes in bone microarchitecture, abdominal fat distribution, body composition or insulin resistance Conclusions: Sex steroid deficiency induced by ADT for prostate cancer results in bone microarchitectural decay and accumulation of visceral and subcutaneous abdominal fat. Increased insulin resistance may arise secondary to visceral fat accumulation, rather than directly due to sex steroid deficiency. TRT in men with classical androgen deficiency results in improved trabecular bone density; other conclusions regarding the effects of TRT are limited by small numbers of study subjects.