Increase in visceral and subcutaneous abdominal fat in men with prostate cancer treated with androgen deprivation therapy

Authors


M. Grossmann, Department of Medicine Austin Health/Northern Health, University of Melbourne, Studley Road, Heidelberg, Vic. 3084, Australia. Tel.: +61 3 9496 5135; Fax: +61 3 9457 5485; E-mail: mathisg@unimelb.edu.au

Summary

Objective  Androgen deprivation therapy (ADT) for prostate cancer is associated with increases in fat mass and risk of type 2 diabetes; however, the relationship between sex steroid deficiency and abdominal fat distribution remains controversial.

Design  We conducted a 12-month prospective observational study at a tertiary referral centre.

Patients and measurements  We investigated changes in abdominal fat distribution and insulin resistance in 26 men (70·6 ± 6·8 years) with nonmetastatic prostate cancer during the first year of ADT.

Results  Twelve months of ADT increased visceral abdominal fat area by 22% (from 160·8 ± 61·7 to 195·9 ± 69·7 cm2; P < 0·01) and subcutaneous abdominal fat area by 13% (from 240·7 ± 107·5 to 271·3 ± 92·8 cm2; P < 0·01). Fat mass increased by 14% (+3·4 kg; P < 0·001) and lean tissue mass decreased by 3·6% (−1·9 kg; P < 0·001). Insulin resistance (HOMA-IR) increased by 12% (2·50 ± 1·12 to 2·79 ± 1·31, P < 0·05). There was no change in fasting glucose or glycated haemoglobin levels. Total testosterone (TT) was inversely associated with visceral fat area independent of oestradiol (E2), but E2 was not associated with visceral fat area independent of TT. Visceral fat area, not TT or E2, was independently associated with insulin resistance.

Conclusions  ADT for prostate cancer results in accumulation of both visceral and subcutaneous abdominal fat. Increased visceral fat area appears more closely linked to testosterone than oestradiol deficiency. Increased insulin resistance may arise secondary to visceral fat accumulation, rather than as a direct result of sex steroid deficiency.

Ancillary