Insulin resistance from fat rather than lack of T

[JimmyToowong]

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

Tuesday, 11 January 2011

Dept. of Medicine, Austin Health/Northern Health, University of Melbourne, Heidelberg, VIC 3084.

Dept. of Medicine, and Nutrition and Dietetics, Monash University, Clayton, VIC 3168; Walter and Eliza Hall Institute of Medical Research, Parkville, VIC 3052; Radiation Oncology Centre, Austin Health, Heidelberg, VIC 3084; Dept. of Surgery, Austin Health/Northern Health, University of Melbourne, Heidelberg, VIC 3084.

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.

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

We investigated changes in abdominal fat distribution and insulin resistance in 26 men (70.6 ± 6.8 years) with non-metastatic prostate cancer during the first year of ADT.

Twelve months ADT increased visceral abdominal fat area by 22% (from 160.8 ± 61.7 to 195.9 ± 69.7 cm(2) ; p< 0.01) and subcutaneous abdominal fat area by 13% (from 240.7 ± 107.5 to 271.3 ± 92.8 cm(2) ; 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 estradiol (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.

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 estradiol deficiency. Increased insulin resistance may arise secondary to visceral fat accumulation, rather than as a direct result of sex steroid deficiency.

Written by:

Hamilton EJ, Gianatti E, Strauss BJ, Wentworth J, Lim-Joon D, Bolton D, Zajac JD, Grossmann M.

Reference: Clin Endocrinol (Oxf). 2010 Nov 30. Epub ahead of print.

PubMed Abstract

PMID: 21118287 Forum: Primary hormone therapy Title: Insulin resistance from fat rather than lack of T

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