Increase in visceral and subcutaneous abdominal fat in men with prostate cancer treated with androgen deprivation therapy
Details
Publication Year 2011-03,Volume 74,Issue #3,Page 377-383
Journal Title
CLINICAL ENDOCRINOLOGY
Publication Type
Journal Article
Abstract
P>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 center dot 6 +/- 6 center dot 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 center dot 8 +/- 61 center dot 7 to 195 center dot 9 +/- 69 center dot 7 cm2; P < 0 center dot 01) and subcutaneous abdominal fat area by 13% (from 240 center dot 7 +/- 107 center dot 5 to 271 center dot 3 +/- 92 center dot 8 cm2; P < 0 center dot 01). Fat mass increased by 14% (+3 center dot 4 kg; P < 0 center dot 001) and lean tissue mass decreased by 3 center dot 6% (-1 center dot 9 kg; P < 0 center dot 001). Insulin resistance (HOMA-IR) increased by 12% (2 center dot 50 +/- 1 center dot 12 to 2 center dot 79 +/- 1 center dot 31, P < 0 center dot 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.
Publisher
WILEY-BLACKWELL
Keywords
TESTOSTERONE REPLACEMENT THERAPY; INSULIN-RESISTANCE; ADIPOSE-TISSUE; METABOLIC SYNDROME; BODY-COMPOSITION; ADIPONECTIN LEVELS; OBESITY; HYPOGONADISM; SENSITIVITY; ADIPOCYTOKINES
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Creation Date: 2011-03-01 12:00:00
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