Abstract


Background: In contrast to hypogonadism from primary testicular failure, obesity-associated hypogonadism is due to the increased conversion of androgen precursors to estrogen in the large adipose tissue volume resulting in hyperestrogenemia. This leads to increased negative feedback inhibition of the hypothalamic-pituitary-gonadal axis resulting in reduced gonadotropin production and consequently low testosterone (T) production by the testis. view more

Background: In contrast to hypogonadism from primary testicular failure, obesity-associated hypogonadism is due to the increased conversion of androgen precursors to estrogen in the large adipose tissue volume resulting in hyperestrogenemia. This leads to increased negative feedback inhibition of the hypothalamic-pituitary-gonadal axis resulting in reduced gonadotropin production and consequently low testosterone (T) production by the testis. Given the difference in the underlying mechanism, it is possible that response to T therapy differs between obese and non-obese men with hypogonadism.
Objective:The objective of this study is to evaluate the response to T therapy among hypogonadal men according to body mass index (BMI).  
Methods and study design: Single arm open-label study, men 40 to 74 yo, with average morning T (2 measurements) <300 ng/dl, given testosterone cypionate 200 mg every 2 weeks IM. Areal bone mineral density (aBMD), body composition by dual energy x-ray absorptiometry (DXA); volumetric BMD (vBMD), leg fat/muscle composition by peripheral quantitative computed tomography (pQCT); T by automated immunoassay, estradiol (E2) by LC/MS; SHBG by ELISA. Hypogonadal symptoms assessed using a questionnaire designed for the study. Subjects were grouped into: 1: BMI <30kg/m2 (n:38), 2: BMI 30 to <35 kg/m2 (n:40), 3: BMI ≥35/kg2(n:27). Group comparison with the different outcomes as dependent variables and the BMI groups as independent variable was performed by ANOVA adjusted for age.
Results: Men (n:105) aged 59.6±8.4 yo, average T 210.4±63.3 ng/dl and BMI of 32.3±5.5 kg/m2 (21.8-48.6 kg/m2) were enrolled. Increase in T and free androgen index (FAI) at 12 mo were lower in group 3 (p 0.03 and 0.08, respectively) resulting in lower FAI levels in this group (p 0.05). E2 was borderline higher in group 3 vs the first 2 groups at 12 mo (p 0.07). E2/T remained higher in group 3 vs groups 1 and 2 at the end of 12 mo (p<0.01).
With T treatment, total and trunk fat significantly decreased from baseline at 6 and 12 mo with no significant difference between groups. Group 1 and 2 had greater changes in lean mass  at 6 and 12 mo  (for both p 0.02). At the 66% tibia, there was a decrease in intermuscular adipose tissue in group 3 vs first 2 groups (p<0.05) and a borderline decrease in muscle area (p 0.06). There were no significant changes in aBMD and vBMD across the BMI at 6 and 12 mo. Groups 1 and 2 had a borderline decrease in endosteal circumference (p 0.07) and increase in cortical thickness (p 0.06) compared to group 3.
Hypogonadal symptoms significantly improved at 6 and 12 mo in groups 1 and 2 while group 3 remained symptomatic (p<0.05).
Conclusion: Our results demonstrate that severely obese hypogonadal men do not benefit from T therapy as much as men with lower BMI. Thus, alternative treatment should be considered for these subjects and best using agents directed at the primary mechanism for obesity-associated hypogonadism.

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