Effect of Testosterone and Estradiol on Insulin Sensitivity in Healthy Older Men

Program: Abstracts - Orals, Featured Poster Presentations, and Posters
Session: SUN 780-806-Determinants of Insulin Resistance & Associated Metabolic Disturbances
Basic/Translational
Sunday, June 16, 2013: 1:45 PM-3:45 PM
Expo Halls ABC (Moscone Center)

Poster Board SUN-799
Cathy C. Lee*1, Li-Jung Liang2, Christian K. Roberts3, M. Albert Thomas3, Justin Cheng4, Stacey Barnett4 and Theodore J Hahn1
1VA Greater Los Angeles GRECC/UCLA, Los Angeles, CA, 2David Geffen School of Medicine at UCLA, Los Angeles, CA, 3University of California, Los Angeles, Los Angeles, CA, 4University of California, Los Angeles
Aging is associated with physiologic changes, such as increased central adiposity and the development of insulin resistance, which significantly increase the risk of diabetes.   In older men, a unifying factor in these changes is an age-associated decrease in testosterone levels with evidence to support that low testosterone levels are independently associated with increased insulin resistance and increased risk of diabetes.  The primary objective of this study was to determine the contribution of testosterone (T) and estrogen (E) on insulin resistance in older men.

Thirty healthy older men age 66 ± 6 years underwent chemical androgen ablation followed by T and/or E replacement. After baseline studies for measurement of serum hormone, glucose and insulin levels, participants were randomized into one of four groups:  1) continuation of T and E, 2) continuation of T only 3) continuation of E only or 4) discontinuation of both T and E.  Repeat studies were performed 6 weeks after randomization.  Changes in basal insulin levels were analyzed using an ANCOVA model that adjusted for baseline insulin and age.  Preliminary data from this prospective study is being presented.

The major outcome variable being presented is changes in basal insulin levels.  There was a significant difference (p=0.023) observed in change from pre- to post-intervention basal insulin levels between the groups receiving E only (estimated post-pre = -1.55, SE=1.34) versus the group receiving no hormone replacement (estimated post-pre = 3.45, SE=1.47). There was also a significant difference (p=0.042) in the change in basal insulin levels between the groups receiving E replacement with or without T replacement (estimated post-pre for with and without T: 2.58 vs. -1.55, respectively).  

This unexpected finding suggests that estrogen may have independent effects on insulin sensitivity.  If estrogen indeed has an independent regulatory role in this regard, this would suggest that aromatase transformation of testosterone to estrogen in men could be important in the effects of testosterone on insulin sensitivity.  In addition, this would be consistent with the important role already demonstrated for estrogen on bone metabolism and with the metabolic effects observed in aromatase deficient males. 

 

Nothing to Disclose: CCL, LJL, CKR, MAT, JC, SB, TJH

*Please take note of The Endocrine Society's News Embargo Policy at http://www.endo-society.org/endo2013/media.cfm

Sources of Research Support: VA Advanced Research Career Development Award; UCLA GCRC NIH/NCRR M01-RR00865; UCLA Hartford Center of Excellence; UCLA CTSI NCRR/NCATS UL1TR000124