Leptin in Postmenopausal Women: Influence of Hormone Therapy, Insulin, and Fat Distribution1
B. A. Gower,
T. R. Nagy,
M. I. Goran2,
A. Smith and
E. Kent
University of Alabama at Birmingham, Department of Nutrition
Sciences, Division of Physiology and Metabolism, and University of
Alabama at Birmingham Obesity Research Center, Birmingham, Alabama
35294-3360
Address correspondence and requests for reprints to: B. A. Gower, University of Alabama at Birmingham, Department of Nutrition Sciences, 441 Webb Building, 1675 University Boulevard, Birmingham, Alabama 35294-3360. E-mail: bgower{at}uab.edu
Whether use of hormone-replacement therapy (HRT) influences
menopause-relatedchanges in body weight is unclear. HRT may affect
energy balanceby influencing synthesis of the adipocyte-derived
hormone leptin.The objectives of this study were to: 1) identify
factors influencingcirculating leptin in postmenopausal women; 2)
determine whetherHRT influences serum leptin after adjusting for
confoundingfactors; and, 3) identify potential independent effects of
HRTor leptin on resting energy expenditure (REE). Subjects were54
postmenopausal women, 45–55 yr old, 35 of whom usedHRT (estrogen plus
progestin). Total and regional body compositionand fat distribution
were determined by dual-energy x-ray absorptiometryand computed
tomography; fasting serum leptin and insulin, byRIA; and REE, by
indirect calorimetry. Stepwise multiple linearregression analysis
indicated that serum leptin could best bepredicted from total fat
mass, fasting serum insulin, and totallean mass [log leptin =
1.08·log fat mass) + (0.46·loginsulin) + (-1.25·log lean mass)
+ 1.88; model R2 = 0.78,P
< 0.001]. Multiple linear regression analysis indicatedthat visceral
fat was independently related to leptin (parameterestimate =
0.23, P < 0.05), after adjusting for sc abdominal
fatand leg fat, as well as lean mass and insulin. After adjustingfor
total fat mass, total lean mass, and fasting insulin, serumleptin did
not differ between users and nonusers of HRT (21.7± 1.0
vs. 20.2 ± 1.3 ng/mL , P =
0.369, adjustedmean ± SE, respectively). Serum
estradiol was inverselycorrelated with (adjusted) leptin in non-HRT
users (r = -0.50),suggesting that ovarian
senescence may lead to an increase inleptin. Multiple linear
regression analysis indicated that REE(adjusted for fat mass, fat-free
mass, and ethnicity) was notassociated with leptin
(P = 0.298) or hormone use status
(P= 0.999; 1323 ± 31 vs.
1316 ± 42 kcal/day, adjustedmean ± SE for
users and nonusers, respectively). Theseresults indicate that, in
postmenopausal women: 1) total fatmass, lean mass, and fasting
insulin, but not HRT, are significantdeterminants of serum leptin; 2)
visceral and sc fat contributeto serum leptin; and, 3) neither HRT nor
leptin is independentlyrelated to REE.
This article has been cited by other articles:
M.-P. St-Onge, L. L. T. Goree, and B. Gower High-Milk Supplementation with Healthy Diet Counseling Does not Affect Weight Loss but Ameliorates Insulin Action Compared with Low-Milk Supplementation in Overweight Children
J. Nutr.,
May 1, 2009;
139(5):
933 - 938.
[Abstract][Full Text][PDF]
J. Munoz and B. A. Gower Relationship between Serum Leptin Concentration and Low-Density Muscle in Postmenopausal Women
J. Clin. Endocrinol. Metab.,
March 1, 2003;
88(3):
1157 - 1161.
[Abstract][Full Text][PDF]
X. Hu, S. C. Juneja, N. J. Maihle, and M. P. Cleary Leptin--A Growth Factor in Normal and Malignant Breast Cells and for Normal Mammary Gland Development
J Natl Cancer Inst,
November 20, 2002;
94(22):
1704 - 1711.
[Abstract][Full Text][PDF]
