| Titre : | Leptin concentrations in women in the San Antonio Heart Study : Effect of menopausal status and postmenopausal hormone replacement therapy. (1997) |
| Auteurs : | S.M. HAFFNER ; L. MYKKANEN ; M.P. STERN ; Department of Medicine. University of Texas Health Science Center at San Antonio. San Antonio TX. USA |
| Type de document : | Article |
| Dans : | American journal of epidemiology (vol. 146, n° 7, 1997) |
| Pagination : | 581-585 |
| Langues: | Anglais |
| Mots-clés : | Obésité ; Ménopause ; Hormone ; Epidémiologie ; Taux ; Plasma sanguin ; Femme ; Homme ; Etats Unis ; Amérique du Nord ; Amérique ; Maladie nutrition |
| Résumé : | [BDSP. Notice produite par INIST 82FR0xcp. Diffusion soumise à autorisation]. Leptin, the product of the human OB gene, is increased in obese individuals, suggesting resistance to its effect. However, there is variability in leptin levels at each level of body mass index, suggesting that genetic and environmental factors other than overall adiposity may regulate leptin concentrations. Leptin concentrations are higher in women relative to men, a difference that is only partially explained by the increased fat depots in women. The authors hypothesized that higher estrogen levels in women might be responsible for the sexual dimorphism in leptin concentrations. To test this hypothesis, they measured leptin concentrations in premenopausal women not on oral contraceptives (PRE) in=53), postmenopausal women on hormone replacement therapy (POSTY) (n=28), and postmenopausal women not on hormone replacement therapy (POSTN) (n=28) in the San Antonio Heart Study, a population-based study of diabetes and cardiovascular risk factors. Analyses were restricted to nondiabetic Mexican Americans. Subjects were well matched on obesity as assessed by body mass index (kg/m2 : PRE=31.0, POSTY=29.8, and POSTN=31.6. Leptin concentrations (ng/ml) were not significantly different among the three groups (PRE=27.6, POSTY=28.3, and POSTN=27.8). The authors conclude that differences in estrogen levels are not likely to explain the sexual dimorphism in leptin concentrations. |
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