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Weight loss results in a small decrease in follicle stimulating hormone in overweight glucose-intolerant postmenopausal women

OBJECTIVE: To examine the impact of a weight loss intervention upon follicle stimulating hormone (FSH) levels in postmenopause. DESIGN AND METHODS: Participants were postmenopausal, overweight, glucose-intolerant women not using exogenous estrogen (n=382) in the Diabetes Prevention Program. Women we...

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Detalles Bibliográficos
Autores principales: Kim, Catherine, Randolph, John F., Golden, Sherita H., Labrie, Fernand, Kong, Shengchun, Nan, Bin, Barrett-Connor, Elizabeth
Formato: Online Artículo Texto
Lenguaje:English
Publicado: 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4276440/
https://www.ncbi.nlm.nih.gov/pubmed/25294746
http://dx.doi.org/10.1002/oby.20917
Descripción
Sumario:OBJECTIVE: To examine the impact of a weight loss intervention upon follicle stimulating hormone (FSH) levels in postmenopause. DESIGN AND METHODS: Participants were postmenopausal, overweight, glucose-intolerant women not using exogenous estrogen (n=382) in the Diabetes Prevention Program. Women were randomized to intensive lifestyle change (ILS) with the goals of weight reduction of at least 7% of initial weight and 150 minutes per week of moderate intensity exercise, metformin 850 mg, or placebo administered twice a day. RESULTS: Randomization to ILS led to small increases in FSH between baseline and 1-year follow-up vs. placebo (2.3 IU/l vs. -0.81 IU/l, p<0.01). Increases in FSH were correlated with decreases in weight (r=-0.165, p<0.01) and E2 (r=-0.464, p<0.0001) after adjustment for age, race/ethnicity, and randomization arm. Changes in FSH were still significantly associated with changes in weight even after adjustment for E2 levels. Metformin users had reductions in weight but non-significant changes in FSH and E2 levels vs. placebo. CONCLUSIONS: Weight loss leads to small increases in FSH among overweight, postmenopausal women, potentially through pathways mediated by endogenous estrogen as well as other pathways.