Middle-aged female rats retain sensitivity to the anorexigenic effect of exogenous estradiol

Jessica Santollo, Dachun Yao, Genevieve Neal-Perry, Anne M. Etgen

Research output: Contribution to journalArticlepeer-review

23 Scopus citations


It is well established that estradiol (E2) decreases food intake and body weight in young female rats. However, it is not clear if female rats retain responsiveness to the anorexigenic effect of E2 during middle age. Because middle-aged females exhibit reduced responsiveness to E2, manifesting as a delayed and attenuated luteinizing hormone surge, it is plausible that middle-aged rats are less responsive to the anorexigenic effect of E2. To test this we monitored food intake in ovariohysterectomized young and middle-aged rats following E2 treatment. E2 decreased food intake and body weight to a similar degree in both young and middle-aged rats. Next, we investigated whether genes that mediate the estrogenic inhibition of food intake are similarly responsive to E2 by measuring gene expression of the anorexigenic genes corticotropin-releasing hormone (CRH), proopiomelanocortin (POMC), the long form of the leptin receptor (Lepr) and serotonin 2C receptors (5HT2CR) and the orexigenic genes agouti-related peptide (AgRP), neuropeptide Y (NPY), prepromelanin-concentrating hormone (pMCH) and orexin in the hypothalamus of young and middle-aged OVX rats treated with E2. As expected, E2 increased expression of all anorexigenic genes while decreasing expression of all orexigenic genes in young rats. Although CRH, 5HT2CR, Lepr, AgRP, NPY and orexin were also sensitive to E2 treatment in middle-aged rats, POMC and pMCH expression were not influenced by E2 in middle-aged rats. These data demonstrate that young and middle-aged rats are similarly sensitive to the anorexigenic effect of E2 and that most, but not all feeding-related genes retain sensitivity to E2.

Original languageEnglish
Pages (from-to)159-164
Number of pages6
JournalBehavioural Brain Research
Issue number1
StatePublished - Jun 15 2012

Bibliographical note

Funding Information:
This work was supported by the Eunice Kennedy Shriver National Institute of Child Health and Human Development/National Institutes of Health through cooperative agreement U54 HD058155 as part of the Specialized Cooperative Centers Program in Reproduction and Infertility Research and by NIH grants P60 DK020541 and T32 AG023475 and the Department of Obstetrics and Gynecology and Women's Health, Albert Einstein College of Medicine .


  • Aging
  • Estradiol
  • Estrogen receptor alpha
  • Food intake

ASJC Scopus subject areas

  • Behavioral Neuroscience


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