Estradiol increases the anorectic effect of central apolipoprotein A-IV

Ling Shen, David Q.H. Wang, Chun Min Lo, Patrick Tso, W. Sean Davidson, Stephen C. Woods, Min Liu

Research output: Contribution to journalArticlepeer-review

25 Scopus citations


Estrogens have potent suppressive effects on food intake and body weight in many species, including humans. Compelling evidence suggests estrogen's anorectic action is through an indirect mechanism by enhancing the strength of other physiological signals that reduce meal size such as apolipoprotein A-IV (apo A-IV), a satiation factor from the gut and brain. We determined whether estradiol, the primary form of estrogen, modulates the anorectic effect of apo A-IV. Intrafourth ventricular administration of low doses of apo A-IV reduced food intake to a greater extent in ovariectomized (OVX) rats cyclically treated with estradiol than in vehicle-treated OVX controls, implying that cyclic estradiol replacement increases the satiating potency of apo A-IV. OVX significantly increased food intake and body weight but decreased apo A-IV gene expression in the nucleus tractus solitarius (NTS). All of these alterations were reversed by cyclic regimen of estradiol treatment. The finding of colocalization of apo A-IV with estrogen receptor-α in the NTS suggests that estradiol might act locally in the NTS to upregulateapoA-IV gene expression. Finally, OVXapoA-IV knockout mice had a smaller feeding response to estradiol because they ate significantly more food and gained more body weight than OVX wild-type controls during the period of cyclic estradiol replacement. These data indicate that an increased signaling of endogenous apo A-IV may partially mediate estradiol-induced inhibitory effect on feeding.

Original languageEnglish (US)
Pages (from-to)3163-3168
Number of pages6
Issue number7
StatePublished - Jul 2010
Externally publishedYes

ASJC Scopus subject areas

  • Endocrinology


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