Apolipoprotein E reduces food intake via PI3K/Akt signaling pathway in the hypothalamus

Ling Shen, David Q.H. Wang, Patrick Tso, Ronald J. Jandacek, Stephen C. Woods, Min Liu

Research output: Contribution to journalArticlepeer-review

20 Scopus citations


Apolipoprotein E (apoE) is a satiation factor. While central apoE administration reduces food intake, the specific intracellular signaling mechanisms activated by apoE remain largely unknown. Using primary cultured hypothalamic neurons, we demonstrated that apoE treatment (50 nM) elicited rapid activation of the phosphatidylinositol-3-kinase (PI3K)/Akt signaling cascade. Specifically, apoE induced the phosphorylation of Akt, peaking at 30 min, and the increased phosphorylation of Akt was significantly attenuated after pretreatment with LY294002 (50. μM), an inhibitor of the PI3K signaling pathway. To determine whether the activation of PI3K by apoE is required for the ability of apoE to reduce food intake, LY294002 (1 nmol) was infused into the 3rd-cerebral ventricle before injection of an anorectic dose of apoE. Consistent with our previous report, apoE (4. μg) exerted significant reduction of food intake in the 4-h fasted rats, compared with saline. Pretreatment with LY294002 significantly attenuated the potency of exogenous apoE to induce satiation, while the same dose of PI3K inhibitor by itself caused only a slight non-significant decrease of food intake. These results indicate that the activation of the PI3K/Akt pathway is necessary for the acute effects of apoE on food intake.

Original languageEnglish (US)
Pages (from-to)124-128
Number of pages5
JournalPhysiology and Behavior
Issue number1
StatePublished - Nov 30 2011
Externally publishedYes


  • Apolipoprotein
  • Body weight
  • Food intake
  • Signaling pathway

ASJC Scopus subject areas

  • Experimental and Cognitive Psychology
  • Behavioral Neuroscience


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