Night eating and obesity in the EP3R-deficient mouse

Manuel Sanchez-Alavez, Izabella Klein, Sara Brownell, Iustin V. Tabarean, Christopher N. Davis, Bruno Conti, Tamas Bartfai

Research output: Contribution to journalArticle

42 Citations (Scopus)

Abstract

Adult mice carrying a null mutation of the prostanoid receptor EP3R (EP3R-/- mice) exhibit increased frequency of feeding during the light cycle of the day and develop an obese phenotype under a normal fat diet fed ad libitum. EP3R-/- mice show increased motor activity, which is not sufficient to offset the increased feeding leading to increased body weight. Altered "nocturnal" activity and feeding behavior is present from a very early age and does not seem to require age-dependent factors for the development of obesity. Obesity in EP3R-/- mice is characterized by elevated leptin and insulin levels and >20% higher body weight compared with WT littermates. Abdominal and subcutaneous fat and increased liver weight account for the weight increase in EP3R-/- mice. These observations expand the roles of prostaglandin E2 signaling in metabolic regulation beyond the reported stimulation of leptin release from adipose tissue to involve actions mediated by EP3R in the regulation of sleep architecture and feeding behavior. The findings add to the growing literature on links between inflammatory signaling and obesity.

Original languageEnglish (US)
Pages (from-to)3009-3014
Number of pages6
JournalProceedings of the National Academy of Sciences of the United States of America
Volume104
Issue number8
DOIs
StatePublished - Feb 20 2007
Externally publishedYes

Fingerprint

Obesity
Eating
Feeding Behavior
Leptin
Body Weight
Abdominal Subcutaneous Fat
Weights and Measures
Age Factors
Photoperiod
Dinoprostone
Prostaglandins
Adipose Tissue
Sleep
Motor Activity
Fats
Insulin
Diet
Phenotype
Mutation
Liver

Keywords

  • Body weight
  • Insulin
  • Leptin
  • Prostanoid receptor
  • Signaling

ASJC Scopus subject areas

  • Genetics
  • General

Cite this

Night eating and obesity in the EP3R-deficient mouse. / Sanchez-Alavez, Manuel; Klein, Izabella; Brownell, Sara; Tabarean, Iustin V.; Davis, Christopher N.; Conti, Bruno; Bartfai, Tamas.

In: Proceedings of the National Academy of Sciences of the United States of America, Vol. 104, No. 8, 20.02.2007, p. 3009-3014.

Research output: Contribution to journalArticle

Sanchez-Alavez, Manuel ; Klein, Izabella ; Brownell, Sara ; Tabarean, Iustin V. ; Davis, Christopher N. ; Conti, Bruno ; Bartfai, Tamas. / Night eating and obesity in the EP3R-deficient mouse. In: Proceedings of the National Academy of Sciences of the United States of America. 2007 ; Vol. 104, No. 8. pp. 3009-3014.
@article{0f47b02e6ff6442a879b35ae622752e4,
title = "Night eating and obesity in the EP3R-deficient mouse",
abstract = "Adult mice carrying a null mutation of the prostanoid receptor EP3R (EP3R-/- mice) exhibit increased frequency of feeding during the light cycle of the day and develop an obese phenotype under a normal fat diet fed ad libitum. EP3R-/- mice show increased motor activity, which is not sufficient to offset the increased feeding leading to increased body weight. Altered {"}nocturnal{"} activity and feeding behavior is present from a very early age and does not seem to require age-dependent factors for the development of obesity. Obesity in EP3R-/- mice is characterized by elevated leptin and insulin levels and >20{\%} higher body weight compared with WT littermates. Abdominal and subcutaneous fat and increased liver weight account for the weight increase in EP3R-/- mice. These observations expand the roles of prostaglandin E2 signaling in metabolic regulation beyond the reported stimulation of leptin release from adipose tissue to involve actions mediated by EP3R in the regulation of sleep architecture and feeding behavior. The findings add to the growing literature on links between inflammatory signaling and obesity.",
keywords = "Body weight, Insulin, Leptin, Prostanoid receptor, Signaling",
author = "Manuel Sanchez-Alavez and Izabella Klein and Sara Brownell and Tabarean, {Iustin V.} and Davis, {Christopher N.} and Bruno Conti and Tamas Bartfai",
year = "2007",
month = "2",
day = "20",
doi = "10.1073/pnas.0611209104",
language = "English (US)",
volume = "104",
pages = "3009--3014",
journal = "Proceedings of the National Academy of Sciences of the United States of America",
issn = "0027-8424",
number = "8",

}

TY - JOUR

T1 - Night eating and obesity in the EP3R-deficient mouse

AU - Sanchez-Alavez, Manuel

AU - Klein, Izabella

AU - Brownell, Sara

AU - Tabarean, Iustin V.

AU - Davis, Christopher N.

AU - Conti, Bruno

AU - Bartfai, Tamas

PY - 2007/2/20

Y1 - 2007/2/20

N2 - Adult mice carrying a null mutation of the prostanoid receptor EP3R (EP3R-/- mice) exhibit increased frequency of feeding during the light cycle of the day and develop an obese phenotype under a normal fat diet fed ad libitum. EP3R-/- mice show increased motor activity, which is not sufficient to offset the increased feeding leading to increased body weight. Altered "nocturnal" activity and feeding behavior is present from a very early age and does not seem to require age-dependent factors for the development of obesity. Obesity in EP3R-/- mice is characterized by elevated leptin and insulin levels and >20% higher body weight compared with WT littermates. Abdominal and subcutaneous fat and increased liver weight account for the weight increase in EP3R-/- mice. These observations expand the roles of prostaglandin E2 signaling in metabolic regulation beyond the reported stimulation of leptin release from adipose tissue to involve actions mediated by EP3R in the regulation of sleep architecture and feeding behavior. The findings add to the growing literature on links between inflammatory signaling and obesity.

AB - Adult mice carrying a null mutation of the prostanoid receptor EP3R (EP3R-/- mice) exhibit increased frequency of feeding during the light cycle of the day and develop an obese phenotype under a normal fat diet fed ad libitum. EP3R-/- mice show increased motor activity, which is not sufficient to offset the increased feeding leading to increased body weight. Altered "nocturnal" activity and feeding behavior is present from a very early age and does not seem to require age-dependent factors for the development of obesity. Obesity in EP3R-/- mice is characterized by elevated leptin and insulin levels and >20% higher body weight compared with WT littermates. Abdominal and subcutaneous fat and increased liver weight account for the weight increase in EP3R-/- mice. These observations expand the roles of prostaglandin E2 signaling in metabolic regulation beyond the reported stimulation of leptin release from adipose tissue to involve actions mediated by EP3R in the regulation of sleep architecture and feeding behavior. The findings add to the growing literature on links between inflammatory signaling and obesity.

KW - Body weight

KW - Insulin

KW - Leptin

KW - Prostanoid receptor

KW - Signaling

UR - http://www.scopus.com/inward/record.url?scp=33847292902&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=33847292902&partnerID=8YFLogxK

U2 - 10.1073/pnas.0611209104

DO - 10.1073/pnas.0611209104

M3 - Article

VL - 104

SP - 3009

EP - 3014

JO - Proceedings of the National Academy of Sciences of the United States of America

JF - Proceedings of the National Academy of Sciences of the United States of America

SN - 0027-8424

IS - 8

ER -