PMID- 24039946
OWN - NLM
STAT- MEDLINE
DCOM- 20140607
LR  - 20211021
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 8
IP  - 9
DP  - 2013
TI  - Improved leptin sensitivity as a potential candidate responsible for the 
      spontaneous food restriction of the Lou/C rat.
PG  - e73452
LID - 10.1371/journal.pone.0073452 [doi]
LID - e73452
AB  - The Lou/C rat, an inbred strain of Wistar origin, was described as a model of 
      resistance to age- and diet-induced obesity. Although such a resistance involves 
      many metabolic parameters described in our previous studies, Lou/C rats also 
      exhibit a spontaneous food restriction due to decreased food consumption during 
      the nocturnal period. We then attempted to delineate the leptin sensitivity and 
      mechanisms implicated in this strain, using different protocols of acute central 
      and peripheral leptin administration. A first analysis of the meal patterns 
      revealed that Lou/C rats eat smaller meals, without any change in meal number 
      compared to age-matched Wistar animals. Although the expression of the recognized 
      leptin transporters (leptin receptors and megalin) measured in the choroid plexus 
      was normal in Lou/C rats, the decreased triglyceridemia observed in these animals 
      is compatible with an increased leptin transport across the blood brain barrier. 
      Improved hypothalamic leptin signaling in Lou/C rats was also suggested by the 
      higher pSTAT3/STAT3 (signal transducer and activator of transcription 3) ratio 
      observed following acute peripheral leptin administration, as well as by the 
      lower hypothalamic mRNA expression of the suppressor of cytokine signaling 3 
      (SOCS3), known to downregulate leptin signaling. To conclude, spontaneous 
      hypophagia of Lou/C rats appears to be related to improved leptin sensitivity. 
      The main mechanism underlying such a phenomenon consists in improved leptin 
      signaling through the Ob-Rb leptin receptor isoform, which seems to consequently 
      lead to overexpression of brain-derived neurotrophic factor (BDNF) and 
      thyrotropin-releasing hormone (TRH).
FAU - Veyrat-Durebex, Christelle
AU  - Veyrat-Durebex C
AD  - Laboratory of Metabolism, Department of Internal Medicine Specialties, Faculty of 
      Medicine, University of Geneva, Geneva, Switzerland.
FAU - Poher, Anne-Laure
AU  - Poher AL
FAU - Caillon, Aurelie
AU  - Caillon A
FAU - Somm, Emmanuel
AU  - Somm E
FAU - Vallet, Philippe
AU  - Vallet P
FAU - Charnay, Yves
AU  - Charnay Y
FAU - Rohner-Jeanrenaud, Francoise
AU  - Rohner-Jeanrenaud F
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20130906
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
RN  - 0 (Leptin)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, Leptin)
RN  - 0 (Suppressor of Cytokine Signaling Proteins)
SB  - IM
MH  - Animals
MH  - *Eating
MH  - Hypothalamus/metabolism
MH  - Leptin/*metabolism
MH  - Male
MH  - Obesity/genetics/*metabolism/physiopathology
MH  - RNA, Messenger/genetics
MH  - Rats
MH  - Rats, Wistar
MH  - Receptors, Leptin/metabolism
MH  - Signal Transduction
MH  - Suppressor of Cytokine Signaling Proteins/genetics
PMC - PMC3765307
COIS- Competing Interests: The authors have declared that no competing interests exist.
EDAT- 2013/09/17 06:00
MHDA- 2014/06/08 06:00
PMCR- 2013/09/06
CRDT- 2013/09/17 06:00
PHST- 2012/12/06 00:00 [received]
PHST- 2013/07/23 00:00 [accepted]
PHST- 2013/09/17 06:00 [entrez]
PHST- 2013/09/17 06:00 [pubmed]
PHST- 2014/06/08 06:00 [medline]
PHST- 2013/09/06 00:00 [pmc-release]
AID - PONE-D-12-38237 [pii]
AID - 10.1371/journal.pone.0073452 [doi]
PST - epublish
SO  - PLoS One. 2013 Sep 6;8(9):e73452. doi: 10.1371/journal.pone.0073452. eCollection 
      2013.