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Acute intermittent hypoxia alters leptin signaling pathways in arcuate nucleus (1107.1)
Author(s) -
Moreau Jason,
McCoy Aaron,
Jones Douglas,
Ciriello John
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.1107.1
Subject(s) - leptin , medicine , endocrinology , arcuate nucleus , hypothalamus , phosphorylation , hypoxia (environmental) , arc (geometry) , energy homeostasis , adipose tissue , signal transduction , stat3 , biology , chemistry , receptor , obesity , microbiology and biotechnology , geometry , mathematics , organic chemistry , oxygen
The effect of acute intermittent hypoxia (AIH) on central pathways involved in metabolic homeostasis was investigated in male wild type Sprague‐Dawley (WT) or leptin deficient (Kilo rat; a homozygous knockout of the leptin gene) rats. Rats were exposed to AIH (8 h) or normoxic control conditions and their hypothalamic arcuate nuclei (ARC) were assessed for changes in protein signaling associated with satiety. AIH reduced body weight, food intake and active cycle locomotion without altering adipose tissue mass compared to WT normoxic controls. These differences were not present in Kilo rats. Plasma concentration of leptin was significantly increased after AIH in WT rats, but was not detectable in the Kilo rat. In ARC, phosphorylation of STAT3 and pro‐opiomelanocortin (POMC) expression were higher in the AIH WT rats, but these differences were absent in Kilo rats. Additionally, POMC‐expressing neurons were activated as determined by immediate early gene FRA‐1/2 expression in the AIH WT rats. Finally, ERK1/2 and its phosphorylation were lower in response to AIH in the WT rat, but these differences were eliminated in the Kilo rat. These data suggest that AIH induces significant alterations to body energy balance through changes in the secretion of leptin which exerts effects on satiety‐inducing pathways within the hypothalamus. Supported by HSF of Ontario. Grant Funding Source : Heart and Stroke Foundation of Ontario