title: Effects of acute intermittent hypoxia on energy balance and hypothalamic feeding pathways.
abstract: This study was done to investigate the effects of acute intermittent hypoxia (IH) on metabolic factors associated with energy balance and body weight, and on hypothalamic satiety-inducing pathways. Adult male Sprague-Dawley rats were exposed to either 8h IH or normoxic control conditions. Food intake, locomotion and body weights were examined after IH. Additionally, plasma levels of leptin, adiponectin corticosterone, insulin and blood glucose were measured following exposure to IH. Furthermore, adipose tissue was removed and analyzed for leptin and adiponectin content. Finally, the hypothalamic arcuate nucleus (ARC) was assessed for alterations in protein signaling associated with satiety. IH reduced body weight, food intake and active cycle locomotion without altering adipose tissue mass. Leptin protein content was reduced while adiponectin content was elevated in adipose tissue after IH. Plasma concentration of leptin was significantly increased while adiponectin decreased after IH. No changes were found in plasma corticosterone, insulin and blood glucose. In ARC, phosphorylation of signal transducer and activator of transcription-3 and pro-opiomelanocortin (POMC) expression were elevated. In addition, POMC-expressing neurons were activated as determined by immediate early gene FRA-1/2 expression. Finally, ERK1/2 and its phosphorylation were reduced in response to IH. These data suggest that IH induces significant alterations to body energy balance through changes in the secretion of leptin which exert effects on satiety-inducing pathways within the hypothalamus.
authors.affiliation: Department of Physiology and Pharmacology, Schulich School of Medicine and Dentistry, The University of Western Ontario, London, ON N6A 5C1, Canada.
authors.forename: J M
authors.initials: JM
authors.lastname: Moreau
authors.forename: J
authors.initials: J
authors.lastname: Ciriello
mesh_terms: D000273:Adipose Tissue / Q000378:metabolism; D000818:Animals; D001786:Blood Glucose / Q000502:physiology; D001835:Body Weight / Q000502:physiology; D004195:Disease Models, Animal; D004326:Drinking / Q000502:physiology; D004734:Energy Metabolism / Q000502:physiology*; D005247:Feeding Behavior; D007031:Hypothalamus / Q000378:metabolism / Q000503:physiopathology*; D000860:Hypoxia / Q000473:pathology* / Q000503:physiopathology*; D020738:Leptin / Q000378:metabolism; D008124:Locomotion / Q000502:physiology; D008297:Male; D009419:Nerve Tissue Proteins / Q000378:metabolism; D011333:Pro-Opiomelanocortin / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D054411:Receptors, Leptin / Q000378:metabolism; D015398:Signal Transduction / Q000502:physiology; D014157:Transcription Factors / Q000378:metabolism
chemical_list: D001786:Blood Glucose; D020738:Leptin; D009419:Nerve Tissue Proteins; D054411:Receptors, Leptin; D014157:Transcription Factors; D011333:Pro-Opiomelanocortin
keywords: ARC; IH; Norm; Ob-Rb; PBS; POMC; SDS; STAT3; TBST; Tris-buffered saline+Tween-20; adiponectin; arcuate nucleus; food intake; intermittent hypoxia; leptin; long-form leptin receptor; normoxic; pSTAT3; phosphate-buffered saline; phosphorylated STAT3; pro-opiomelanocortin; signal transducer and activator of transcription-3; sodium dodecyl sulfate