title: Tail suspension increases energy expenditure independently of the melanocortin system in mice.
abstract: Space travelers experience anorexia and body weight loss in a microgravity environment, and microgravity-like situations cause changes in hypothalamic activity. Hypothalamic melanocortins play a critical role in the regulation of metabolism. Therefore, we hypothesized that microgravity affects metabolism through alterations in specific hypothalamic signaling pathways, including melanocortin signaling. To address this hypothesis, the microgravity-like situation was produced by an antiorthostatic tail suspension in wild-type and agouti mice, and the effect of tail suspension on energy expenditure and hypothalamic gene expression was examined. Energy expenditure was measured using indirect calorimetry before and during the tail suspension protocol. Hypothalamic tissues were collected for gene expression analysis at the end of the 3 h tail suspension period. Tail suspension significantly increased oxygen consumption, carbon dioxide production, and heat production in wild-type mice. Tail suspension-induced increases in energy expenditure were not attenuated in agouti mice. Although tail suspension did not alter hypothalamic proopiomelanocortin (POMC) and agouti-related protein (AGRP) mRNA levels, it significantly increased hypothalamic interleukin 6 (Il-6) mRNA levels. These data are consistent with the hypothesis that microgravity increases energy expenditure and suggest that these effects are mediated through hypothalamic signaling pathways that are independent of melanocortins, but possibly used by Il-6.
authors.affiliation: Department of Physiology, University of Manitoba, 745 Bannatyne Avenue, Winnipeg, MB R3E 0J9, Canada.
authors.forename: Pei San
authors.initials: PS
authors.lastname: Lew
authors.forename: Davie
authors.initials: D
authors.lastname: Wong
authors.forename: Takafumi
authors.initials: T
authors.lastname: Yamaguchi
authors.forename: Arnold
authors.initials: A
authors.lastname: Leckstrom
authors.forename: Jacquie
authors.initials: J
authors.lastname: Schwartz
authors.forename: Janice G
authors.initials: JG
authors.lastname: Dodd
authors.forename: Tooru M
authors.initials: TM
authors.lastname: Mizuno
mesh_terms: D002001:Adipose Tissue, Brown / Q000378:metabolism; D054369:Agouti-Related Protein / Q000378:metabolism; D000818:Animals; D001774:Blood Chemical Analysis; D015153:Blotting, Western; D004734:Energy Metabolism / Q000502:physiology*; D015870:Gene Expression / Q000502:physiology; D019417:Hindlimb Suspension / Q000502:physiology*; D006728:Hormones / Q000097:blood; D007031:Hypothalamus / Q000502:physiology; D015850:Interleukin-6 / Q000096:biosynthesis; D007700:Kinetics; D008297:Male; D053486:Melanocortins / Q000096:biosynthesis* / Q000235:genetics; D008660:Metabolism / Q000502:physiology; D051379:Mice; D008810:Mice, Inbred C57BL; D011333:Pro-Opiomelanocortin / Q000378:metabolism; D012313:RNA / Q000096:biosynthesis / Q000235:genetics; D020133:Reverse Transcriptase Polymerase Chain Reaction; D015398:Signal Transduction / Q000502:physiology; D014893:Weightlessness
chemical_list: D054369:Agouti-Related Protein; D006728:Hormones; D015850:Interleukin-6; D053486:Melanocortins; D012313:RNA; D011333:Pro-Opiomelanocortin