title: GH does not modulate the early fasting-induced release of free fatty acids in mice.
abstract: Fasting results in the mobilization of adipose stores and the elevation of levels of free fatty acids (FFA). In humans, this process is driven by a release in GH. Little is known regarding the role of GH in modulating this process during early stages of fasting in the mouse. Confirmation of the role of GH in modulating FFA release in the fasting mouse is of particular importance given the frequent use of mouse models to study metabolic mechanisms. Here, we correlate the initial release of FFA throughout fasting in mice with pulsatile GH secretion. Observations illustrate the rapid release of FFA in response to food withdrawal. This does not correlate with a rise in GH secretion. Rather, we observed a striking loss in pulsatile secretion of GH throughout the first 6 h of fasting, suggesting that GH does not modulate the initial release of FFA in the mouse in response to fasting. This was confirmed in GH receptor knockout mice, in which we observed a robust fasting-induced rise in FFA. We further illustrate the dynamic relationship between the orexigenic and anorexigenic hormones ghrelin and leptin during fasting in the mouse. Our findings show an initial suppression of leptin and the eventual rise in circulating levels of acyl-ghrelin with fasting. However, altered acyl-ghrelin and leptin secretion occurs well after the rise in FFA and the suppression of GH secretion. Consequently, we conclude that although acyl-ghrelin and leptin may modulate the physiological response to drive food intake, these changes do not contribute to the initial loss of pulsatile GH secretion. Rather, it appears that the suppression of GH secretion in fasting may occur in response to an elevation in fasting levels of FFA or physiological stress. Observations highlight a divergent role for GH in modulating FFA release between man and mouse.
authors: School of Biomedical Sciences, University of Queensland, St. Lucia, Brisbane, Queensland 4072, Australia.
authors: F J
authors: FJ
authors: Steyn
authors: J W
authors: JW
authors: Leong
authors: L
authors: L
authors: Huang
authors: H Y
authors: HY
authors: Tan
authors: T Y
authors: TY
authors: Xie
authors: C
authors: C
authors: Nelson
authors: M J
authors: MJ
authors: Waters
authors: J D
authors: JD
authors: Veldhuis
authors: J
authors: J
authors: Epelbaum
authors: C
authors: C
authors: Chen
mesh_terms: D000818:Animals; D003345:Corticosterone / Q000097:blood; D005215:Fasting / Q000097:blood / Q000502:physiology*; D005230:Fatty Acids, Nonesterified / Q000097:blood / Q000378:metabolism*; D015870:Gene Expression; D054439:Ghrelin / Q000097:blood; D013006:Growth Hormone / Q000097:blood / Q000378:metabolism / Q000502:physiology*; D006801:Humans; D007031:Hypothalamus / Q000502:physiology; D007334:Insulin-Like Growth Factor I / Q000378:metabolism; D020738:Leptin / Q000097:blood; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D023421:Models, Animal; D010902:Pituitary Gland / Q000502:physiology; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D017481:Receptors, Somatostatin / Q000235:genetics; D011986:Receptors, Somatotropin / Q000172:deficiency / Q000235:genetics; D015398:Signal Transduction; D013045:Species Specificity; D013997:Time Factors
chemical_list: D005230:Fatty Acids, Nonesterified; D054439:Ghrelin; D020738:Leptin; D012333:RNA, Messenger; D017481:Receptors, Somatostatin; D011986:Receptors, Somatotropin; D007334:Insulin-Like Growth Factor I; D013006:Growth Hormone; D003345:Corticosterone