The Rise in Growth Hormone during Starvation Does
Not Serve to Maintain Glucose Levels or Lean Mass
but Is Required for Appropriate Adipose Tissue
Response in Female Mice
posted on 2014-04-15, 00:00authored byManuel D. Gahete, José Córdoba-Chacón, Raúl M. Luque, Rhonda D. Kineman
In mice, GH levels rise in response to short-term fasting or starvation (food restriction to 40% of ad
libitum intake), similar to that which occurs in humans in response to fasting or anorexia. Recent
studies using acyl-ghrelin knockout mice have suggested that the rise inGHduring food restriction
is essential to support glucose levels. To directly test this hypothesis, adult-onset isolated GH
deficient (AOiGHD) mice and their GH-replete littermate controls were provided40%of ad libitum
food intake for 11 d. As previously shown, food restriction increased GH levels in controls, and this
response was not observed inAOiGHDmice. In both controls andAOiGHD,food restriction resulted
in an initial decline in glucose, which stabilized to 82–85% of ad libitum-fed values by d 2. In
addition, loss of lean mass in response to food restriction was not altered by GH status. However,
the loss of fat mass and the associated rise in circulating free fatty acids and ketones was blunted
in starved AOiGHD mice compared with controls. Taken together, these results suggest a rise ofGH
during starvation is not required to support glucose levels and muscle mass but may be important
in supporting fat mobilization.
Funding
This work was supported by the Department of Veterans
Affairs, Veterans Health Administration, Office of Research and
Development Merit Award, and National Institutes of Health
Grants R21AG031465 and R01DK088133 (to R.D.K.); Fundacion
Caja Madrid and “Sara Borrell” program (Grant CD11/
00276) (to M.D.G.); Fundacion Alfonso Martin Escudero (to
J.C.-C.); and Grants CTS-5051, BFU2010-19300, Centro de Investigación
Biomédica en Red Fisiopatología de la Obesidad y
Nutrición, and Grant RYC-2007-00186 (to R.M.L.).