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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

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posted on 2014-04-15, 00:00 authored by Manuel 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.).

History

Publisher Statement

This is a copy of an article published in the Endocrinology © 2013 Endocrine Society. The publication is available at http://endo.endojournals.org/

Publisher

Endocrine Society

Language

  • en_US

issn

1945-7170

Issue date

2013-01-01

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