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Growth hormone overexpression in the central nervous system results in hyperphagia-induced obesity associated with insulin resistance and dyslipidemia

Bohlooly, M; Olsson, B; Bruder, CEG; Linden, D; Sjogren, K; Bjursell, M; Egecioglu, E; Svensson, L; Brodin, P and Waterton, JC, et al. (2005) In Diabetes 54(1). p.51-62
Abstract
It is well known that peripherally administered growth hormone (GH) results in decreased body fat mass. However, GH-deficient patients increase their food intake when substituted with GH, suggesting that GH also has an appetite stimulating effect. Transgenic mice with an overexpression of bovine GH in the central nervous system (CNS) were created to investigate the role of GH in CNS. This study shows that overexpression of GH in the CNS differentiates the effect of GH on body fat mass from that on appetite. The transgenic mice were not GH-deficient but were obese and showed increased food intake as well as increased hypothalamic expression of agouti-related protein and neuropeptide Y. GH also had an acute effect on food intake following... (More)
It is well known that peripherally administered growth hormone (GH) results in decreased body fat mass. However, GH-deficient patients increase their food intake when substituted with GH, suggesting that GH also has an appetite stimulating effect. Transgenic mice with an overexpression of bovine GH in the central nervous system (CNS) were created to investigate the role of GH in CNS. This study shows that overexpression of GH in the CNS differentiates the effect of GH on body fat mass from that on appetite. The transgenic mice were not GH-deficient but were obese and showed increased food intake as well as increased hypothalamic expression of agouti-related protein and neuropeptide Y. GH also had an acute effect on food intake following intra-cerebroventricular injection of C57BL/6 mice. The transgenic mice were severely hyperinsulinemic and showed a marked hyperplasia of the islets of Langerhans. In addition, the transgenic mice displayed alterations in serum lipid and lipoprotein levels and hepatic gene expression. In conclusion, GH overexpression in the CNS results in hyperphagia-induced obesity indicating a dual effect of GH with a central stimulation of appetite and a peripheral lipolytic effect. (Less)
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Contribution to journal
publication status
published
subject
in
Diabetes
volume
54
issue
1
pages
51 - 62
publisher
American Diabetes Association Inc.
external identifiers
  • pmid:15616010
  • wos:000226247500007
  • scopus:19944426672
ISSN
1939-327X
language
English
LU publication?
yes
id
bc24d06f-8bd6-41ec-a989-4658d460666a (old id 257552)
alternative location
http://diabetes.diabetesjournals.org/cgi/content/abstract/54/1/51
date added to LUP
2007-08-14 08:43:24
date last changed
2017-06-11 04:36:35
@article{bc24d06f-8bd6-41ec-a989-4658d460666a,
  abstract     = {It is well known that peripherally administered growth hormone (GH) results in decreased body fat mass. However, GH-deficient patients increase their food intake when substituted with GH, suggesting that GH also has an appetite stimulating effect. Transgenic mice with an overexpression of bovine GH in the central nervous system (CNS) were created to investigate the role of GH in CNS. This study shows that overexpression of GH in the CNS differentiates the effect of GH on body fat mass from that on appetite. The transgenic mice were not GH-deficient but were obese and showed increased food intake as well as increased hypothalamic expression of agouti-related protein and neuropeptide Y. GH also had an acute effect on food intake following intra-cerebroventricular injection of C57BL/6 mice. The transgenic mice were severely hyperinsulinemic and showed a marked hyperplasia of the islets of Langerhans. In addition, the transgenic mice displayed alterations in serum lipid and lipoprotein levels and hepatic gene expression. In conclusion, GH overexpression in the CNS results in hyperphagia-induced obesity indicating a dual effect of GH with a central stimulation of appetite and a peripheral lipolytic effect.},
  author       = {Bohlooly, M and Olsson, B and Bruder, CEG and Linden, D and Sjogren, K and Bjursell, M and Egecioglu, E and Svensson, L and Brodin, P and Waterton, JC and Isaksson, OGP and Sundler, Frank and Ahrén, Bo and Ohlsson, C and Oscarsson, J and Tornell, J},
  issn         = {1939-327X},
  language     = {eng},
  number       = {1},
  pages        = {51--62},
  publisher    = {American Diabetes Association Inc.},
  series       = {Diabetes},
  title        = {Growth hormone overexpression in the central nervous system results in hyperphagia-induced obesity associated with insulin resistance and dyslipidemia},
  volume       = {54},
  year         = {2005},
}