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Am J Physiol Endocrinol Metab (May 7, 2003). doi:10.1152/ajpendo.00444.2002
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Submitted on October 16, 2002
Accepted on April 26, 2003

Bovine Growth Hormone Transgenic Mice Have Major Alterations in Hepatic Expression of Metabolic Genes

Bob Olsson1*, Mohammad Bohlooly-Y1, Ola Brusehed1, Olle G. P. Isaksson2, Bo Ahren3, Sven-Olof Olofsson4, Jan Oscarsson5, and Jan Tornell6

1 Department of Physiology, Goteborg University, Goteborg, 405 30, Sweden; Department of Internal Medicine, Sahlgrenska University Hospital, Goteborg, 413 45, Sweden
2 Department of Internal Medicine, Sahlgrenska University Hospital, Goteborg, 413 45, Sweden
3 Department of Medicine, Lund University, Lund, 221 84, Sweden
4 Department of Medical Biochemistry, Goteborg University, Goteborg, 405 30, Sweden; Wallenberg Laboratory for Cardiovascular Disease, Sahlgrenska University Hospital, Goteborg, 413 45, Sweden
5 Department of Physiology, Goteborg University, Goteborg, 405 30, Sweden; Wallenberg Laboratory for Cardiovascular Disease, Sahlgrenska University Hospital, Goteborg, 413 45, Sweden
6 Department of Physiology, Goteborg University, Goteborg, 405 30, Sweden; AstraZeneca Transgenics & Comparative Genomics Centre, AstraZeneca R&D, Molndal, 431 83, Sweden

* To whom correspondence should be addressed. E-mail: bob.olsson{at}medic.gu.se.

Transgenic mice over expressing growth hormone (GH) have been extensively used to study the chronic effects of elevated serum levels of GH. GH is known to have many acute effects in the liver but little is known about the chronic effects of GH over expression on hepatic gene expression. Therefore, we used DNA micro-array to compare gene expression in livers from bovine GH transgenic mice (bGH) and littermates. Hepatic expression of PPAR{alpha} and genes involved in fatty acid activation, peroxisomal and mitochondrial {beta}-oxidation and production of ketone bodies was decreased. In line with this expression profile, bGH transgenic mice had a reduced ability to form ketone bodies both in the fed and fasted state. Although the bGH mice were hyperinsulinemic the expression of SREBP-1 and most lipogenic enzymes regulated by SREBP-1 was reduced, indicating that these mice are different from other insulin resistant models with respect to expression of SREBP-1 and its down-stream genes. This study also provides several candidate genes for the well-known association between elevated GH levels and cardiovascular disease e.g. decreased expression of scavenger receptor class B type I (SR-BI), hepatic lipase (HL), serum paraoxonase (PON-1) and increased expression of serum amyloid A-3 protein (SAA3). We conclude that bGH transgenic mice display marked changes in hepatic genes coding for metabolic enzymes and suggest that GH directly or indirectly regulates many of these hepatic genes via decreased expression of PPAR{alpha} and SREBP-1.




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