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Dual age-dependent effect of ghrelin administration on serum level of insulin-like growth factor-1 and gastric growth in young rats
Authors:Warzecha Zygmunt  Dembiński Artur  Ceranowicz Piotr  Dembiński Marcin  Cieszkowski Jakub  Bielański Władysław  Pawlik Wiesław W  Kuwahara Atsukazu  Kato Ikuo
Affiliation:Department of Physiology, Jagiellonian University Medical College, 16 Grzegórzecka Street, 31-531 Kraków, Poland.
Abstract:Ghrelin is a circulating growth hormone-releasing peptide primarily isolated from human and rat stomach. The aim of present study was to investigate the effect of ghrelin administration on gastric growth in suckling, and young peripubertal 7-week-old rats. Rats were treated for 7 days with saline or ghrelin (4, 8 or 16 nmol/kg/dose) intraperitoneally twice a day. Suckling rats were treated from the fist postnatal day. Results: Treatment with ghrelin did not affect animal weight in suckling rats; whereas in 7-week-old animals, administration of ghrelin caused a significant increase in body weight. In suckling rats, ghrelin decreased the gastric weight, DNA synthesis and DNA content. In young 7-week-old peripubertal rats, treatment with ghrelin increased food intake and animal body weight. This effect was accompanied with a significant increase in gastric mucosa weight, DNA synthesis and DNA content. Treatment with ghrelin increased serum level of growth hormone in all rats tested, but this result was much higher in 7-week-old peripubertal rats than in suckling rats. Serum level of insulin-like growth factor-1 was not affected by ghrelin administration in suckling rats. In contrast, ghrelin caused a significant increase in serum level of insulin-like growth factor-1 in 7-week-old peripubertal rats. We conclude that administration of ghrelin exhibits biphasic effect on gastric growth in young rats: in suckling rats, ghrelin reduces gastric growth, whereas in young 7-week-old animals, treatment with ghrelin stimulates gastric growth. The growth-promoting effect of ghrelin in the stomach seems to depend on the stimulation of food intake and the release of insulin-like growth factor-1.
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