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Liver-derived IGF-I regulates GH secretion at the pituitary level in mice.

Artikel i vetenskaplig tidskrift
Författare Kristina Wallenius
Klara Sjögren
X D Peng
S Park
Ville Wallenius
J L Liu
M. Umaerus
H Wennbo
Olle Isaksson
L Frohman
R Kineman
Claes Ohlsson
John-Olov Jansson
Publicerad i Endocrinology
Volym 142
Nummer/häfte 11
Sidor 4762-70
ISSN 0013-7227
Publiceringsår 2001
Publicerad vid Institutionen för invärtesmedicin, Avdelningen för internmedicin
Institutionen för invärtesmedicin
Sidor 4762-70
Språk en
Länkar www.ncbi.nlm.nih.gov/entrez/query.f...
Ämnesord Animals, Female, Growth Hormone, blood, genetics, secretion, Growth Hormone-Releasing Hormone, pharmacology, Hypothalamus, metabolism, Insulin-Like Growth Factor I, analysis, genetics, physiology, Liver, anatomy & histology, metabolism, Male, Mice, Mice, Knockout, genetics, Neuropeptides, physiology, Organ Size, Pituitary Gland, secretion, Proteins, genetics, RNA, Messenger, metabolism, Receptors, Cell Surface, physiology, Receptors, Prolactin, genetics
Ämneskategorier Medicin och Hälsovetenskap

Sammanfattning

We have reported that liver-specific deletion of IGF-I in mice (LI-IGF-I-/-) results in decreased circulating IGF-I and increased GH levels. In the present study, we determined how elimination of hepatic IGF-I modifies the hypothalamic-pituitary GH axis to enhance GH secretion. The pituitary mRNA levels of GH releasing factor (GHRF) receptor and GH secretagogue (GHS) receptor were increased in LI-IGF-I-/- mice, and in line with this, their GH response to ip injections of GHRF and GHS was increased. Expression of mRNA for pituitary somatostatin receptors, hypothalamic GHRF, somatostatin, and neuropeptide Y was not altered in LI-IGF-I-/- mice, whereas hypothalamic IGF-I expression was increased. Changes in hepatic expression of major urinary protein and the PRL receptor in male LI-IGF-I-/- mice indicated an altered GH release pattern most consistent with enhanced GH trough levels. Liver weight was enhanced in LI-IGF-I-/- mice of both genders. In conclusion, loss of liver-derived IGF-I enhances GH release by increasing expression of pituitary GHRF and GHS receptors. The enhanced GH release in turn affects several liver parameters, in line with the existence of a pituitary-liver axis.

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