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Göteborgs universitets publikationer

Liver-derived IGF-I regulates kidney size, sodium reabsorption, and renal IGF-II expression.

Författare och institution:
Johan Svensson (Institutionen för medicin, avdelningen för invärtesmedicin); Åsa Tivesten (Institutionen för medicin, avdelningen för invärtesmedicin); Klara Sjögren (Institutionen för medicin, avdelningen för invärtesmedicin); Olle Isaksson (Institutionen för medicin, avdelningen för invärtesmedicin); Göran Bergström (Institutionen för medicin, avdelningen för molekylär och klinisk medicin); Subburaman Mohan (-); Johan Mölne (Institutionen för biomedicin, avdelningen för patologi); Jörgen Isgaard (Institutionen för medicin, avdelningen för invärtesmedicin); Claes Ohlsson (Institutionen för medicin, avdelningen för invärtesmedicin)
Publicerad i:
The Journal of endocrinology, 193 ( 3 ) s. 359-66
Artikel, refereegranskad vetenskaplig
Sammanfattning (abstract):
The GH/-IGF-I axis is important for kidney size and function and may also be involved in the development of renal failure. In this study, the role of liver-derived endocrine IGF-I for kidney size and function was investigated in mice with adult liver-specific IGF-I inactivation (LI-IGF-I(-/-) mice). These mice have an 80-85% reduction of serum IGF-I level and compensatory increased GH secretion. Seven-month-old as well as 24-month-old LI-IGF-I(-/-) mice had decreased kidney weight. Glomerular filtration rate, assessed using creatinine clearance as well as creatinine clearance corrected for body weight, was unchanged. The 24-h urine excretion of sodium and potassium was increased in the LI-IGF-I(-/-) mice. In the 24-month-old mice, there was no between-group difference in kidney morphology. Microarray and real-time PCR (RT-PCR) analyses showed a high renal expression of IGF-II in the control mice, whereas in the LI-IGF-I(-/-) mice, there was a tissue-specific decrease in the renal IGF-II mRNA levels (-79%, P < 0.001 vs controls using RT-PCR). In conclusion, deficiency of circulating liver-derived IGF-I in mice results, despite an increase in GH secretion, in a global symmetrical decrease in kidney size, increased urinary sodium and potassium excretion, and a clear down regulation of renal IGF-II expression. However, the LI-IGF-I(-/-) mice did not develop kidney failure or nephrosclerosis. One may speculate that liver-derived endocrine IGF-I induces renal IGF-II expression, resulting in symmetrical renal growth.
Ämne (baseras på Högskoleverkets indelning av forskningsämnen):
Animals, Extracellular Matrix Proteins, genetics, GTP-Binding Proteins, genetics, Gene Expression Profiling, Gene Expression Regulation, Growth Hormone, secretion, Insulin-Like Growth Factor I, genetics, physiology, Insulin-Like Growth Factor II, analysis, genetics, metabolism, Kidney, anatomy & histology, metabolism, Liver, metabolism, Mice, Mice, Knockout, Oligonucleotide Array Sequence Analysis, Organ Size, Potassium, metabolism, urine, Protein-Lysine 6-Oxidase, genetics, RNA, Messenger, analysis, Reverse Transcriptase Polymerase Chain Reaction, Sodium, metabolism, urine
Postens nummer:
Posten skapad:
2007-10-25 13:36
Posten ändrad:
2011-01-20 10:00

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