Flyvbjerg A, Marshall S M, Frystyk J, Rasch R, Bornfeldt K E, Arnqvist H, Jensen P K, Pallesen G, Orskov H
Institute of Experimental Clinical Research, University of Aarhus, Denmark.
Am J Physiol. 1992 Jun;262(6 Pt 2):F1023-31. doi: 10.1152/ajprenal.1992.262.6.F1023.
We investigated insulin-like growth factor I (IGF-I) in the kidney during the initial renal enlargement induced by dietary K depletion in rats. Kidney weight increase was significant after 3 days of K depletion and amounted to 29% after 7 days compared with pair-fed controls [839 +/- 34 vs. 648 +/- 17 mg (SE), P less than 0.01]. The kidney growth occurred despite almost complete arrest in body weight gain in K-depleted animals (8 +/- 3 vs. 34 +/- 4 g/7 days in controls, P less than 0.01). Whole kidney protein, RNA, and DNA estimations indicated that cellular hypertrophy during the first 4 days was followed by hyperplasia. Immunoassayable kidney IGF-I concentration increased by 106% (673 +/- 30 vs. 327 +/- 14 ng/g, P less than 0.01) in K-depleted animals 24 h after induction of K depletion, stayed elevated until day 4, and returned to control levels on day 7. After K depletion for 24 h, IGF-I immunostaining was markedly increased in the medullary parts of the collecting ducts from K-depleted animals, whereas kidney IGF-I gene expression (IGF-I mRNA) had decreased by 36%. The increase in total kidney IGF-I concentration and immunostainable IGF-I in collecting ducts in kidneys from K-depleted rats precedes the renal hypertrophy and thereby suggests a renotropic role for IGF-I. The increase in kidney IGF-I concentration is not associated with increased IGF-I mRNA levels, indicating that non-transcriptional mechanisms may be responsible for the renal IGF-I accumulation.
我们研究了大鼠饮食缺钾诱导的最初肾脏增大过程中肾脏内的胰岛素样生长因子I（IGF-I）。缺钾3天后肾脏重量显著增加，与配对喂食的对照组相比，7天后增加了29%[839±34 vs. 648±17 mg（标准误），P<0.01]。尽管缺钾动物的体重增加几乎完全停止（对照组为34±4 g/7天，缺钾组为8±3 g/7天，P<0.01），但肾脏仍在生长。全肾蛋白质、RNA和DNA测定表明，最初4天细胞肥大后接着是细胞增生。缺钾动物在缺钾诱导24小时后，可免疫测定的肾脏IGF-I浓度增加了106%（673±30 vs. 327±14 ng/g，P<0.01），持续升高至第4天，第7天恢复到对照水平。缺钾24小时后，缺钾动物集合管髓质部分的IGF-I免疫染色明显增加，而肾脏IGF-I基因表达（IGF-I mRNA）下降了36%。缺钾大鼠肾脏中总肾脏IGF-I浓度的增加以及集合管中可免疫染色的IGF-I在肾脏肥大之前出现，因此提示IGF-I具有促肾生长作用。肾脏IGF-I浓度的增加与IGF-I mRNA水平的增加无关，表明非转录机制可能是肾脏IGF-I积累的原因。
