title: IGF, type I IGF receptor and IGF-binding protein mRNA expression in kidney and liver of potassium-depleted and normal rats infused with IGF-I.
abstract: Dietary potassium (K) depletion is known to reduce body weight gain and organ growth, except for kidney which increases in weight. This renal hypertrophy is preceded by increased renal IGF-I levels. In the present study, we investigated IGF-I and -II, type I IGF receptor and IGF-binding protein (IGFBP) mRNA expression in liver and kidney of K-depleted and normal rats infused with vehicle or recombinant human IGF-I. Body weight gain was almost completely arrested in K-depleted rats without any stimulatory effect of IGF-I infusion. Both absolute and relative kidney weight (kidney weight/body weight) were significantly increased in K-depleted rats and this was further enhanced by IGF-I infusion. In contrast, relative liver weight was comparable in the different groups and unaffected by IGF-I infusion. IGF-I mRNA expression was significantly lower in kidney and liver of K-depleted animals whereas type I IGF receptor levels were unchanged. In contrast, in kidney, K depletion increased IGFBP-1 and -2 mRNA expression with no additional effect of IGF-I infusion. In liver of K-depleted animals, IGFBP-1 mRNA expression was increased whereas increased IGFBP-1 and -2 mRNA expression was observed when these animals were infused with IGF-I. These observations may point towards a differential mode of action of the IGFBPs. In kidney increased IGFBP-1 and -2 mRNA expression may enhance IGF-I bioavailability with subsequent kidney growth. In liver, with clearly detectable type I IGF receptor mRNA expression, increased IGFBP levels may protect from IGF-I-induced organ growth by decreasing IGF-I bioavailability.
authors.affiliation: Department of Pediatrics, Erasmus University/Sophia Children's Hospital, Rotterdam, The Netherlands.
authors.forename: J W
authors.initials: JW
authors.lastname: van Neck
authors.forename: A
authors.initials: A
authors.lastname: Flyvbjerg
authors.forename: A G
authors.initials: AG
authors.lastname: Schuller
authors.forename: R R
authors.initials: RR
authors.lastname: Rosato
authors.forename: C
authors.initials: C
authors.lastname: Groffen
authors.forename: M
authors.initials: M
authors.lastname: van Kleffens
authors.forename: D
authors.initials: D
authors.lastname: Lindenbergh-Kortleve
authors.forename: I
authors.initials: I
authors.lastname: Dørup
authors.forename: S L
authors.initials: SL
authors.lastname: Drop
mesh_terms: D000818:Animals; D001786:Blood Glucose / Q000032:analysis; D005260:Female; D015870:Gene Expression; D018969:Insulin-Like Growth Factor Binding Proteins / Q000235:genetics*; D007334:Insulin-Like Growth Factor I / Q000008:administration & dosage / Q000235:genetics* / Q000378:metabolism; D007668:Kidney / Q000378:metabolism* / Q000473:pathology; D008099:Liver / Q000378:metabolism* / Q000473:pathology; D009929:Organ Size; D011191:Potassium Deficiency / Q000097:blood / Q000235:genetics*; D012333:RNA, Messenger / Q000235:genetics; D051381:Rats; D017208:Rats, Wistar; D017526:Receptor, IGF Type 1 / Q000235:genetics*; D013977:Tibia / Q000033:anatomy & histology; D015430:Weight Gain
chemical_list: D001786:Blood Glucose; D018969:Insulin-Like Growth Factor Binding Proteins; D012333:RNA, Messenger; D007334:Insulin-Like Growth Factor I; D017526:Receptor, IGF Type 1