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Growth hormone (GH)-transgenic insulin-like growth factor 1 (IGF1)-deficient mice
allow dissociation of excess GH and IGF1 effects on glomerular and tubular
growth
#MMPMID26997624
Blutke A
; Schneider MR
; Wolf E
; Wanke R
Physiol Rep
2016[Mar]; 4
(5
): ? PMID26997624
show ga
Growth hormone (GH)-transgenic mice with permanently elevated systemic levels of
GH and insulin-like growth factor 1 (IGF1) reproducibly develop renal and
glomerular hypertrophy and subsequent progressive glomerulosclerosis, finally
leading to terminal renal failure. To dissociate IGF1-dependent and -independent
effects of GH excess on renal growth and lesion development in vivo, the kidneys
of 75 days old IGF1-deficient (I(-/-)) and of IGF1-deficient GH-transgenic mice
(I(-/-)/G), as well as of GH-transgenic (G) and nontransgenic wild-type control
mice (I(+/+)) were examined by quantitative stereological and functional
analyses. Both G and I(-/-)/G mice developed glomerular hypertrophy, hyperplasia
of glomerular mesangial and endothelial cells, podocyte hypertrophy and foot
process effacement, albuminuria, and glomerulosclerosis. However, I(-/-)/G mice
exhibited less severe glomerular alterations, as compared to G mice. Compared to
I(+/+) mice, G mice exhibited renal hypertrophy with a significant increase in
the number without a change in the size of proximal tubular epithelial (PTE)
cells. In contrast, I(-/-)/G mice did not display significant PTE cell
hyperplasia, as compared to I(-/-) mice. These findings indicate that GH excess
stimulates glomerular growth and induces lesions progressing to
glomerulosclerosis in the absence of IGF1. In contrast, IGF1 represents an
important mediator of GH-dependent proximal tubular growth in GH-transgenic mice.
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