ArticlePhysiological reports2016
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.
Article in Physiological reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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20 citing papers in PubMed, 32 citations in OpenAlex.
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- The growth hormone/IGF-1 axis is a risk factor for long-term kidney allograft failure.JCI insight · 2025Article
- The canine vibrissal system as a highly innervated and functional sensory organ.Scientific reports · 2025Article
- Decreased β-cell volume and insulin secretion but preserved glucose tolerance in a growth hormone insensitive pig model.Pituitary · 2024Article
- A case report: Alport syndrome and growth hormone deficiency associated with a newTranslational pediatrics · 2024Article
- Proteomic Identification of Plasma Components inMarine drugs · 2023Article
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- Renal effects of growth hormone in health and in kidney disease.Pediatric nephrology (Berlin, Germany) · 2021Article
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- The intrinsic circadian clock in podocytes controls glomerular filtration rate.Scientific reports · 2019Article
- Metabolic syndrome and extensive adipose tissue inflammation in morbidly obese Göttingen minipigs.Molecular metabolism · 2018Article
- Sampling Strategies and Processing of Biobank Tissue Samples from Porcine Biomedical Models.Journal of visualized experiments : JoVE · 2018Article
- Practicable methods for histological section thickness measurement in quantitative stereological analyses.PloS one · 2018Article
- Novel Actions of Growth Hormone in Podocytes: Implications for Diabetic Nephropathy.Frontiers in medicine · 2017Review
- 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.Physiological reports · 2016Article
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- Targeting growth hormone function: strategies and therapeutic applications.Signal transduction and targeted therapyReview
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Authors and funding
4 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
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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