Document Detail


The glomerular podocyte as a target of growth hormone action: implications for the pathogenesis of diabetic nephropathy.
MedLine Citation:
PMID:  21067510     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Involvement of the growth hormone (GH) / insulin-like growth factor 1 (IGF-I) axis in the pathogenesis of diabetic nephropathy (DN) is strongly suggested by studies investigating the impact of GH excess and deficiency on renal structure and function. GH excess in both the human (acromegaly) and in transgenic animal models is characterized by significant structural and functional changes in the kidney. In the human a direct relationship has been noted between the activity of the GH/IGF-1 axis and renal hypertrophy, microalbuminuria, and glomerulosclerosis. Conversely, states of GH deficiency or deficiency or inhibition of GH receptor (GHR) activity confer a protective effect against DN. The glomerular podocyte plays a central and critical role in the structural and functional integrity of the glomerular filtration barrier and maintenance of normal renal function. Recent studies have revealed that the glomerular podocyte is a target of GH action and that GH's actions on the podocyte could be detrimental to the structure and function of the podocyte. These results provide a novel mechanism for GH's role in the pathogenesis of DN and offer the possibility of targeting the GH/IGF-1 axis for the prevention and treatment of DN.
Authors:
P Anil Kumar; Frank C Brosius; Ram K Menon
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Review    
Journal Detail:
Title:  Current diabetes reviews     Volume:  7     ISSN:  1875-6417     ISO Abbreviation:  Curr Diabetes Rev     Publication Date:  2011 Jan 
Date Detail:
Created Date:  2010-12-29     Completed Date:  2011-04-27     Revised Date:  2012-02-06    
Medline Journal Info:
Nlm Unique ID:  101253260     Medline TA:  Curr Diabetes Rev     Country:  United Arab Emirates    
Other Details:
Languages:  eng     Pagination:  50-5     Citation Subset:  IM    
Affiliation:
Pediatrics & Communicable Diseases, University of Michigan, Ann Arbor, MI 48109-0718, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Diabetic Nephropathies / etiology*,  metabolism,  pathology,  physiopathology
Disease Progression
Human Growth Hormone / metabolism*,  physiology*
Humans
Insulin-Like Growth Factor I / metabolism,  physiology
Kidney Glomerulus / metabolism*,  pathology,  physiopathology
Models, Biological
Podocytes / metabolism*,  pathology
Receptors, Somatotropin / agonists,  metabolism
Grant Support
ID/Acronym/Agency:
DK49845/DK/NIDDK NIH HHS; P60DK-20572/DK/NIDDK NIH HHS; R24 DK082841-04/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
0/Receptors, Somatotropin; 12629-01-5/Human Growth Hormone; 67763-96-6/Insulin-Like Growth Factor I

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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