Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011881 (diabetic nephropathy)
 10,836 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This review has updated recent facets of evidence for the significance of the GH/IGF system in the development of diabetic kidney disease. It seems evident, however, that there is still an extensive number of questions that need to be answered before diabetic kidney disease is fully understood. The knowledge we have today indicates that GH/IGF axis, through a complex system comprising GHR, GHBP, IGFs, IGF receptors and IGFBPs may be responsible for both early and late renal changes in experimental diabetes (Fig. 3). In view of the complexity of the GH/IGF system, it will be a challenge to fully characterize the renal effects of GH/IGFs in diabetic kidney disease. There is no doubt that information on this topic will occur with increasing pace in the near future and that a understanding of the above-mentioned mechanisms will allow the further development of existing antagonists and design of new drugs, which may prove to be useful for therapeutic manipulation in the treatment of diabetic nephropathy. The development of long-acting somatostatin analogues and GH antagonists, both with a specific action on the GH/IGF axis, seems to be one important step ahead. The combined administration of one of these antagonists with other drugs with a well described renoprotective action (such as ACE inhibitors) opens an interesting new dimension.
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PMID:Role of growth hormone, insulin-like growth factors (IGFs) and IGF-binding proteins in the renal complications of diabetes. 928 96

Growth hormone (GH) may have a role in the development of diabetic nephropathy. The effect of experimental diabetes on renal expression of the growth hormone receptor gene products, including the receptor itself (GHR) and its binding protein (GHBP) was examined. Adult female rats received i.v. streptozotocin and were killed at 7, 30, 90 and 180 days after the induction of diabetes. Diabetic animals had a pronounced increase in kidney weight and progressive albuminuria. In renal cortex, no change was seen in GHR mRNA levels throughout the observation period of 6 months, while a significant increase in cortical GHBP mRNA levels was observed after 1 month of diabetes and sustained for the rest of the study period. Immunohistochemical analysis of kidney sections revealed a stronger staining for GHBP at the cortical and inner medullary areas in the diabetic animals. These data indicate that although the GHR and GHBP mRNAs originate from the same gene, their renal levels are differentially regulated during the development of experimental diabetic kidney disease, suggesting a functional role for GHBP.
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PMID:Differential expression of renal growth hormone receptor and its binding protein in experimental diabetes mellitus. 1099 Apr 43