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- December 1, 2008 |
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CME on Diabetes is a website built to transmit top-level CME conferences given by international experts in endocrinology, insulin resistance, prediabetes, metabolic syndrome and type 2 diabetes. More than 2.6 million slides have been viewed since the website launch. Thank you for your continued support and commitment!
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"Strategies to prevent diabetic renal disease (bench to bedside)"Prof. Mark E. Cooper (biography)
English - 2004-06-26 - 37 minutes
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 | (34 slides) |
Summary :
In this presentation Dr. Cooper presents scientific data relating to possible future therapeutic interventions for preventing diabetic renal disease.
The metallopeptidase enzymes such as angiotensin converting enzyme (ACE) and neutral endopeptidase (NEP) are homologous, so it is possible to make a drug targeting both enzymes. Inhibition of both enzymes with the drug omapatrilat showed a greater attenuation of albuminuria compared to ACE inhibition alone in an animal model of of progressive diabetic renal injury.
Advanced glycation is thought to be a very important pathway for the development of diabetic complications. Advanced glycation endproducts (AGEs) can be reduced either by glycemic control, providing less substrate for AGE formation, or, by drugs that prevent the formation of AGEs from early glycated proteins, prevent AGEs attaching to their receptors, or actually cleave preformed AGEs.
Dr. Cooper also talks about the possible role of PKC inhibition and growth factor inhibition in the prevention of disease.
Copyright © 2004 E-MedHosting.com Inc
Learning objectives :
After viewing this presentation the participant will be able to discuss scientific data relating to possible therapeutic interventions to prevent diabetic renal disease:
- Dual ACE and NEP inhibition
- Reduction of AGEs
- PKC beta inhibition
- Growth factor inhibition
Bibliographic references :
M. E. Cooper. Interaction of metabolic and haemodynamic factors in mediating experimental diabetic nephropathy Diabetologia 2001; 44(11):1957 - 1972.
B. J. Davis, C. I. Johnston, L. M. Burrell, W. C. Burns, E. Kubota, Z. Cao, M. E. Cooper and T. J. Allen. Renoprotective effects of vasopeptidase inhibition in an experimental model of diabetic nephropathy Diabetologia 2003;46(7):961 - 971.
Josephine M. Forbes, Louis Teo Loon Yee, Vicki Thallas, Markus Lassila, Riccardo Candido, Karin A. Jandeleit-Dahm, Merlin C. Thomas, Wendy C. Burns, Elizabeth K. Deemer, Susan M. Thorpe, Mark E. Cooper, and Terri J. Allen. Advanced Glycation End Product Interventions Reduce Diabetes-Accelerated Atherosclerosis Diabetes 2004; 53:1813-1823.
Forbes JM, Thallas V, Thomas MC, Founds HW, Burns WC, Jerums G, Cooper ME. The breakdown of preexisting advanced glycation end products is associated with reduced renal fibrosis in experimental diabetes. FASEB J. 2003 Sep;17(12):1762-4.
Forbes JM, Soulis T, Thallas V, Panagiotopoulos S, Long DM, Vasan S, Wagle D, Jerums G, Cooper ME.Renoprotective effects of a novel inhibitor of advanced glycation. Diabetologia 2001 Jan;44(1):108-14.
DAISUKE KOYA, MASAKAZU HANEDA, HIROKO NAKAGAWA, KEIJI ISSHIKI, HARUHISA SATO, SHIRO MAEDA, TOSHIRO SUGIMOTO, HITOSHI YASUDA, ATSUNORI KASHIWAGI, D. KIRK WAYS, GEORGE L. KING§ and RYUICHI KIKKAWA.Amelioration of accelerated diabetic mesangial expansion by treatment with a PKC ß inhibitor in diabetic db/db mice, a rodent model for type 2 diabetes FASEB.2000;14:439-447.
Park L, Raman KG, Lee KJ, Lu Y, Ferran LJ Jr, Chow WS, Stern D, Schmidt AM.Suppression of accelerated diabetic atherosclerosis by the soluble receptor for advanced glycation endproducts.
Nat Med. 1998 Sep;4(9):1025-31.
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