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  Franšais - August 16, 2011
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 Presentation

"Insulin Resistance and B-Cell Dysfunction: Changing the Consequences of the Disease Continuum"

Dr. Samuel Dagogo-Jack (biography)
English - 2003-06-16 - 34 minutes
(21 slides)

Summary :
The prediabetic state is characterized by IFG or IGT, but we have more information about IGT since its use in the large clinical trials, and it is not clear whether they predict the same outcomes. It was recently shown that individuals with IFG were as insulin resistant as those with established type 2 diabetes, and beta cell function was elevated. (Dagogo-Jack S et al. Diabetes. 2003; 52: (suppl 1):A285.

From the UKPDS data, it can be estimated that decline in beta cell function would have begun about a decade before diagnosis (Lebovitz H. Diabetes Rev. 1999; 7(3):139-53), and so it is of major interest now to determine how beta cells die. Although there is no unified hypothesis for this, it has been shown that inhibitors of iNOS (inducible nitric oxide synthase), as well as the PPAR-gamma agonist 15-deoxyPGJ2 protected beta cells from cytokine-mediated death (Corbett JA et al. J ExpMed 1995; 181: 559).

Here we will look at the performance of PPAR agonists in clinical trials and new information about the effects of rosiglitazone on improving beta cell function.

Learning objectives :
The participant will learn new information about IFG, and the role of PPAR gamma agonists in improving beta cell function:

- IFG individuals were found to be as insulin resistant as those with type 2 diabetes, and had elevated beta cell function (Dagogo-Jack S et al. Diabetes. 2003; 52: (suppl 1):A285.

- Rosiglitazone improves beta cell function in monotherapy and in combination (Data on file, GlaxoSmithKline).

Bibliographic references :
Corbett JA, McDaniel ML. Intraislet release of interleukin 1 inhibits beta cell function by inducing beta cell expression of inducible nitric oxide synthase. J Exp Med. 1995 Feb 1;181(2):559-68.

   


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