| Autor: |
Portha, Bernard, Lacraz, G., Dolz, M., Homo-Delarche, F., Giroix, M.-H., Movassat, J. |
| Předmět: |
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| Zdroj: |
Expert Review of Endocrinology & Metabolism; Nov2007, Vol. 2 Issue 6, p785-795, 11p, 1 Color Photograph, 2 Diagrams, 3 Graphs |
| Abstrakt: |
Increasing evidence indicates that decreased functional β-cell mass is the hallmark of Type 2 diabetes mellitus. Therefore, the debate focuses on the possible mechanisms responsible for abnormal islet microenvironment, decreased β-cell number, impaired β-cell function and their multifactorial etiologies. The information available on the Goto—Kakizaki/Par rat line, one of the best characterized animal models of spontaneous Type 2 mellitus, are reviewed in such a perspective. We propose that the defective β-cell mass and function in the Goto—Kakizaki/Par model reflect the complex interactions of multiple pathogenic players, including several independent loci containing genes responsible for some diabetic traits (but not decreased β-cell mass), gestational metabolic impairment inducing an epigenetic programming of the pancreas (decreased β-cell neogenesis), which is transmitted to the next generation, and loss of β-cell differentiation due to chronic exposure to hyperglycemia, inflammatory mediators, oxidative stress and perturbed islet microarchitecture. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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