| Autor: |
Ahmed, Sahid, Clark, Anne, Matthews, David R., DPhil |
| Zdroj: |
Current Opinion in Endocrinology & Diabetes; August 1997, Vol. 4 Issue: 4 p300-307, 8p |
| Abstrakt: |
The deterioration in non-insulin dependent diabetes is associated with progressive failure of β cells. Decline in β-cell function is likely to be exacerbated by increased insulin resistance. Progressive deterioration of (3-cell function cannot be influenced by either insulin or sulfonylurea therapy. The pathophysiology of failure is still unknown, though possibilities include islet amyloid formation, so-called “glucose toxicity,” and lateonset autoimmunity (latent autoimmune diabetes of adults). Raised proinsulin levels may be one marker of β-cell failure. Maturity-onset diabetes of the young results from mutations in genes coding for islet proteins causing persistent β-cell dysfunction. Identification of a single causative factor is unlikely in such a heterogeneous disease. |
| Databáze: |
Supplemental Index |
| Externí odkaz: |
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