WEDNESDAY, Jan. 6 (HealthDay News) -- Tetracycline reduces the progression of diabetes in lines of mice that develop the disease along with islet β-cell dysfunction and β-cell loss, according to research published in the January issue of Diabetes.
Jacqueline F. Aitken, Ph.D., of the University of Auckland in New Zealand, and colleagues analyzed data from experiments on human amylin/islet amyloid polypeptide (hA/hIAPP) transgenic mice. In human type 2 diabetes, amyloid deposits in the islets of Langerhans contain hA/hIAPP.
The researchers found that diabetes developed in both homozygous and hemizygous mice, though more quickly in the former group. Amyloid deposition was not seen in homozygous mice with severe early-onset disease, but was seen in hemizygous animals, in which it was positively associated with lifespan. The use of tetracycline reduced hyperglycemia, delayed the onset and progression of diabetes, and improved longevity in hemizygous animals in a dose-dependent manner.
"In summary, our findings show that islet β-cell dysfunction and not mature extracellular amyloid is the underpinning cause for diabetes pathogenesis in hemizygous hA/hIAPP transgenic mice. Moreover, deposition of microscopically visible amyloid was positively correlated with lifespan, showing that tissue hA/hIAPP deposits are not intrinsically cytotoxic. Treatment with an effective dosage of tetracycline delayed the onset and impeded the progression of diabetes in hemizygous mice. Consequently, any intervention that allows progressive deposition of (apparently benign) islet amyloid through mechanisms that reduce the cytotoxicity of prefibrillar aggregates might be expected to prevent islet β-cell degeneration," the authors write.
Abstract
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