Type 1 diabetes (T1D) is a chronic, multifactorial disorder that results from a contretemps of genetic and environmental factors. Autoimmune attack and functional inhibition of the insulin-producing β cells in the pancreas lead to the inability of β cells to metabolize glucose, and thus results the hallmark clinical symptom of diabetes: abnormally high blood glucose levels. Treatment and protection from T1D require a detailed knowledge of the molecular effectors and the mechanism(s) of cell death leading to β-cell demise. Primary islets and surrogate β cells have been utilized in vitro to investigate in isolation-specific mechanisms associated with progression to T1D in vivo. This review focuses on the data obtained from these experiments. Studies using transformed β cells of human sources are described.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3703770 | PMC |
http://dx.doi.org/10.1111/j.1365-2362.2012.02711.x | DOI Listing |
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