β-cell (beta-cell) impairment is central to the development and progression of human diabetes, as a result of the combined effects of genetic and acquired factors. Reduced islet number and/or reduced β cells amount in the pancreas of individuals with Type 2 diabetes have been consistently reported. This is mainly due to increased β cell death, not adequately compensated for by regeneration. In addition, several quantitative and/or qualitative defects of insulin secretion have been observed in Type 2 diabetes, both in vivo and ex vivo with isolated islets. All this is associated with modifications of islet cell gene and protein expression. With the identification of several susceptible Type 2 diabetes loci, the role of genotype in affecting β-cell function and survival has been addressed in a few studies and the relationships between ge notype and β-cell phenotype investigated. Among acquired factors, the importance of metabolic insults (in particular glucotoxicity and lipotoxicity) in the natural history of β-cell damage has been widely underlined. Continuous improvements in our knowledge of the β cells in human Type 2 diabetes will lead to more targeted and effective strategies for the prevention and treatment of the disease.
CITATION STYLE
Marchetti, P., Bugliani, M., Boggi, U., Masini, M., & Marselli, L. (2013). The pancreatic β cells in human type 2 diabetes. Advances in Experimental Medicine and Biology, 771, 288–309. https://doi.org/10.1007/978-1-4614-5441-0_22
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