THE PANCREATIC β CELLS IN HUMAN TYPE 2 DIABETES

被引:0
|
作者
Marchetti, Piero [1 ]
Bugliani, Marco [1 ]
Boggi, Ugo [1 ]
Masini, Matilde [1 ]
Marselli, Lorella [1 ]
机构
[1] Univ Pisa, Dept Endocrinol & Metab, Pisa, Italy
来源
关键词
FREE FATTY-ACIDS; INSULIN-SECRETION; OXIDATIVE STRESS; HUMAN ISLETS; HIGH GLUCOSE; GLUTATHIONE-PEROXIDASE; ENDOPLASMIC-RETICULUM; PROTEIN EXPRESSION; CAUSES APOPTOSIS; B-CELLS;
D O I
暂无
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
beta-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 beta cells amount in the pancreas of individuals with Type 2 diabetes have been consistently reported. This is mainly due to increased beta 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 modi fications of islet cell gene and protein expression. With the identification of several susceptible Type 2 diabetes loci, the role of genotype in affecting beta-cell function and survival has been addressed in a few studies and the relationships between genotype and beta-cell phenotype investigated. Among acquired factors, the importance of metabolic insults (in particular glucotoxicity and lipotoxicity) in the natural history of beta-cell damage has been widely underlined. Continuous imp rovements in our knowledge of the [ 3 cells in hum an Type 2 diabetes will lead to more targeted and effective strategies for the prevent ion and treatment of the disease.
引用
收藏
页码:288 / 309
页数:22
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