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Islet gene expression and function in type 2 diabetes; studies in the Goto‐Kakizaki rat and humans
Author(s) -
Östenson C.G.,
Efendic S.
Publication year - 2007
Publication title -
diabetes, obesity and metabolism
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.445
H-Index - 128
eISSN - 1463-1326
pISSN - 1462-8902
DOI - 10.1111/j.1463-1326.2007.00787.x
Subject(s) - islet , endocrinology , medicine , type 2 diabetes , diabetes mellitus , beta cell , insulin , pancreatic islets , beta (programming language) , pathogenesis , biology , secretion , computer science , programming language
Defective β‐cell function with resulting impairment of glucose‐stimulated insulin release is a critical factor in the pathogenesis of type 2 diabetes. Accumulated studies in pancreatic islets of the spontaneously diabetic Goto‐Kakizaki (GK) rat suggest that this is a useful animal model of type 2 diabetes. The GK rat is non‐obese, and abnormal glucose regulation develops early in life in association with impaired insulin secretion. There are some differences in islet morphology and function reported between different GK rat colonies. In addition to reduction of β‐cell mass, a number of β‐cell defects have been described with possible relevance for the reduced insulin secretion. Interestingly, some of these defects have also been shown in isolated islets from type 2 diabetic humans. The polygenic nature of diabetes heredity in the GK rat may well resemble the genetic basis in the majority of patients with type 2 diabetes. Here, we review studies concerning β‐cell function and islet gene expression in the GK rat and compare it with the limited number of investigations on similar topics in isolated islets from patients with type 2 diabetes.