Jamileh Movassat

TL;DR: It is demonstrated that in the GK rat, the deficit of total beta- cell mass as observed in the adult animal is related to impaired beta-cell development, which must be considered as a primary and crucial event in the sequence leading to overt diabetes in this NIDDM model.

TL;DR: This review is aimed to illustrate to what extend the Goto-Kakizaki rat, one of the best characterized animal models of spontaneous T2D, has proved be a valuable tool offering sufficient commonalities to study these aspects.

TL;DR: This paper examines the developmental programming of glucose intolerance/diabetes by disturbed intrauterine metabolic condition experimentally obtained in various rodent models of maternal protein restriction, caloric restriction, overnutrition or diabetes, with a focus on the alteration of the developing beta-cell mass.

TL;DR: It is proposed that the development of T2D in the GK model results from the complex interaction of multiple events: several susceptibility loci containing genes responsible for some diabetic traits; gestational metabolic impairment inducing an epigenetic programming of the offspring pancreas and the major insulin target tissues; and environmentally induced loss of β-cell differentiation due to chronic exposure to hyperglycemia/hyperlipidemia, inflammation, and oxidative stress.

TL;DR: Several convergent data suggest that the permanently reducedbeta-cell mass in the GK/Par rat reflects a limitation of beta-cell neogenesis during early fetal life, and it is conceivable that some genes among the set involved in GK diabetes belong to the subset of genes controlling early beta- cell development.