作者: Bernard Portha , Marie-Hélène Giroix , Cecile Tourrel-Cuzin , Hervé Le-Stunff , Jamileh Movassat
DOI: 10.1007/978-1-62703-068-7_9
关键词:
摘要: Type 2 diabetes mellitus (T2D) arises when the endocrine pancreas fails to secrete sufficient insulin cope with metabolic demand because of β-cell secretory dysfunction and/or decreased mass. Defining nature pancreatic islet defects present in T2D has been difficult, part human islets are inaccessible for direct study. This review is aimed illustrate what extent Goto Kakizaki rat, one best characterized animal models spontaneous T2D, proved be a valuable tool offering commonalities study this aspect. A comprehensive compendium multiple functional GK abnormalities so far identified proposed perspective, together their time-course and interactions. special focus given toward pathogenesis defective number function model. It that development model results from complex interaction events: (1) several susceptibility loci containing genes responsible some diabetic traits; (2) gestational impairment inducing an epigenetic programming offspring major target tissues; (3) environmentally induced loss differentiation due chronic exposure hyperglycemia/hyperlipidemia, inflammation, oxidative stress.