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Dysregulation of glucose homeostasis in nicotinamide nucleotide transhydrogenase knockout mice is independent of uncoupling protein 2

Parker, Nadeene ; Vidal-Puig, Antonio J ; Azzu, Vian ; Brand, Martin D

BBA - Bioenergetics, December 2009, Vol.1787(12), pp.1451-1457 [Peer Reviewed Journal]

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  • Title:
    Dysregulation of glucose homeostasis in nicotinamide nucleotide transhydrogenase knockout mice is independent of uncoupling protein 2
  • Author: Parker, Nadeene ; Vidal-Puig, Antonio J ; Azzu, Vian ; Brand, Martin D
  • Description: Glucose intolerance in C57Bl/6 mice has been associated with mutations in the nicotinamide nucleotide transhydrogenase ( ) gene. It has been proposed that the absence of NNT from mitochondria leads to increased mitochondrial reactive oxygen species production and subsequent activation of uncoupling protein 2 (UCP2). Activation of UCP2 has been suggested to uncouple electron transport from ATP synthesis in pancreatic beta cell mitochondria thereby decreasing glucose tolerance due to decreased insulin secretion through lower ATP/ADP ratios. The hypothesis tested in this paper is that UCP2 function is required for the dysregulation of glucose homeostasis observed in NNT ablated mice. Single and double and knockout mouse lines were used to measure glucose tolerance, whole animal energy balance and biochemical characteristics of mitochondrial uncoupling. As expected, glucose tolerance was diminished in mice lacking NNT. This...
  • Is Part Of: BBA - Bioenergetics, December 2009, Vol.1787(12), pp.1451-1457
  • Identifier: ISSN: 0005-2728 ; E-ISSN: 1879-2650 ; DOI: 10.1016/j.bbabio.2009.06.005
  • Subjects: Uncoupling Protein 2 (Ucp2) ; Nicotinamide Nucleotide Transhydrogenase (Nnt) ; Proton Leak ; Glucose Tolerance ; Glucose Stimulated Insulin Secretion (Gsis) ; Chemistry
  • Language: English

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