Modulation of mitochondria and NADPH oxidase function by the nitrate-nitrite-NO pathway in metabolic disease with focus on type 2 diabetes

We examine recent research related to the effects of bioactive nitrogen oxide species on mitochondrial function with emphasis on type 2 diabetes

Tomas A. Schiffer; Jon O. Lundberg; Eddie Weitzberg; Mattias Carlström

2020

Scholarcy highlights

  • Mitochondria play fundamental role in maintaining cellular metabolic homeostasis, and metabolic disorders including type 2 diabetes have been associated with mitochondrial dysfunction
  • Pathophysiological mechanisms are coupled to increased production of reactive oxygen species and oxidative stress, together with reduced bioactivity/signaling of nitric oxide
  • A diet rich in green leafy vegetables, which contains high concentrations of inorganic nitrate, has been shown to reduce the risk of T2D. To this regard research has shown that in addition to the classical NO synthase dependent pathway, nitrate from our diet can work as an alternative precursor for NO and other bioactive nitrogen oxide species via serial reductions of nitrate
  • This non-conventional pathway may act as an efficient back-up system during various pathological conditions when the endogenous NOS system is compromised
  • Attention has been directed towards the effects of nitrate/nitrite on mitochondrial functions including beiging/browning of white adipose tissue, PGC-1α and SIRT3 dependent AMPK activation, GLUT4 translocation and mitochondrial fusion-dependent improvements in glucose homeostasis, as well as dampening of NADPH oxidase activity
  • We examine recent research related to the effects of bioactive nitrogen oxide species on mitochondrial function with emphasis on T2D

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