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Mitochondrial uncoupling has no effect on microvascular complications in type 2 diabetes

Lucy M Hinder1, Kelli M Sas2, Phillipe D O'Brien1

  • 1Department of Neurology, University of Michigan, Ann Arbor, MI, 48109, USA.

Scientific Reports
|January 31, 2019
PubMed

Insights

Targeting mitochondria with niclosamide ethanolamine (NEN) did not improve type 2 diabetes (T2D) or its complications, including diabetic peripheral neuropathy (DPN), diabetic kidney disease (DKD), and diabetic retinopathy (DR). This suggests global mitochondrial uncoupling is not a viable therapy for T2D complications.

Area of Science:

  • Mitochondrial biology
  • Diabetes complications
  • Metabolic diseases

Background:

  • Diabetic peripheral neuropathy (DPN), diabetic kidney disease (DKD), and diabetic retinopathy (DR) are major causes of morbidity and mortality in type 2 diabetes (T2D).
  • Current therapies offer limited impact on the pathogenesis of these T2D complications.
  • Tissue-specific mitochondrial adaptations in T2D are known, but their causal role in dysfunction is unclear.

Purpose of the Study:

  • To investigate the therapeutic potential of mitochondrial uncoupling using niclosamide ethanolamine (NEN) in T2D.
  • To determine the effects of NEN on the development of T2D and its complications (DPN, DKD, DR) in a mouse model.

Main Methods:

  • BKS-db/db mice, a model for T2D, were treated with NEN from 6 to 24 weeks of age.
  • Evaluated the impact of NEN treatment on T2D progression and the development of DPN, DKD, and DR.

Main Results:

  • NEN treatment showed minimal effect on the development of T2D.
  • NEN treatment did not significantly alter the progression of DPN, DKD, or DR.
  • Global mitochondrial uncoupling did not provide therapeutic benefit for the studied diabetic complications.

Conclusions:

  • Targeting mitochondria globally with an uncoupling agent like NEN is unlikely to be an effective therapeutic strategy for DPN, DKD, or DR in T2D.
  • Further research is needed to understand tissue-specific metabolic reprogramming in the pathogenesis of diabetic complications.

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