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Impact of obesity-induced type 2 diabetes on long-term outcomes following stroke.

Authors
  • Bhaskar, Sonu1, 2, 3, 4, 5
  • 1 Department of Neurology and Neurophysiology, Liverpool Hospital, Sydney, NSW, Australia [email protected] , (Australia)
  • 2 The University of New South Wales (UNSW), South West Sydney Clinical School, Sydney, NSW, Australia. , (Australia)
  • 3 NSW Brain Clot Bank and Neurovascular Imaging Lab, Ingham Institute for Applied Medical Research, Liverpool, NSW, Australia. , (Australia)
  • 4 South Western Sydney Local Health District (SWSLHD), South Western Sydney Research, Liverpool, NSW, Australia. , (Australia)
  • 5 Western Sydney University, School of Medicine, South Western Sydney Clinical School, Liverpool, NSW, Australia. , (Australia)
Type
Published Article
Journal
Clinical Science
Publisher
Portland Press
Publication Date
Jul 31, 2019
Volume
133
Issue
14
Pages
1603–1607
Identifiers
DOI: 10.1042/CS20190492
PMID: 31331992
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Diabetes is associated with poor recovery profiles following stroke. The pathophysiological mechanisms by which diabetes mediates neurological recovery after stroke are debatable. A recent paper published in the Clinical Science by Pintana et al. (Clinical Science (2019)133, 1367-1386) provides a possible explanation for the underlying mechanisms of poor long-term motor recovery after stroke in obesity-induced diabetes animal model. Authors report that stroke-induced neurogenesis and parvalbumin (PV)+ interneuron-mediated neuroplasticity is severely impaired due to obesity-induced type 2 diabetes (T2D). Poor long-term motor recovery after stroke in comorbid obese and diabetic mice was not associated with stroke-induced grey or white matter damage. Understanding these mechanisms is crucial to develop therapeutic strategies to improve recovery in the obesity-induced diabetic population. The strength of the present study lies in the use of a comorbid obese/diabetic animal model, which is more likely to reflect the clinical scenario. However, these findings should be understood from the context of this specific animal model and whether these findings hold true for another variant of the obesity/T2D model warrants further consideration. This is an interesting study from the perspective of understanding the stroke pathology in T2D; however, the interaction of microvascular changes (including vascular modelling, angiogenesis), oxidative stress and insulin resistance (IR) associated with T2D and poor recovery profile merit further discussions. Given the increasing burden of obesity, diabetes and/or stroke globally, understanding of mechanisms may be useful in developing cardiovascular risk management pathways in this subgroup of population who are at increased risk of poor clinical outcomes following acute stroke. © 2019 The Author(s). Published by Portland Press Limited on behalf of the Biochemical Society.

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