Alterations in Energy Metabolism, Mitochondrial Function and Redox Homeostasis in GK Diabetic Rat Tissues Treated with Aspirin.
CYP 450s
GK rat
aspirin
diabetes
mitochondrial bioenergetics
redox metabolism
Journal
Life (Basel, Switzerland)
ISSN: 2075-1729
Titre abrégé: Life (Basel)
Pays: Switzerland
ID NLM: 101580444
Informations de publication
Date de publication:
12 Jan 2022
12 Jan 2022
Historique:
received:
12
12
2021
revised:
04
01
2022
accepted:
10
01
2022
entrez:
21
1
2022
pubmed:
22
1
2022
medline:
22
1
2022
Statut:
epublish
Résumé
Our recent studies have demonstrated that aspirin treatment prevents inflammatory and oxidative stress-induced alterations in mitochondrial function, improves glucose tolerance and pancreatic endocrine function and preserves tissue-specific glutathione (GSH)-dependent redox homeostasis in Goto-Kakizaki (GK) diabetic rats. In the current study, we have investigated the mechanism of action of aspirin in maintaining mitochondrial bioenergetics and redox metabolism in the liver and kidneys of GK rats. Aspirin reduced the production of reactive oxygen species (ROS) and oxidative stress-induced changes in GSH metabolism. Aspirin treatment also improved mitochondrial respiratory function and energy metabolism, in addition to regulating the expression of cell signaling proteins that were altered in diabetic animals. Ultrastructural electron microscopy studies revealed decreased accumulation of glycogen in the liver of aspirin-treated diabetic rats. Hypertrophic podocytes with irregular fusion of foot processes in the renal glomerulus and detached microvilli, condensed nuclei and degenerated mitochondria observed in the proximal convoluted tubules of GK rats were partially restored by aspirin. These results provide additional evidence to support our previous observation of moderation of diabetic complications by aspirin treatment in GK rats and may have implications for cautious use of aspirin in the therapeutic management of diabetes.
Identifiants
pubmed: 35054496
pii: life12010104
doi: 10.3390/life12010104
pmc: PMC8780217
pii:
doi:
Types de publication
Journal Article
Langues
eng
Subventions
Organisme : Sheikh Hamdan Bin Rashid Al Maktoum Award for Medical Sciences
ID : MRG-01/2011-2012
Organisme : Research Committee, College of Medicine, UAE University
ID : NP-14/01 and NP-20/13
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