ArticleAmerican journal of physiology. Heart and circulatory physiology2019
Effects of prolonged type 2 diabetes on mitochondrial function in cerebral blood vessels.
Article in American journal of physiology. Heart and circulatory physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- APOE4 negates the effects of ovarian hormones on cerebrovascular endothelial and mitochondrial function.The Journal of physiology · 2026Article
- Predictive Model for In-Hospital Death in Older Patients with Type 2 Diabetes Mellitus: A Multicenter Retrospective Study in Southwest China.Diabetes, metabolic syndrome and obesity : targets and therapy · 2025Article
- Three-dimensional object geometry of mitochondria-associated signal: 3-D analysis pipeline for two-photon image stacks of cerebrovascular endothelial mitochondria.American journal of physiology. Heart and circulatory physiology · 2024Article
- The role of telomerase reverse transcriptase in the mitochondrial protective functions of Angiotensin-(1-7) in diabetic CD34Biochemical pharmacology · 2024Article
- Oxidative Regulation of Vascular CaAntioxidants (Basel, Switzerland) · 2022Review
- Detrimental effects of transient cerebral ischemia on middle cerebral artery mitochondria in female rats.American journal of physiology. Heart and circulatory physiology · 2022Article
- Associations between serum mitokine levels and outcomes in stable COPD: an observational prospective study.Scientific reports · 2022Observational
- Oxidative Stress, GTPCH1, and Endothelial Nitric Oxide Synthase Uncoupling in Hypertension.Antioxidants & redox signaling · 2021Review
- GSTM1-null allele predicts rapid disease progression in nondialysis patients and mortality among South Indian ESRD patients.Molecular and cellular biochemistry · 2020Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 2 countries.
Funding
Abstract
One of the major characteristics of hyperglycemic states such as type 2 diabetes is increased reactive oxygen species (ROS) generation. Since mitochondria are a major source of ROS, it is vital to understand the involvement of these organelles in the pathogenesis of ROS-mediated conditions. Therefore, we investigated mitochondrial function and ROS production in cerebral blood vessels of 21-wk-old Zucker diabetic fatty obese rats and their lean controls. We have previously shown that in the early stages of insulin resistance, and short periods of type 2 diabetes mellitus, only mild differences exist in mitochondrial function. In the present study, we examined mitochondrial respiration, mitochondrial protein expression, and ROS production in large-surface cerebral arteries. We used 21-wk-old animals exposed to peak glucose levels for 7 wk and compared them with our previous studies on younger diabetic animals. We found that the same segments of mitochondrial respiration (basal respiration and proton leak) were diminished in diabetic groups as they were in younger diabetic animals. Levels of rattin, a rat humanin analog, tended to decrease in the diabetic group but did not reach statistical significance (
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.