scholarly journals Impaired Mitochondrial Respiration in Large Cerebral Arteries of Rats with Type 2 Diabetes

2017 ◽  
Vol 54 (1) ◽  
pp. 1-12 ◽  
Author(s):  
Ivan Merdzo ◽  
Ibolya Rutkai ◽  
Venkata N.L.R. Sure ◽  
Catherine A. McNulty ◽  
Prasad V.G. Katakam ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Mitochondrial Respiration ◽  
Cerebral Arteries

scholarly journals Modifications in Retinal Mitochondrial Respiration Precede Type 2 Diabetes and Protracted Microvascular Retinopathy

2017 ◽  
Vol 58 (10) ◽  
pp. 3826 ◽  
Author(s):  
Woo Hyun Han ◽  
Jonathan Gotzmann ◽  
Sharee Kuny ◽  
Hui Huang ◽  
Catherine B. Chan ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Mitochondrial Respiration

scholarly journals Effect of Hyperglycemia on Mitochondrial Respiration in Type 2 Diabetes

2009 ◽  
Vol 94 (4) ◽  
pp. 1372-1378 ◽  
Author(s):  
Rasmus Rabøl ◽  
Patricia M. V. Højberg ◽  
Thomas Almdal ◽  
Robert Boushel ◽  
Steen B. Haugaard ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Mitochondrial Respiration

Opposite effects of pioglitazone and rosiglitazone on mitochondrial respiration in skeletal muscle of patients with type 2 diabetes

2010 ◽  
Vol 12 (9) ◽  
pp. 806-814 ◽  
Author(s):  
R. Rabøl ◽  
R. Boushel ◽  
T. Almdal ◽  
C. N. Hansen ◽  
T. Ploug ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Skeletal Muscle ◽  
Mitochondrial Respiration

scholarly journals Inhibitory Effect of Metformin on Oxidation of NADH-Dependent Substrates in Rat Liver Homogenate

2011 ◽  
pp. 835-839 ◽  
Author(s):  
E. PÁLENÍČKOVÁ ◽  
M. CAHOVÁ ◽  
Z. DRAHOTA ◽  
L. KAZDOVÁ ◽  
M. KALOUS
Keyword(s):  
Type 2 Diabetes ◽  
Mitochondrial Respiration ◽  
Complex I ◽  
Liver Homogenate ◽  
Inhibitory Effect ◽  
Small Samples ◽  
Inhibitory Effects ◽  
Experimental Conditions ◽  
Wet Weight

Metformin is widely used in the treatment of Type 2 diabetes, however, mechanisms of its antihyperglycemic effect were not yet fully elucidated. Complex I of mitochondrial respiration chain is considered as one of the possible targets of metformin action. In this paper, we present data indicating that the inhibitory effect of metformin can be tested also in liver homogenate. Contrary to previous findings on hepatocytes or mitochondria under our experimental conditions, lower metformin concentrations and shorter time of preincubation give significant inhibitory effects. These conditions enable to study the mechanism of the inhibitory effect of metformin in small samples of biological material (50-100 mg wet weight) and compare more experimental groups of animals because isolation of mitochonria is unnecessary.

scholarly journals Regional Anatomic Differences in Skeletal Muscle Mitochondrial Respiration in Type 2 Diabetes and Obesity

2010 ◽  
Vol 95 (2) ◽  
pp. 857-863 ◽  
Author(s):  
R. Rabøl ◽  
S. Larsen ◽  
P. M. V. Højberg ◽  
T. Almdal ◽  
R. Boushel ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Skeletal Muscle ◽  
Mitochondrial Respiration ◽  
Diabetes And Obesity

scholarly journals Type 2 Diabetes and Cardiovascular Factors Contrasted with Fibrinolysis Disorders in the Blood of Patients with Peripheral Arterial Disease

Medicina ◽  
2019 ◽  
Vol 55 (7) ◽  
pp. 395 ◽  
Author(s):  
Radosław Wieczór ◽  
Anna Maria Wieczór ◽  
Arleta Kulwas ◽  
Danuta Rość
Keyword(s):  
Type 2 Diabetes ◽  
Endothelial Dysfunction ◽  
Peripheral Arterial Disease ◽  
Plasminogen Activator ◽  
Cerebral Arteries ◽  
Arterial Disease ◽  
Peripheral Arterial ◽  
Pai 1 ◽  
D Dimer

Background and objectives: Both in the pathogenesis of type 2 diabetes (DM 2) and Peripheral Arterial Disease (PAD), a vital role is played by endothelial dysfunction. Metabolic disorders found in DM 2 (hyperglycemia, insulin resistance), endothelial dysfunction, and increased inflammation lead to intensified atherothrombosis. The fibrinolysis system comprises a natural compensatory mechanism in case of hypercoagulability. The aim of this study was to assess concentrations of selected fibrinolysis parameters in the blood of patients with symptomatic PAD, including in particular concurrent DM 2 and other cardiovascular factors. Materials and Methods: In the group of 80 patients with PAD (27 F/53 M) and 30 healthy volunteers (10 F/20 M), the following parameters were measured: Concentrations of fibrinogen, tissue-Plasminogen Activator (t-PA Ag), Plasminogen Activator Inhibitor-1 (PAI-1 Ag), D-dimer, and platelet (PLT) count. Results: In the blood of patients with PAD and concomitant DM 2 significantly higher concentrations of fibrinogen were found in comparison with patients with PAD and without diabetes (p = 0.044). No significant impact was observed in individuals with atherosclerotic complications (manifested by coronary artery disease, atherosclerosis of cerebral arteries) and selected cardiovascular risk factors (smoking, LDL and triglyceride concentrations, BP values) on the levels of t-PA, PAI-1, D-dimer, and PLT count. It was found that t-PA Ag and PAI-1 Ag values tended to rise along with a BMI increase in the subgroups of subjects (with normal body mass, overweight, and obesity), but no statistically significant differences were observed. However, two significant positive correlations were reported between t-PA Ag and BMI, as well as between PAI-1 Ag and BMI. Conclusions: Type 2 diabetes in peripheral arterial disease affects the concentration of fibrinogen causing its increase, which is connected with the inflammation and prothrombotic process in the course of both conditions. The concurrence of atherosclerosis of coronary or cerebral arteries, smoking, LDL and TG concentrations, and BP value do not have a significant impact on the levels of analyzed fibrinolysis parameters. A positive correlation between BMI and t-PA Ag and PAI-1 Ag concentrations needs to be supported in further studies on a larger number of overweight and obese patients.

scholarly journals Effects of prolonged type 2 diabetes on mitochondrial function in cerebral blood vessels

2019 ◽  
Vol 317 (5) ◽  
pp. H1086-H1092 ◽  
Author(s):  
Ivan Merdzo ◽  
Ibolya Rutkai ◽  
Venkata N. L. R. Sure ◽  
Prasad V. G. Katakam ◽  
David W. Busija
Keyword(s):  
Diabetes Mellitus ◽  
Reactive Oxygen Species ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Mitochondrial Function ◽  
Mitochondrial Respiration ◽  
Ros Production ◽  
Oxygen Species ◽  
Cerebral Blood Vessels

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 ( P = 0.08). Other mitochondrial proteins were unaffected, which might indicate the existence of compensatory mechanisms with extension of this relatively mild form of diabetes. Superoxide levels were significantly higher in large cerebral vessels of diabetic animals compared with the control group. In conclusion, prolonged dietary diabetes leads to stabilization, rather than deterioration, of metabolic status in the cerebral circulation, despite continued overproduction of ROS. NEW & NOTEWORTHY We have characterized for the first time the dynamics of mitochondrial function during the progression of type 2 diabetes mellitus with regard to mitochondrial respiration, protein expression, and reactive oxygen species production. In addition, this is the first measurement of rattin levels in the cerebral vasculature, which could potentially lead to novel treatment options.

scholarly journals Endurance training remodels skeletal muscle phospholipid composition and increases intrinsic mitochondrial respiration in men with Type 2 diabetes

2019 ◽  
Vol 51 (11) ◽  
pp. 586-595 ◽  
Author(s):  
Maria F. Pino ◽  
Natalie A. Stephens ◽  
Alexey M. Eroshkin ◽  
Fanchao Yi ◽  
Andrew Hodges ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Skeletal Muscle ◽  
Insulin Sensitivity ◽  
Endurance Training ◽  
Mitochondrial Function ◽  
Mitochondrial Respiration ◽  
Phospholipid Composition ◽  
Rna Seq ◽  
Mitochondrial Dna Copy Number

The effects of exercise training on the skeletal muscle (SKM) lipidome and mitochondrial function have not been thoroughly explored in individuals with Type 2 diabetes (T2D). We hypothesize that 10 wk of supervised endurance training improves SKM mitochondrial function and insulin sensitivity that are related to alterations in lipid signatures within SKM of T2D (males n = 8). We employed integrated multi-omics data analyses including ex vivo lipidomics (MS/MS-shotgun) and transcriptomics (RNA-Seq). From biopsies of SKM, tissue and primary myotubes mitochondrial respiration were quantified by high-resolution respirometry. We also performed hyperinsulinemic-euglycemic clamps and blood draws before and after the training. The lipidomics analysis revealed that endurance training (>95% compliance) increased monolysocardiolipin by 68.2% ( P ≤ 0.03), a putative marker of mitochondrial remodeling, and reduced total sphingomyelin by 44.8% ( P ≤ 0.05) and phosphatidylserine by 39.7% ( P ≤ 0.04) and tended to reduce ceramide lipid content by 19.8%. Endurance training also improved intrinsic mitochondrial respiration in SKM of T2D without alterations in mitochondrial DNA copy number or cardiolipin content. RNA-Seq revealed 71 transcripts in SKM of T2D that were differentially regulated. Insulin sensitivity was unaffected, and HbA1c levels moderately increased by 7.3% despite an improvement in cardiorespiratory fitness (V̇o2peak) following the training intervention. In summary, endurance training improves intrinsic and cell-autonomous SKM mitochondrial function and modifies lipid composition in men with T2D independently of alterations in insulin sensitivity and glycemic control.

Relationship Between Mitochondrial Respiration and Glucose Tolerance in Individuals at Risk of Type 2 Diabetes

2017 ◽  
Vol 49 (5S) ◽  
pp. 1021
Author(s):  
Justin J. Reid ◽  
Adam R. Konopka ◽  
William M. Castor ◽  
Jaime L. Laurin ◽  
Chistopher A. Wolff ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
At Risk ◽  
Glucose Tolerance ◽  
Mitochondrial Respiration
Sign in / Sign up

Export Citation Format

Share Document