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MitoQ Healthy Living Blog

Diabetes

  • The mitochondrial-targeted antioxidant MitoQ ameliorates metabolic syndrome features in obesogenic diet-fed rats better than Apocynin or Allopurinol

    The prevalence of metabolic syndrome (MetS) components including obesity, dyslipidemia, insulin resistance (IR), and hepatic steatosis is rapidly increasing in wealthy societies. It is accepted that inflammation/oxidative stress are involved in the initiation/evolution of the MetS features. The present work was designed to evaluate the effects of three major cellular ROS production systems on obesity, glucose tolerance, and hepatic steatosis development and on oxidative stress onset .. (more)

  • A mitochondrial-targeted coenzyme q analog prevents weight gain and ameliorates hepatic dysfunction in high-fat-fed mice.

    We hypothesized that the mitochondrial-targeted antioxidant, mitoquinone (mitoQ), known to have mitochondrial uncoupling properties, might prevent the development of obesity and mitigate liver dysfunction by increasing energy expenditure, as opposed to reducing energy intake. We administered mitoQ or vehicle (ethanol) to obesity-prone C57BL/6 mice fed high-fat (HF) or normal-fat (NF) diets. MitoQ (500 µM) or vehicle (ethanol) was added to the drinking water for 28 weeks. MitoQ significantly reduced total body mass and fat mass ... (more)

  • Prevention of diabetic nephropathy in Ins2(+/)⁻(AkitaJ) mice by the mitochondria-targeted therapy MitoQ

    Mitochondrial production of ROS (reactive oxygen species) is thought to be associated with the cellular damage resulting from chronic exposure to high glucose in long-term diabetic patients. We hypothesized that a mitochondria-targeted antioxidant would prevent kidney damage in the Ins2(+/)⁻(AkitaJ) mouse model (Akita mice) of Type 1 diabetes. To test this we orally administered a mitochondria-targeted ubiquinone (MitoQ) over a 12-week period and assessed tubular and glomerular function. Fibrosis and pro-fibrotic signalling pathways were determined by immunohistochemical analysis, and mitochondria were isolated from the kidney for functional assessment. MitoQ treatment improved tubular and glomerular function in the Ins2(+/)⁻(AkitaJ) mice. MitoQ did not have a significant effect on plasma creatinine levels, but decreased urinary albumin levels to the same level as non-diabetic controls. Consistent with previous studies, renal mitochondrial function showed no significant change between any of the diabetic or wild-type groups. Importantly, interstitial fibrosis and glomerular damage were significantly reduced in the treated animals. The pro-fibrotic transcription factors phospho-Smad2/3 and β-catenin showed a nuclear accumulation in the Ins2(+/)⁻(AkitaJ) mice, which was prevented by MitoQ treatment. These results support the hypothesis that mitochondrially targeted therapies may be beneficial in the treatment of diabetic nephropathy. They also highlight a relatively unexplored aspect of mitochondrial ROS signalling in the control of fibrosis. (more)

  • Mitochondrial Dysfunction and Complications Associated with Diabetes

    Diabetes is a metabolic syndrome that results in chronically increased blood glucose (hyperglycaemia) due to defects either in insulin secretion consequent to the loss of beta cells in the pancreas (Type 1) or to loss of insulin sensitivity in target organs in the presence of normal insulin secretion (Type 2). Long term hyperglycaemia can lead to a number of serious health-threatening pathologies, or complications, especially in the kidney, heart, retina and peripheral nervous system. (more)

  • Mitochondria-targeted antioxidants protect pancreatic β-cells against oxidative stress and improve insulin secretion in glucotoxicity and glucolipotoxicity.

    Mitochondrial oxidative damage is thought to play a key role in pancreatic β-cell failure in the pathogenesis of type 2 diabetes. Despite this, the potential of mitochondria-targeted antioxidants to protect pancreatic β-cells against oxidative stress has not yet been studied. Therefore, we investigated if mitochondria-targeted antioxidants protect pancreatic β-cells such as RINm5F and HIT-T15 cells against oxidative stress under glucotoxic and glucolipotoxic conditions. (more)

  • Boosting mitochondrial biogenesis in white adipocytes: A route towards improved insulin sensitivity?

    Mitochondria are the central players in cellular bioenergetics. Via the tricarboxylic acid (TCA) cycle and the oxidative phosphorylation (OXPHOS) process of the respiratory chain, energy supplied by nutrients is converted to adenosine triphosphate (ATP). Impaired mitochondrial OXPHOS capacity plays a crucial role in the pathogenesis of numerous disorders [1]. In recent years, research interests are increasingly focused on a potential link between white adipocyte mitochondrial dysfunction and the pathogenesis of obesity driven insulin resistance and diabetes mellitus type 2 (T2DM). (more)

  • Accelerated aging as evidenced by increased telomere shortening and mitochondrial DNA depletion in patients with type 2 diabetes.

    Although shortened telomeres were shown associated with several risk factors of diabetes, there is lack of data on their relationship with mitochondrial dysfunction. Therefore, we compared the relationship between telomere length and mitochondrial DNA (mtDNA) content in patients with type 2 diabetes mellitus (T2DM; n = 145) and in subjects with normal glucose tolerance (NGT; n = 145). (more)

  • The mitochondria-targeted antioxidant MitoQ decreases features of the metabolic syndrome in ATM+/–/ApoE–/– mice

    A number of recent studies suggest that mitochondrial oxidative damage may be associated with atherosclerosis and the metabolic syndrome. However, much of the evidence linking mitochondrial oxidative damage and excess reactive oxygen species (ROS) with these pathologies is circumstantial. (more)

  • Mitochondrial function, energy expenditure, aging and insulin resistance.

    Mitochondria are the cells' powerhouse that produce the ubiquitous energy currency (ATP) by consuming oxygen, producing water and building up the proton motive force. Oxygen consumption is a classical means of assessing energy expenditure, one component of energy balance. When energy balance is positive, weight increases. This is observed during the dynamic phase of obesity, and during body composition changes associated with aging. Whether intrinsic defaults in mitochondria occur is the matter of this review.(more)

  • Diabetic Kidney Disease Linked to Reduced Mitochondrial Function

    Significant differences in the levels of 12 metabolites between patients with diabetes mellitus andchronic kidney disease (CKD) and others indicate that mitochondria suppression is a fundamental characteristic of diabetes-related kidney disease. (more)

     

     

     

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