cytochrome c/obesitas

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Therapeutic assessment of cytochrome C for the prevention of obesity through endothelial cell-targeted nanoparticulate system.

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Because the functional apoptosis-initiating protein, cytochrome C (CytC) is rapidly cleared from the circulation (t1/2 (half-life): 4 minutes), it cannot be used for in vivo therapy. We report herein on a hitherto unreported strategy for delivering exogenous CytC as a potential and safe antiobesity

Activities of cytochrome c oxidase and citrate synthase in lymphocytes of obese and normal-weight subjects.

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BACKGROUND Obesity represents a heterogeneous group of disorders associated with broad spectrum of metabolic and endocrine abnormalities. The metabolic changes in obesity may also concern the efficacy of mitochondrial system of energy provision. The aim of our study was to analyse activities of

Circulating levels of cytochrome C, gamma-glutamyl transferase, triglycerides and unconjugated bilirubin in overweight/obese patients with non-alcoholic fatty liver disease.

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Non-alcoholic fatty liver disease, characterized by hepatocyte apoptosis, is distinct in fatty liver and non-alcoholic steatohepatitis, the more severe form. Apoptotic cell death is caspase-dependent and associated with mitochondrial membrane depolarization and cytochrome c release. Adhering to the

Anti-obesity and anti-tumor pro-apoptotic peptides are sufficient to cause release of cytochrome c from vesicles.

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Peptides that target tissue for an apoptotic death have potential as therapeutics in a variety of disease conditions. The class of peptides described herein enters the cell through a specific receptor-mediated interaction. Once inside the cell, the peptide migrates toward the mitochondria, where the

Bariatric Surgery Reduces Elevated Urinary Mitochondrial DNA Copy Number in Patients With Obesity.

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Obesity is an independent risk factor for chronic kidney disease. Recently, urinary mitochondrial DNA (mtDNA) has been used as a surrogate marker of mitochondrial damage in various kidney diseases. However, there are no data regarding its use in patients with obesity or the change in

PGC-1alpha's relationship with skeletal muscle palmitate oxidation is not present with obesity despite maintained PGC-1alpha and PGC-1beta protein.

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Reduced skeletal muscle mitochondrial content and fatty acid oxidation are associated with obesity and insulin resistance. Although the exact mechanisms remain elusive, this may result from impaired mitochondrial biogenesis or reductions in the mitochondrial reticulum network. Therefore, the purpose

High free fatty acids level related with cardiac dysfunction in obese rats.

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OBJECTIVE To determine whether reducing free fatty acids (FFAs) concentration has a protective effect on cardiac structure and function in high-fat-diet-induced obese rat. METHODS Sprague-Dawley rats were randomly divided into normal control, obesity and fenofibrate group. After 8 or 16 weeks, the

Melinjo (Gnetum gnemon L.) seed extract induces uncoupling protein 1 expression in brown fat and protects mice against diet-induced obesity, inflammation, and insulin resistance.

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Dietary supplementation with melinjo (Gnetum gnemon L.) seed extract (MSE) has been proposed as an anti-obesity strategy. However, it remains unclear how MSE modulates energy balance. We tested the hypothesis that dietary MSE reduces energy intake and/or increases physical activity and metabolic

Roux-en-Y gastric bypass improves hepatic mitochondrial function in obese rats.

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BACKGROUND Obesity-related fatty liver disease is linked to mitochondrial dysfunction and oxidative stress. Nuclear factor (erythroid-derived 2)-like 2 (Nrf2) regulates mitochondrial function and is a transcriptor of multiple genes that produce antioxidants. Because Roux-en-Y gastric bypass (RYGB)

Mutations in COA3 cause isolated complex IV deficiency associated with neuropathy, exercise intolerance, obesity, and short stature.

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BACKGROUND We investigated a subject with an isolated cytochrome c oxidase (COX) deficiency presenting with an unusual phenotype characterised by neuropathy, exercise intolerance, obesity, and short stature. RESULTS Blue-native polyacrylamide gel electrophoresis (BN-PAGE) analysis showed an almost

Physical exercise promotes memory capability by enhancing hippocampal mitochondrial functions and inhibiting apoptosis in obesity-induced insulin resistance by high fat diet.

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A high-fat diet induces obesity in mice, leading to insulin resistance, decreased mitochondrial function, and increased apoptosis in the hippocampus, which eventually result in memory loss. The present study investigated the effect of physical exercise on memory, hippocampal mitochondrial function,

Exendin-4 protected against critical limb ischemia in obese mice.

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This study tested the hypothesis that exendin-4 protects against critical limb ischemia (CLI) in obese mice undergoing hypoxic stress (H). B6 mice were categorized into aged-matched control (C)-H (group 1-A), obesity (induced by high-fat diet) (O)-H (group 1-B), C-H-CLI (group 2-A), O-H-CLI (group

The coexistence of nocturnal sustained hypoxia and obesity additively increases cardiac apoptosis.

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BACKGROUND nocturnal sustained hypoxia during sleeping time has been reported in severe obesity, but no information regarding the cardiac molecular mechanism in the coexistence of nocturnal sustained hypoxia and obesity is available. This study evaluates whether the coexistence of nocturnal

Impact of obesity control on circulating level of endothelial progenitor cells and angiogenesis in response to ischemic stimulation.

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OBJECTIVE We tested the hypothesis that obesity reduced circulating number of endothelial progenitor cells (EPCs), angiogenic ability, and blood flow in ischemic tissue that could be reversed after obesity control. METHODS 8-week-old C57BL/6J mice (n=27) were equally divided into group 1 (fed with

Mitochondrial apoptotic signaling is elevated in cardiac but not skeletal muscle in the obese Zucker rat and is reduced with aerobic exercise.

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Mitochondrial apoptosis and apoptotic signaling modulations by aerobic training were studied in cardiac and skeletal muscles of obese Zucker rats (OZR), a rodent model of metabolic syndrome. Comparisons were made between left ventricle, soleus, and gastrocnemius muscles from OZR (n = 16) and

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