Skeletal muscle metabolism is highly dependent on mitochondrial function, with impaired mitochondrial biogenesis associated with the development of metabolic diseases such as insulin resistance and type 2 diabetes. Mitochondria display substantial plasticity in skeletal muscle, and are highly sensitive to levels of physical activity. It is thought that physical activity promotes mitochondrial biogenesis in skeletal muscle through increased expression of genes encoded in both the nuclear and the mitochondrial genome; however, how this process is co-ordinated at the cellular level is poorly understood. Nuclear receptors (NRs) are key signalling proteins capable of integrating environmental factors and mitochondrial function, thereby providing a potential link between exercise and mitochondrial biogenesis. The aim of this review is to highlight the function of NRs in skeletal muscle mitochondrial biogenesis and discuss the therapeutic potential of NRs for the management and treatment of chronic ...

TY - JOUR. T1 - Obesity modifies the stoichiometry of mitochondrial proteins in a way that is distinct to the subcellular localization of the mitochondria in skeletal muscle. AU - Kras, Katon A.. AU - Langlais, Paul R.. AU - Hoffman, Nyssa. AU - Roust, Lori R.. AU - Benjamin, Tonya R.. AU - De Filippis, Elena A.. AU - Dinu, Valentin. AU - Katsanos, Christos S.. N1 - Funding Information: This work was supported by National Institutes of Health/ National Institute of Diabetes and Digestive and Kidney Diseases grant R01DK094062 (CSK). PY - 2018/12. Y1 - 2018/12. N2 - Background: Skeletal muscle mitochondrial content and function appear to be altered in obesity. Mitochondria in muscle are found in well-defined regions within cells, and they are arranged in a way that form distinct subpopulations of subsarcolemmal (SS) and intermyofibrillar (IMF) mitochondria. We sought to investigate differences in the proteomes of SS and IMF mitochondria between lean subjects and subjects with obesity. Methods: We ...

This study was designed to examine energetic behaviour of skeletal muscle subsarcolemmal and intermyofibrillar mitochondrial populations. The data show tha

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One of the hallmarks of peripheral insulin resistance is an imbalance in lipid metabolism favoring storage, rather than oxidation, of fatty acids. Lipid accumulation is known to play a causative role in the pathogenesis of insulin resistance (27), and several investigations suggest this effect is secondary to impaired lipid disposal pathways (35, 51, 54, 56-58). Alternatively, endurance exercise training increases whole body fatty acid oxidation, which is linked, in part, to enhanced skeletal muscle mitochondrial content and hence elevated oxidative capacity, an adaptation believed to play a major role in the exercise training-mediated alleviation of insulin resistance (10, 18). Although these studies provide strong evidence indicating a positive relationship between oxidative capacity and improved insulin action, it is largely speculative, since most of the information has been collected from subjects with a preexisting insulin-resistant condition. Obscuring the issue further is the fact that ...

We used training response variation in muscle mitochondrial function in vivo (measured by PCr recovery rate) after 10 weeks of aerobic training to classify individuals with type 2 diabetes as nonresponders or responders. Individuals classified as nonresponders did not improve insulin sensitivity and worsened glycemic control with training, whereas responders improved insulin sensitivity. The training response variation in muscle mitochondrial function in vivo was marked by a distinct pretraining molecular pattern in muscle tissue and in myogenic progenitor cells (HSkMCs) of nonresponders compared with responders. DNA methylation and RNA expression patterns showed elevations in antioxidant defense, insulin signaling, and mitochondrial metabolism in nonresponders, which were reflected in vivo by higher pretraining muscle mitochondrial function and insulin sensitivity in these same individuals.. On average, exercise-training interventions improve muscle mitochondrial function (25,26) and even ...

Objective: We examined in insulin resistant muscle if, in contrast to long-standing dogma, mitochondrial fatty acid oxidation is increased, and whether this is attributed to an increased nuclear content of peroxisome proliferator-activated receptor γ co-activator 1α (PGC1α) and the adaptations of specific mitochondrial sub-populations.. Research design and methods: Skeletal muscles from male control and ZDF rats were used to determine; 1) intramuscular lipid distribution, 2) subsarcolemmal (SS) and intermyofibrillar (IMF) mitochondrial morphology, 3) rates of palmitate oxidation in SS and IMF mitochondria, and 4) the sub-cellular localization of PGC1α. Electotransfection of PGC1α-cDNA into lean animals tested the notion that increased nuclear PGC1α preferentially targeted SS mitochondria.. Results: TEM analysis revealed that in ZDF animals the number (+50%), width (+69%) and density (+57%) of SS mitochondria were increased (P,0.05). In contrast, IMF mitochondria remained largely unchanged. ...

The present study showed that early life exposure to large, phospholipid-coated lipid droplets leads to altered expression of markers for mitochondrial oxidative capacity in RP WAT and m. tibialis. Although functional mitochondrial capacity was not measured, these markers suggest that adapted mitochondrial oxidative capacity may underlie the previously reported reduced body fat accumulation in adolescence and adulthood [18-20].. Programming of metabolic health is well established, but possible underlying mechanisms are still largely unknown although many have been suggested. Aberrant mitochondrial function has been suggested in a limited amount of studies as possible link between adverse fetal environment and the development of T2D [22, 34]. Yet, little is known on how nutritional programming may improve lifelong metabolic health and protect against obesity.. In the present study, markers for mitochondrial oxidative capacity appeared to be increased due to the supramolecular structure of milk ...

Reduced skeletal muscle mitochondrial function might be a contributing mechanism to the myopathy and activity based limitations that typically plague patients with peripheral arterial disease (PAD). We hypothesized that mitochondrial dysfunction, myofiber atrophy, and muscle contractile deficits are...

Sigma-Aldrich offers abstracts and full-text articles by [Robert A Jacobs, Anne-Kristine Meinild, Nikolai B Nordsborg, Carsten Lundby].

Regular exercise has proven benefits in preventing and treating type 2 diabetes, but many patients find it tough to meet the American Diabetes Association guidelines of 150 minutes of moderate to vigorous exercise a week. A new study, conducted by researchers at McMaster University, suggests that there could be a better way. In a small proof-of-principle study in eight type 2 diabetes patients, the researchers found that exercising at a very high intensity, but for a mere 30 minutes a week within a 75 minute total time commitment, lowered overall blood sugar concentrations, reduced post-meal blood sugar spikes, and increased skeletal mitochondrial capacity, a marker of metabolic health. The findings suggest that exercising harder, but in a significantly shorter amount of time, could provide benefits similar to longer, but more moderate, activity.. The article is entitled Low-Volume High-Intensity Interval Training Reduces Hyperglycemia and Increases Muscle Mitochondrial Capacity in Patients ...

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(2009) Rönn et al. PLoS ONE. BACKGROUND: Impaired oxidative capacity of skeletal muscle mitochondria contribute to insulin resistance and type 2 diabetes (T2D). Furthermore, mRNA expression of genes involved in oxidative phosp...

Oxygen consumption (VO2), carbon dioxide production, pulmonary ventilation (Ve), and the respiratory quotient (RER) were measured using an on-line system (Medical Graphics CPX, Saint Paul, Minneapolis, MN, USA) while the subjects breathed through a low-resistance breathing valve. Gases with known VO2 and carbon dioxide consumption concentrations were used for gas analyser calibration. The heart rate was obtained from a continuously recorded electrocardiogram signal. Blood samples were drawn without stasis from a venous catheter in the forearm. In the blood samples the following parameters were assessed: blood lactate, p-pyruvate, free fatty acids (FFA), p-glycerol, p-norepinephrine and p-epinephrine. The blood- lactate levels were immediately measured using an electrolyte metabolite analyser (EML 105; Radiometer, Copenhagen). The samples were immediately frozen for later analyses of FFA, glycerol, p-pyruvate and plasma lactate using Cobas Fara 2 (Roche Diagnostics, Basel, Switzerland), whereas ...

Mitochondria play a key role in the energy metabolism in skeletal muscle. A new concept has emerged suggesting that impaired mitochondrial oxidative capacity in skeletal muscle may be the underlying defect that causes insulin resistance. According to current knowledge, the causes and the underlying molecular mechanisms at the origin of decreased mitochondrial oxidative capacity in skeletal muscle still remain to be elucidated. The present review focuses on recent data investigating these issues in the area of metabolic disorders and describes the potential causes, mechanisms and consequences of mitochondrial dysfunction in the skeletal muscle.

Low-volume high-intensity interval training (HIT) is emerging as a time-efficient exercise strategy for improving health and fitness. This form of exercise has not been tested in type 2 diabetes and thus we examined the effects of low-volume HIT on glucose regulation and skeletal muscle metabolic ca …

Flight Muscle Mitochondria This image is of non-human tissue. Flight muscle is the most powerful type of muscle, to cope with the aerobic demands of flying the balance of muscle fibres and mitochondria has to be optimal. Here we see flight muscle from a bird in a transverse cut. Mitochondria generate the energy that cells need to function. The energy made by the mitochondria is in the form of a chemical called adenosine triphosphate or ATP. The mitochondria are the pink/red structures in this image. Cellular level art, paint on silk, digitised.

Abstract Peroxisome proliferator-activated receptor-γ coactivator (PGC)-1α has been shown to play critical roles in regulating mitochondria biogenesis, respiration, and muscle oxidative phenotype. Furthermore, reductions in the expression of PGC-1α in muscle have been implicated in the pathogenesis of type 2 diabetes. To determine the effect of increased muscle-specific PGC-1α expression on muscle mitochondrial function and…

TY - JOUR. T1 - Angiotensin II reduces mitochondrial content in skeletal muscle and affects glycemic control. AU - Mitsuishi, Masanori. AU - Miyashita, Kazutoshi. AU - Muraki, Ayako. AU - Itoh, Hiroshi. PY - 2009/3. Y1 - 2009/3. N2 - OBJECTIVE-Blockade of angiotensin (Ang) II has been shown to prevent new-onset type 2 diabetes. We focused on the effects of AngII on muscle mitochondria, especially on their biogenesis, as an underlining mechanism of type 2 diabetes. RESEARCH DESIGN AND METHODS-C2C12 cells and C57bl/6 mice were used to examine roles for AngII in the regulation of muscle mitochondria and to explore whether the effect was mediated by type 1 AngII receptor (AT1R) or type 2 receptor (AT2R). RESULTS-C2C12 cells treated with 10-8-10 -6 mol/l AngII reduced the mitochondrial content associated with downregula- tion of the genes involved in mitochondrial biogenesis. The action of AngII was diminished by blockade of AT2R but not AT1R, whereas overexpression of AT2R augmented the effect. ...

Submitter supplied) Skeletal muscle insulin resistance, decreased phosphatidylinositol 3-kinase (PI3K) activation and altered mitochondrial function are hallmarks of type 2 diabetes. We created mice with a muscle-specific knockout of p110α or p110β, the two major catalytic subunits of PI3K. We find that mice with muscle-specific knockout of p110α, but not p110β, display impaired muscle insulin signaling and reduced muscle size due to enhanced proteasomal and autophagic activity. more... ...

Previous studies examining the effect of different fatty acids on insulin action have reported improved glucose tolerance and insulin tolerance in rodents fed high-fat diets rich in MCFAs compared with LCFAs (11,18,19). Our current study reveals the tissues responsible for the favorable effect of MCFAs on whole-body glucose metabolism, as well as a mechanistic basis for these effects. We have made the intriguing observation that insulin action in skeletal muscle and adipose tissue is preserved at the level of low-fat-fed controls when animals consume a high-fat diet rich in MCFAs. In muscle, the lack of induction of insulin resistance with MCFA high-fat feeding is associated with a substantial increase in mitochondrial oxidative capacity, which is sufficient to prevent lipid accumulation in this tissue. However, the liver of MCFA-fed animals accumulated greater amounts of triglycerides, likely due to upregulation of lipogenic pathways, and as such, hepatic insulin action was reduced after MCFA ...

1. L. E. Bakeeva, Chentsov YuS, and V. P. Skulachev, Mitochondrial framework (reticulum mitochondriale) in rat diaphragm muscle, Biochim. Biophys. Acta 501(3), 349-369 (1978). [CrossRef] [PubMed] 2. M. Picard, K. White, and D. M. Turnbull, Mitochondrial morphology, topology, and membrane interactions in skeletal muscle: a quantitative three-dimensional electron microscopy study, J. Appl. Physiol. 114(2), 161-171 (2013). [CrossRef] [PubMed] 3. M. Picard, B. J. Gentil, M. J. McManus, K. White, K. St Louis, S. E. Gartside, D. C. Wallace, and D. M. Turnbull, Acute exercise remodels mitochondrial membrane interactions in mouse skeletal muscle, J. Appl. Physiol. 115(10), 1562-1571 (2013). [CrossRef] [PubMed] 4. B. Glancy, L. M. Hartnell, D. Malide, Z. X. Yu, C. A. Combs, P. S. Connelly, S. Subramaniam, and R. S. Balaban, Mitochondrial reticulum for cellular energy distribution in muscle, Nature 523(7562), 617-620 (2015). [CrossRef] [PubMed] 5. J. B. Gale, Mitochondrial swelling associated ...

Although there is no specific treatment for any of the mitochondrial myopathies, physical therapy along with vitamin treatment may extend the range of movement of muscles and improve dexterity.

The current study aims at assessing the impact of Type 1 diabetes and HbA1c on muscle oxygen delivery and on muscle mitochondrial capacity. Our hypothesis is that these both steps of the oxygen cascade might be involved in the aerobic fitness impairment usually observed in poor-controlled patients.. Adults with Type 1 diabetes, aged 18-40 years, without microvascular and macrovascular diabetic complications, will be recruited among patients that regularly attend the unit of diabetology of the University Hospital of Lille and the regional hospital of Roubaix. They will be separated into 2 groups according to their glycaemic control at entrance in the study (HbA1c , 7%, HbA1c , 8%). Subsequently, two healthy control groups (checked by an OGTT) will be selected to strictly match the patients with Type 1 diabetes (age, sex, BMI, number of hours of physical activity per week, tobacco smoking). This is a cross-sectional study including 4 groups.. On their first visit, after the determination of HbA1c, ...

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PMID: 31838512 Open Access Bodis K, Jelenik T, Lundbom J, Markgraf DF, Strom A, Zaharia OP, Karusheva Y, Burkart V, Muessig K, Kupriyanova Y, Ouni M, Wolkersdorfer M, Hwang JH, Ziegler D, Schuermann A, Roden M, Szendroedi J (2019) J Clin Endocrinol Metab Abstract: Impaired adipose tissue (AT) function might induce recent-onset type 2 diabetes (T2D). Understanding AT energy metabolism could yield novel targets for the treatment of T2D. Recently diagnosed male T2D patients and healthy humans (controls, CON) of similar abdominal subcutaneous AT (SAT)-thickness, fat mass and age (n=14 each), underwent hyperinsulinemic-euglycemic clamps with [6,6-2H2]glucose and indirect calorimetry. We assessed mitochondrial efficiency (coupling: state 3/4o; proton leak: state 4o/u) via high-resolution respirometry in superficial (SSAT) and deep (DSAT) SAT-biopsies, hepatocellular lipids (HCL) and fat mass by proton-magnetic-resonance-spectroscopy and -imaging. T2D patients (known diabetes duration: 2.5 [0.1; 5.0] ...

? A In this study, the mitochondrial efficiency and metabolic activity regulation of cancer cells were discussed, which revealed that the reactive ox..

Respiration rates of muscle mitochondria in flying hummingbirds range from 7 to 10 ml of O2 per cm3 of mitochondria per min, which is about 2 times higher than the range obtained in the locomotory muscles of mammals running at their maximum aerobic capacities (VO2max). Capillary volume density is higher in hummingbird flight muscles than in mammalian skeletal muscles. Mitochondria occupy approximately 35% of fiber volume in hummingbird flight muscles and cluster beneath the sarcolemmal membrane adjacent to capillaries to a greater extent than in mammalian muscles. Measurements of protein content, citrate synthase activity, and respiratory rates in vitro per unit mitochondrial volume reveal no significant differences between hummingbird and mammalian skeletal muscle mitochondria. However, inner membrane surface areas per unit mitochondrial volume [Sv(im,m)] are higher than those in mammalian muscle. We propose that both mitochondrial volume densities and Sv(im,m) are near their maximum ...

Compartmentalization of high-energy phosphate carriers between intracellular micro-compartments is a phenomenon that ensures efficient energy use. To connect these sites, creatine kinase (CK) and adenylate kinase (AK) energy-transfer networks, which are functionally coupled to oxidative phosphorylation (OXPHOS), could serve as important regulators of cellular energy fluxes. Here, we introduce how selective permeabilization of cellular outer membrane and high-resolution respirometry can be used to study functional coupling between CK or AK pathways and OXPHOS in different cells and tissues. Using the protocols presented here the ability of creatine or adenosine monophosphate to stimulate OXPHOS through CK and AK reactions, respectively, is easily observable and quantifiable. Additionally, functional coupling between hexokinase and mitochondria can be investigated by monitoring the effect of glucose on respiration. Taken together, high-resolution respirometry in combination with permeabilization is a

The investigators will determine whether people with high muscle mitochondrial capacity produce higher amount of reactive oxygen species (ROS) on consuming high fat /high glycemic diet and thus exhibit elevated cellular oxidative damage. The investigators previously found that Asian Indian immigrants have high mitochondrial capacity in spite of severe insulin resistance. Somalians are another new immigrant population with rapidly increasing prevalence of diabetes. Both of these groups traditionally consume low caloric density diets, and the investigators hypothesize that when these groups are exposed to high-calorie Western diets, they exhibit increased oxidative stress, oxidative damage, and insulin resistance. The investigators will compare Somalians and NE Americans who are matched for age, BMI, and sex. The investigators will measure ROS production in skeletal muscle following high fat/high glycemic diet vs. healthy diet. The investigators will compare the oxidative damage to proteins, DNA, ...

Cachexia causes metabolic alterations in skeletal muscle mitochondria stimulated by inflammatory imbalance towards pro-inflammatory signaling. Previous work by our group has demonstrated that exercise significantly increases muscle mass in cases of advanced tumors in transgenic mice. Furthermore, we have discovered that the natural product Nexrutine® has anti-inflammatory properties which can be beneficial in protecting mitochondria. PURPOSE: To compare the effects of exercise and Nexrutine® on mitochondrial density in skeletal muscle taken from transgenic adenocarcinoma of the mouse prostate (TRAMP) models. METHODS: This project is a continuation of a larger study investigating the effects of exercise and Nexrutine® on the attenuation of muscle wasting in TRAMP mice. For this analysis, gastrocnemius from 14 TRAMP mice from control (n=5), Nexrutine® (600 mg/kg; n=5), and voluntary wheel running (VWR) groups (n=4) that completed 20 weeks of intervention were used. Mitochondrial activity was

Metabolic reprogramming in skeletal muscles in the human and animal models of amyotrophic lateral sclerosis (ALS) may be an important factor in the diseases progression. We hypothesized that swim training, a modulator of cellular metabolism via changes in muscle bioenergetics and oxidative stress, ameliorates the reduction in muscle strength in ALS mice. In this study, we used transgenic male mice with the G93A human SOD1 mutation B6SJL-Tg (SOD1,sup>G93A,/sup>) 1Gur/J and wild type B6SJL (WT) mice. Mice were subjected to a grip strength test and isolated skeletal muscle mitochondria were used to perform high-resolution respirometry. Moreover, the activities of enzymes involved in the oxidative energy metabolism and total sulfhydryl groups (as an oxidative stress marker) were evaluated in skeletal muscle. ALS reduces muscle strength (-70% between 11 and 15 weeks, p , 0.05), modulates muscle metabolism through lowering citrate synthase (CS) (-30% vs. WT, p = 0.0007) and increasing cytochrome c ...

Mitochondrial myopathies: Diagnosis, exercise intolerance, and treatment options. Plasma malondialdehyde increases transiently after ischemic forearm exercise

We have developed a novel method to quantitatively analyze mitochondrial positioning in three dimensions. Using this method, we compared the relative positioning of mitochondria in adult rat and rainbow trout (Oncorhynchus mykiss) ventricular myocytes. Energetic data suggest that trout, in contrast to the rat, have two subpopulations of mitochondria in their cardiomyocytes. Therefore, we speculated whether trout cardiomyocytes exhibit two types of mitochondrial patterns. Stacks of confocal images of mitochondria were acquired in live cardiomyocytes. The images were processed and mitochondrial centers were detected automatically. The mitochondrial arrangement was analyzed by calculating the three-dimensional probability density and distribution functions describing the distances between neighboring mitochondrial centers. In the rat (8 cells with a total of 7,546 mitochondrial centers), intermyofibrillar mitochondria are highly ordered and arranged in parallel strands. These strands are separated ...

PMID: 11231295 Trumbeckaite S, Opalka JR, Neuhof C, Zierz S, Gellerich FN (2001) Eur J Biochem Abstract: The involvement of mitochondrial dysfunction in septic disturbances of tissues is controversial. The aim of this study was to investigate the effects of endotoxininduced sepsis on the function of heart and skeletal muscle mitochondria. Rabbits were made septic by subcutaneous injection of endotoxin (lipopolysaccharide, LPS) from Escherichia coli at concentrations of 100 or 150 mg LPS´kg21 24 h prior to the experiments. Mitochondrial respiration was measured in saponin-skinned muscle fibers and compared with photometrically detected activities of respiratory chain enzymes as well as with function of perfused hearts. In heart fibers a dosage of 100 mg LPS´kg21 caused a significant decrease of state 3-respiration for the substrates pyruvate (238%), octanoyl-carnitine (238%) and succinate (230%) with correspondingly decreased respiratory control indexes (RCI). In addition, endotoxin caused a ...

Mitochondria play a key role in the pathogenesis of different diseases including the pathologies of the heart. According to the World Health Organization, chronic diseases are responsible for 63% of all deaths in the world, with cardiovascular disease as the leading cause of death. New findings of the cardiac muscle mitochondria functions can be further used to develop new therapeutic strategies. The most important parameters of heart mitochondrial activity are oxidative phosphorylation capacity and mitochondrial membrane potential. With these two properties of mitochondria we can determine the coupling state of respiration and the impact of the mitochondrial substrate on the membrane potential [1]. The Fluorescence module for the Oxygraph-2k (Oroboros Instruments, Innsbruck) combines optical measurement with high-resolution respirometry and with this new technology it is possible to detect changes in both parameters simultaneously. The experiments were carried out in mouse heart homogenate. The ...

Proper function of the endoplasmic reticulum (ER) and mitochondria is crucial for cellular homeostasis, and dysfunction at either site has been linked to pathophysiological states, including metabolic diseases. Although the ER and mitochondria play distinct cellular roles, these organelles also form physical interactions with each other at sites defined as mitochondria-associated ER membranes (MAMs), which are essential for calcium, lipid and metabolite exchange. Here we show that in the liver, obesity leads to a marked reorganization of MAMs resulting in mitochondrial calcium overload, compromised mitochondrial oxidative capacity and augmented oxidative stress. Experimental induction of ER-mitochondria interactions results in oxidative stress and impaired metabolic homeostasis, whereas downregulation of PACS-2 or IP3R1, proteins important for ER-mitochondria tethering or calcium transport, respectively, improves mitochondrial oxidative capacity and glucose metabolism in obese animals. These findings

A brief reminder of the benefits of bicarbonate: Regulation of hydrogen ions (H + ) or pH within homeostatic concentrations is critical for proper physiological function. The factors contributing to the change in muscle pH seen during intense exercise are numerous and the role of each factor remains hotly debated. However, classically it is believed that a large contributor of H + is through the accumulation of lactate produced from glycolysis. Next to internal buffers, which are exhausted relatively quickly, the shuttling of H + and lactate across the sarcolemma is also believed to play an important role in the maintenance of pH during intense exercise. This is due to the extracellular buffering capacity HCO3 - which is believed to promote the efflux of H + from active muscles ( Hollidge-Horvat. 2000; Bishop. 2004 ...

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As noted above, the MTT assay is really a metabolic assay because the MTT molecule needs to enter a cell and get converted to Formazan using NADPH. While the exact mechanism of MTTs metabolism isnt clear, this means the mitochondria needs to be intact and functioning. So, if you add a cytotoxic material which reduces mitochondrial efficiency, you might get weird results. In this case, its useful to also know other live/dead assays. The other major cell viability assays that are used in research include:. Cell Titer Blue: Similar to the MTT Assay, this assay involves incubating cells with resazurin (blue) and forming resorfurin (pink) after the cells metabolize it. Generally the metabolism takes 1-4 hours but it is much more sensitive than the MTT assay because you can measure the product via fluorescence (Ex/Em 560 nm/590 nm). The main advantage of this assay is that you dont need to resolubilize the product in DMF/SDS so its much simpler. This is also a great high throughput assay!. Trypan ...

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Growth restriction impacts on offspring development and increases their risk of disease in adulthood which is exacerbated with second hits. The aim of this study was to investigate if blood pressure, glucose tolerance, and skeletal muscle mitochondrial biogenesis were altered in 12-month-old male and female offspring with prenatal or postnatal growth restriction. Bilateral uterine vessel ligation induced uteroplacental insufficiency and growth restriction in offspring (Restricted). A sham surgery was also performed during pregnancy (Control) and some litters from sham mothers had their litter size reduced (Reduced litter), which restricted postnatal growth. Growth-restricted females only developed hypertension at 12 months, which was not observed in males. In Restricted females only homeostasis model assessment for insulin resistance was decreased, indicating enhanced hepatic insulin sensitivity, which was not observed in males. Plasma leptin was increased only in the Reduced males at 12 ...

Mitochondria are small, energy-producing structures vital to the energy needs of the body. Genetic mutations cause mitochondria to fail to produce the energy needed by cells and organs which can cause severe disease and death. These genetic mutations are likely to be in the mitochondrial DNA (mtDNA), or possibly in the nuclear DNA (nDNA). The goal of this review is to assess the current understanding of mitochondrial diseases. This review focuses on the pathology, causes, risk factors, symptoms, prevalence data, symptomatic treatments, and new research aimed at possible preventions and/or treatments of mitochondrial diseases. Mitochondrial myopathies are mitochondrial diseases that cause prominent muscular symptoms such as muscle weakness and usually present with a multitude of symptoms and can affect virtually all organ systems. There is no cure for these diseases as of today. Treatment is generally supportive and emphasizes symptom management. Mitochondrial diseases occur infrequently and hence

TY - JOUR. T1 - Disruption of Snf3/Rgt2 glucose sensors decreases lifespan and caloric restriction effectiveness through Mth1/Std1 by adjusting mitochondrial efficiency in yeast. AU - Choi, Kyung Mi. AU - Kwon, Young Yon. AU - Lee, Cheol-Koo. PY - 2015/1/30. Y1 - 2015/1/30. N2 - Down-regulation of intracellular nutrient signal pathways was proposed to be a primary mechanism of caloric restriction (CR)-mediated lifespan extension. However, the link between lifespan and glucose sensors in the plasma membrane was poorly understood in yeast. Herein, a mutant that lacked glucose sensors (snf3Δrgt2Δ) had impaired glucose fermentation, showed decreased chronological lifespan (CLS), and reduced CLS extension by CR. The mutant also had reduced mitochondrial efficiency, as inferred by increased mitochondrial superoxide and decreased ATP levels. Mth1 and Std1, which are downstream effectors of the Snf3/Rgt2 pathway, were required for viability through mitochondrial function but not fermentative ...

TY - JOUR. T1 - Pgc-1α as a pivotal factor in lipid and metabolic regulation. AU - Cheng, Ching Feng. AU - Ku, Hui Chen. AU - Lin, Heng. PY - 2018/11/2. Y1 - 2018/11/2. N2 - Traditionally, peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α), a 91 kDa transcription factor, regulates lipid metabolism and long-chain fatty acid oxidation by upregulating the expression of several genes of the tricarboxylic acid cycle and the mitochondrial fatty acid oxidation pathway. In addition, PGC-1α regulates the expression of mitochondrial genes to control mitochondria DNA replication and cellular oxidative metabolism. Recently, new insights showed that several myokines such as irisin and myostatin are epigenetically regulated by PGC-1α in skeletal muscles, thereby modulating systemic energy balance, with marked expansion of mitochondrial volume density and oxidative capacity in healthy or diseased myocardia. In addition, in our studies evaluating whether PGC-1α overexpression in ...

MCFAs reduce adiposity and preserve insulin action in muscle and adipose, despite inducing steatosis and insulin resistance in the liver. Dietary supplementation with MCFAs may therefore be beneficial for preventing obesity and peripheral insulin resistance.

Diabetes Care. 2010 Oct 26. [Epub ahead of print] Body and Liver Fat Mass Rather Than Muscle Mitochondrial Function Determines Glucose Metabolism in Women with a History of Gestational Diabetes. Prikoszovich T, Winzer C, Schmid AI, Szendroedi J, Chmelik M, Pacini G, Krssák M, Moser E, Funahashi T, Waldhäusl W, Kautzky-Willer A, Roden M. Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria ...

Mitochondria - what are they & why are they so important? Mitochondria are the primary energy producers in the body. The typical cell contains an average of 1,000 mitochondria. Given that there are 10 to the 13th power cells in a healthy adult, healthy and productive mitochondria are critical to maintain the bodys

2. When the cell needs more energy, the mitochondria can reproduce by growing larger and then dividing. For example, say you want to get in shape. As you exercise more of the mitochondria in your muscles will increase in number and navigate to the edges of the cell, which allows these muscle cells to have more energy. ...

Learn about mitochondria and how to enhance them for better health. Mitochondria are known as the powerhouses of the cell. They are organelles that ac...

This article from Science magazine explains some theories about why we have DNA in the mitochondria of our cells, as well as in the nucleus of the cell. Mitochondria are the powerhouses of our cells, providing the energy needed for functioning and replicating.. Why do our cells powerhouses have their own DNA?. ...

Metagenics MitoVive Mitochondria and Cell Function Support provides nutritional assistance for mitochondrial function and neuromuscular health.

Mitochondria are having their time in the spotlight after years of being ignored. Discover everything you need to know about these cellular powerhouses.

Have you heard mitochondria? Do you know there is a way to maximize mitochondira performance in your body to fight aging, check out at Younggolucky.com !

The cell is the basic structural and functional unit in all living organisms. Living forms vary in size but they are all made up of […]. ...

మైటోకాండ్రియాలు (Mitochondria) కణంలో పాక్షిక స్వతంత్ర ప్రతిపత్తిగల సూక్ష్మాంగాలు. ఇవి స్థూపాకారంలోగాని, గోళాకారంలోగాని ఉంటాయి. ఒక్కొక్కటిగా గాని సమూహాలుగా గాని ఉండవచ్చు. జీవనక్రియలు చురుకుగా సాగే కణాలలో ఇది చాలా అధికసంఖ్యలో ఉంటాయి. ఇవి రెండు పొరలతో ఏర్పడిన సూక్ష్మాంగాలు. ఈ పొరలు కణత్వచాన్ని పోలి ఉంటాయి. దీనివెలుపలి పొర చదునుగా ఉండగా, లోపలి పొర ముడతలుగా ఏర్పడి ఉంటుంది. ఈ ముడతలను ...

2019 8/15 リンク追記 リファレンスゲノムの構築とキュレーションに多大な努力が注がれている (ref.1-5)。これらのリファレンスアセンブリは結果を比較するための共通の表現を提供し、それらはシーケンスアラインメントとアノテーションを行う広範囲の下流ツ… ...

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