Effect of Acute Exercise Or Fasting on Mitochondrial Function and High Fat Diet-induced Insulin Resistance PDF Download
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Author: Oh Sung Kwon
Publisher:
ISBN:
Category : Insulin resistance
Languages : en
Pages : 54
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Book Description
A high-fat diet leads to an accumulation of lipid in skeletal muscle, and the development of both mitochondrial dysfunction and insulin resistance. Recently, our lab reported that lipid overload leads to elevated H2O2 emission from muscle mitochondria, and that mitochondrial-targeted scavenging of H2O2 completely prevents the development of high fat diet-induced insulin resistance. These findings raise the possibility that interventions which acutely restore cellular metabolic balance in muscle may also acutely restore insulin sensitivity. We hypothesized that mitochondrial function and insulin sensitivity can be restored in skeletal muscle of high-fat fed rats by creating an acute deficit in metabolic balance via 2 h low-intensity treadmill exercise or 16 h fasting. Male Sprague-Dawley rats (125-150g) were either maintained on a standard high carbohydrate- diet or fed a high-fat (60%) diet for 6 weeks and divided into three groups the day before the study: one group was maintained on the normal high-fat diet, another group was fasted overnight (16 h), and a third group completed a single 2 h bout of low-intensity treadmill exercise (10 m/min) and then were given normal overnight ad libitum access to the high-fat diet. Oral glucose tolerance tests were administrated to assess insulin action. Red gastrocnemius muscles were harvested and permeabilized fibers prepared for determination of mitochondrial respiratory function and H2O2 emission. A single 16 h fast significantly (P
Author: Oh Sung Kwon
Publisher:
ISBN:
Category : Insulin resistance
Languages : en
Pages : 54
Get Book Here
Book Description
A high-fat diet leads to an accumulation of lipid in skeletal muscle, and the development of both mitochondrial dysfunction and insulin resistance. Recently, our lab reported that lipid overload leads to elevated H2O2 emission from muscle mitochondria, and that mitochondrial-targeted scavenging of H2O2 completely prevents the development of high fat diet-induced insulin resistance. These findings raise the possibility that interventions which acutely restore cellular metabolic balance in muscle may also acutely restore insulin sensitivity. We hypothesized that mitochondrial function and insulin sensitivity can be restored in skeletal muscle of high-fat fed rats by creating an acute deficit in metabolic balance via 2 h low-intensity treadmill exercise or 16 h fasting. Male Sprague-Dawley rats (125-150g) were either maintained on a standard high carbohydrate- diet or fed a high-fat (60%) diet for 6 weeks and divided into three groups the day before the study: one group was maintained on the normal high-fat diet, another group was fasted overnight (16 h), and a third group completed a single 2 h bout of low-intensity treadmill exercise (10 m/min) and then were given normal overnight ad libitum access to the high-fat diet. Oral glucose tolerance tests were administrated to assess insulin action. Red gastrocnemius muscles were harvested and permeabilized fibers prepared for determination of mitochondrial respiratory function and H2O2 emission. A single 16 h fast significantly (P
Author: Beatrice Morio
Publisher: Academic Press
ISBN: 0128117524
Category : Medical
Languages : en
Pages : 460
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Book Description
Mitochondria in Obesity and Type 2 Diabetes: Comprehensive Review on Mitochondrial Functioning and Involvement in Metabolic Diseases synthesizes discoveries from laboratories around the world, enhancing our understanding of the involvement of mitochondria in the etiology of diseases, such as obesity and type 2 diabetes. Chapters illustrate and provide an overview of key concepts on topics such as the role of mitochondria in adipose tissue, cancer, cardiovascular comorbidities, skeletal muscle, the liver, kidney, and more. This book is a must-have reference for students and educational teams in biology, physiology and medicine, and researchers.
Author: Chien-Te Lin
Publisher:
ISBN:
Category : Insulin resistance
Languages : en
Pages : 147
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Book Description
Mitochondrial respiratory capacity and oxidative stress have been implicated in the development of insulin resistance (IR) and type II diabetes. A causative role of mitochondrial oxidative stress in the etiology of diet-induced IR has been suggested. Metabolic oversupply causes mitochondrial oxidative stress and leads to IR; however, how the other side of the metabolic balance equation, energy expenditure, may compensate for oversupply is less appreciated. Based on the principles of bioenergetics, in the condition of substrate oversupply without sufficient energy expenditure, the mitochondrial membrane potential ([delta psi subscript m]) is high and an exponential increase in superoxide generation occurs within a small range of [delta psi subscript m] exceeding about -160mV. The inverse occurs when the mitochondrial energy expenditure rises. In this context, it was hypothesized that a mild increase in energy expenditure can sufficiently attenuate the over-nutrition caused H2O2 emission and IR. To examine this hypothesis acutely, Sprague-Dawley (S-D) rats received a lipid oral gavage with or without 1h of subsequent low intensity exercise. Mitochondria of permeabilized skeletal muscle fibers were studied. The results show that, without a change in respiratory capacity, a single lipid loading quickly elevated [delta psi subscript m], mitochondrial H2O2 emitting potential ([subscript m]E[subscript]H2O2) and reduced calcium retention capacity (an index of the resistance of mitochondrial permeability transition) in state IV and/or under "clamped" physiological state III respiration conditions. These effects can be quickly and sufficiently attenuated by a single bout of postprandial low intensity exercise. These findings provide evidence that mitochondrial H2O2 production/emission and related effects, but not respiratory capacity, are acutely and dynamically regulated by the metabolic status of skeletal muscle. Further, to examine this hypothesis chronically, S-D rats were high fat diet (HFD, 60%) fed for 7 weeks with or without either low intensity exercise or [beta]-guanidinopropionic acid ([beta]-GPA), which chronically elevates mitochondrial energy turnover. The results show that HFD decreased insulin action and increased [subscript]mE[subscript]H2O2, whereas both were preserved by either exercise or [beta]-GPA. The treatment effects of HFD, exercise or [beta]-GPA were mitochondrial respiratory function and fatty acid oxidation rate independent. However, 5'-AMP-activated protein kinase (AMPK) activity, an energy sensing kinase that increases glucose uptake, was also increased by [beta]-GPA treatment. To determine whether AMPK mediated the [beta]-GPA-induced improvements in insulin action, skeletal and cardiac muscle-specific AMPK [alpha]2 catalytic subunit dominant negative mutated (non-functional) mice and their wild-type littermates were fed a HFD with or without [beta]-GPA for 10 weeks. [Beta]-GPA treatment again prevented the increase in [subscript]mE[subscript]H2O2 and IR in both wild-type and AMPK[alpha]2 dominant negative mice fed a HFD. These findings indicate that AMPK[alpha]2 does not mediate the effects of [beta]-GPA on insulin action, supporting the hypothesis that the reduction in mitochondrial H2O2 emission is a primary mechanism by which exercise and [beta]-GPA attenuate HFD-induced IR. In the context of both acute and chronic manipulation of positive (oversupply) and negative (expenditure) cellular energy balance, together these findings support the concept that the governance of mitochondrial oxidant production is a primary factor regulating insulin sensitivity in skeletal muscle. Following the principles of bioenergetics, these data demonstrate that a mild increase in energy expenditure can sufficiently attenuate the HFD-induced H2O2 emission and IR. On the mitochondrial level, the balance of substrate supply and energy expenditure on a daily basis is critical for maintaining a proper cellular redox environment, function and whole body metabolic status.
Author: Lawrence H. Lash
Publisher: Elsevier
ISBN: 1483218619
Category : Science
Languages : en
Pages : 527
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Book Description
Methods in Toxicology, Volume 2: Mitochondrial Dysfunction provides a source of methods, techniques, and experimental approaches for studying the role of abnormal mitochondrial function in cell injury. The book discusses the methods for the preparation and basic functional assessment of mitochondria from liver, kidney, muscle, and brain; the methods for assessing mitochondrial dysfunction in vivo and in intact organs; and the structural aspects of mitochondrial dysfunction are addressed. The text also describes chemical detoxification and metabolism as well as specific metabolic reactions that are especially important targets or indicators of damage. The methods for measurement of alterations in fatty acid and phospholipid metabolism and for the analysis and manipulation of oxidative injury and antioxidant systems are also considered. The book further tackles additional methods on mitochondrial energetics and transport processes; approaches for assessing impaired function of mitochondria; and genetic and developmental aspects of mitochondrial disease and toxicology. The text also looks into mitochondrial DNA synthesis, covalent binding to mitochondrial DNA, DNA repair, and mitochondrial dysfunction in the context of developing individuals and cellular differentiation. Microbiologists, toxicologists, biochemists, and molecular pharmacologists will find the book invaluable.
Author: Sheri R. Colberg
Publisher: American Diabetes Association
ISBN: 158040507X
Category : Medical
Languages : en
Pages : 554
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Book Description
Physical movement has a positive effect on physical fitness, morbidity, and mortality in individuals with diabetes. Although exercise has long been considered a cornerstone of diabetes management, many health care providers fail to prescribe it. In addition, many fitness professionals may be unaware of the complexities of including physical activity in the management of diabetes. Giving patients or clients a full exercise prescription that take other chronic conditions commonly accompanying diabetes into account may be too time-consuming for or beyond the expertise of many health care and fitness professionals. The purpose of this book is to cover the recommended types and quantities of physical activities that can and should be undertaken by all individuals with any type of diabetes, along with precautions related to medication use and diabetes-related health complications. Medications used to control diabetes should augment lifestyle improvements like increased daily physical activity rather than replace them. Up until now, professional books with exercise information and prescriptions were not timely or interactive enough to easily provide busy professionals with access to the latest recommendations for each unique patient. However, simply instructing patients to “exercise more” is frequently not motivating or informative enough to get them regularly or safely active. This book is changing all that with its up-to-date and easy-to-prescribe exercise and physical activity recommendations and relevant case studies. Read and learn to quickly prescribe effective and appropriate exercise to everyone.
Author: Laelie Allison Snook
Publisher:
ISBN:
Category :
Languages : en
Pages :
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Book Description
Nutrient uptake into skeletal muscle involves the redistribution of specific transport proteins to the plasma membrane, events that are tightly regulated by various cellular signals, including the hormone insulin. However, a dysregulatation in nutrient homeostasis causes insulin resistance, a process related to attenuated skeletal muscle glucose transporter (GLUT4), and exaggerated redistribution of fatty acid transporters (i.e. FAT/CD36), at the plasma membrane. Therefore, this thesis investigated the hormonal regulation of nutrient uptake, as well as the ability of prior exercise training to combat high fat diet induced metabolic perturbations. Study one examined post-prandial control of GLUT4 subcellular localization in muscle. This study demonstrated that a mixed carbohydrate- and fat-containing meal increased circulating GIP and improved whole body glucose clearance. Moreover, in skeletal muscle, GIP directly stimulated glucose uptake and increased plasmalemmal GLUT4 independent of insulin, highlighting a novel mechanism for GIP. Hyperinsulinemia has been proposed to result in FAT/CD36 redistribution to the plasma membrane, influencing ectopic lipid accumulation and insulin resistance. However, study two demonstrated that although a pharmacological dose of insulin is sufficient to cause fatty acid transporter plasmalemmal accumulation, this relocation is brief and cannot explain the responses observed post-prandially or during a high-fat challenge. Rather, acute and chronic translocation of fat transporters was matched to increased circulating free fatty acids, suggesting lipids may regulate fatty acid transporter subcellular location. Adipose tissue metabolism is known to influence whole body insulin sensitivity, and is responsive to exercise training. Therefore, in the third study I utilized prior exercise training to examine the protective effects on high fat diet-induced insulin resistance, and potential mechanisms in diverse tissues. I determined that prior training blunted high fat diet-induced weight gain and glucose intolerance independently of food intake and cage activity, responses associated with increased mitochondrial enzyme content in white adipose tissue and increased UCP-1 content in brown adipose tissue. Together, this thesis adds to our understanding of the signals mediating nutrient transporter cycling in skeletal muscle, potentially providing new targets for the treatment of insulin resistance. Additionally, this thesis further emphasizes the importance of regular exercise on metabolic health, specifically in the face of nutrient over-consumption.
Author: Richard Weindruch
Publisher: Charles C Thomas Pub Limited
ISBN: 9780398054960
Category : Health & Fitness
Languages : en
Pages : 436
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Book Description
Author: E. Madison Robison
Publisher:
ISBN:
Category :
Languages : en
Pages : 239
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Book Description
Cardiac mitochondrial phospholipids, notably cardiolipin (CL), regulate inner mitochondrial membrane (IMM) organization and protein function, particularly the enzymes associated with respiration. In a range of metabolic diseases, CL and other phospholipids undergo acyl chain remodeling, which would presumably impair respiratory activity. In diet-induced obesity, the influence of cardiac remodeling on respiratory enzyme activity and mitochondrial respiration is poorly studied. Thus, we first established the effect of diet-induced obesity on the mitochondrial phospholipidome and subsequent influences on mitochondrial function using two different dietary models. Surprisingly, the high fat diet and western diet remodeled the phospholipidome, but both obesogenic diets had no influence on cardiac mitochondrial supercomplex formation, respiratory enzyme activities, or respiration. Therefore, we next investigated how extremely remodeling with dietary n-3 polyunsaturated fatty acids (n-3 PUFAs) in the context of obesity, would influence the mitochondrial phospholipidome and thereby respiration. The rationale for focusing on n-3 PUFAs was that these fatty acids are generally considered cardioprotective but paradoxically are elevated in several metabolic diseases. Dietary supplementation with eicosapentaenoic acid (EPA) or docosahexaenoic acid (DHA) extensively remodeled the phospholipidome. Particularly, CL acyl chains were remodeled to include DHA at the loss of linoleic acid, which is incorporated into 90% of CL species. Strikingly, supplementation with DHA reduced the activities of several respiratory enzymes, although overall respiration was not affected. We tested the hypothesis that the reduction in enzymatic activity with DHA was driven by the replacement of linoleic acid with DHA in CL species. Indeed, fusion of linoleic acid to mitochondria isolated from DHA-fed mice, rescued the impairments in the CL lipidome and thereby several respiratory complex activities. These results suggest that increased DHA in the myocardium in differing diseases may be targeting enzymatic activity. Taken together, the data establish that obesity by itself in mice does not disrupt respiratory enzyme activity despite remodeling of CL acyl chains. However, extensive remodeling with n-3 PUFAs has a strong influence. Finally, this study has implications for future nutritional studies on the balance between linoleic acid and n-3 PUFAs in the heart, which is an area of ongoing debate.
Author: Derick Han
Publisher: CRC Press
ISBN: 1482236982
Category : Medical
Languages : en
Pages : 522
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Book Description
" excellent, well-organized, and timely."-Lester Packer and Enrique Cardenas, University of Southern California, Los Angeles, from the Series PrefaceThe liver is a vital organ that is responsible for a wide range of functions, most of which are essential for survival. The multitude of functions the liver performs makes it vulnerable to a wide range
Author: Alan R. Saltiel
Publisher: Springer Science & Business Media
ISBN: 0387722041
Category : Medical
Languages : en
Pages : 223
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Book Description
More than 18 million people in the United States have diabetes mellitus, and about 90% of these have the type 2 form of the disease. This book attempts to dissect the complexity of the molecular mechanisms of insulin action with a special emphasis on those features of the system that are subject to alteration in type 2 diabetes and other insulin resistant states. It explores insulin action at the most basic levels, through complex systems.
