4 edition of Role of oxidative stress in two models of insulin resistance within primary rat adipocytes found in the catalog.
Role of oxidative stress in two models of insulin resistance within primary rat adipocytes
Charles Young Cho
Thesis (M.Sc.) -- University of Toronto, 1999.
|Series||Canadian theses = -- Thèses canadiennes|
|The Physical Object|
|Pagination||2 microfiches : negative. --|
Recently, considerable attention has been given to the role of increased oxidative stress in the development of AII-induced hypertension and vascular injury. 17,18 We, therefore, considered the possibility that oxidative stress is involved in the molecular mechanism underlying AII-induced insulin resistance and examined the effects of tempol, a Cited by: Adipokines play important roles in metabolic homeostasis and disease. We have recently identified a novel adipokine Metrnl, also known as Subfatin, for its high expression in subcutaneous fat. Here, we demonstrate a prodifferentiation action of Metrnl in white adipocytes. Adipocyte-specific knockout of Metrnl exacerbates insulin resistance induced by high-fat diet Cited by: Title: Dysregulation of Glycogen Synthase Kinase-3 in Skeletal Muscle and the Etiology of Insulin Resistance and Type 2 Diabetes VOLUME: 6 ISSUE: 5 Author(s):Erik J. Henriksen Affiliation:Department of Physiology, P.O. Box , University of Arizona, Tucson, AZ , USA. Keywords:GSK-3, Insulin resistance, Skeletal muscle, Inhibitors, Zucker rat, Oxidative stress Cited by: Progranulin (PGRN) has recently emerged as an important regulator for insulin resistance. However, the direct effect of progranulin in adipose insulin resistance associated with the autophagy mechanism is not fully understood. In the present study, progranulin was administered to 3T3-L1 adipocytes and C57BL/6 J mice with/without specific inhibitors of oxidative stress Cited by:
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Oxidative stress induces insulin resistance. Oxidative stress plays the major role in the association with the insulin resistance pathogenesis by insulin signals disruption and adipocytokines dysregulation[8,9].
In rat models, oxidative stress enhances insulin by: A currently favoured hypothesis is that oxidative stress, through a single unifying mechanism of superoxide production, is the common pathogenic factor leading to insulin resistance, β-cell dysfunction, impaired glucose tolerance (IGT) and ultimately to type 2 DM (T2DM) (2).Cited by: The condition of oxidative stress arises when oxidant production exceeds antioxidant activity in cells and plasma.
The overabundance of oxidants is mechanistically connected with the multifactorial etiology of insulin resistance, primarily in skeletal muscle tissue, and the subsequent development of type 2 by: The following sections will review first the specific role of oxidative stress in the etiology of insulin resistance and subsequently the utility of antioxidant interventions to ameliorate oxidant stress-associated insulin-resistant states.
Origins of Oxidative Stress in Various Cell TypesCited by: 2. Role of Oxidative Stress in Myocardial Insulin Resistance Insulin resistance (IR) that a Insulin resistance (IR) that accompanies the metabolic syndrome and type 2 diabetes increases the risk of cardiovascular disease.
Myocardial IR and mitochondrial (MITO) dysfunction are observed in IR rodents. Insulin Resistance And Oxidative Stress Induced by A Fructose-Rich Diet In Rat Adipose Tissue We have already shown that the We have already shown that the administration of a fructose-rich diet (FRD) to normal rats induces a state of insulin resistance (IR) and an increase of oxidative stress markers (OS) in different tissues.
The seemingly conflicting role of ROS in insulin signaling may be explained by the degree and context by which ROS is generated. It has been proposed that transient and low-grade oxidative stress be beneficial, whereas sustained oxidative stress may promote insulin resistance.
A similar scenario has also been observed for physical exercise-induced enhancement of insulin by: Improvements in skeletal muscle insulin-dependent glucose uptake and whole body IR in rats overexpressing ANG II by ARB or SOD mimetic indicate that oxidative stress plays an important role in ANG II-mediated insulin by: In contrast, several antioxidants improve the insulin signaling of muscle cells for glucose uptake and reduce the production of Role of oxidative stress in two models of insulin resistance within primary rat adipocytes book products, which supports a role for oxidative stress in the development of insulin resistance.
The accumulation of oxidative products found in exercise-induced muscle damage indicates a close Cited by: Insulin resistance and the consequence of declined of insulin secretion are the principle of the T2DM patho-genesis[11,12,15,16].
The late complications of diabetes have been associated and implicated in their etiology with oxidative stress. The influence of oxidative stress on insulin resistance, dyslipidemia, abnormal lipoprotein. Insulin resistance is a major risk factor for various metabolic diseases, such as type 2 diabetes, cardiovascular disease, and some cancers.
Although its underlying mechanisms are elusive, insulin-responsive tissues such as adipose tissue undergo oxidative stress during insulin by: 3.
Sirt1 is decreased in a rat model of NAFLD and Sirt1 hepatic deficiency leads to oxidative damage and insulin resistance. Thus, there is a strong mechanistic link between deficiencies of proteins controlling mitochondrial biogenesis, function, and antioxidant capacity and the development of fatty liver disease, stimulating great interest in Cited by: Oxidative stress, and more specifically oxidative damage to proteins, is increasingly thought to play a central, mechanistic role in this context as it is associated with modifications in the activities of biological compounds and cellular processes that Cited by: Oxidative stress plays a pathological role in the development of various diseases including diabetes, atherosclerosis, or cancer.
Systemic oxidative stress results from an imbalance between oxidants derivatives production and antioxidants defenses. Reactive oxygen species (ROS) are generally considered to be detrimental for health. However, evidences have been Cited by: Oxidative stress-induced reactive oxygen species are associated with the clinical manifestation of insulin resistance.
Evidence suggests that antioxidant treatment may reduce this incidence. This study determined whether glucose oxidase (GO)-induced insulin resistance in cultured skeletal muscle cells could be ameliorated by pre-treatment with gamma-tocopherol Cited by: The development of metabolic dysfunctions like diabetes and insulin resistance in mammals is regulated by a myriad of factors.
Oxidative stress seems to play a central role in this process as recent evidence shows a general increase in oxidative damage and a decrease in oxidative defense associated with several metabolic by: A role for cell senescence and p53 in the development of insulin resistance (or prediabetes) has been obscure.
Issei Komuro and colleagues now show that premature cell senescence occurs in the Cited by: These complications are the consequence of various pathophysiological mechanisms, including metabolic syndromes and oxidative stress.
The primary features of metabolic syndrome include weight gain, hypertension, cholesterol abnormalities, hyperuricemia and insulin resistance .Cited by: Role of oxidative stress in impaired insulin signaling associated with exercise-induced muscle damage Article Literature Review in Free Radical Biology and Medicine 65(6).
Oxidative stress is a mechanistic link between obesity and insulin resistance due to the high level of reactive oxygen species (ROS) generated under the effect of the increased amount of free fatty acids (FFA) and other substances delivered from fat adipocyte to peripheral tissues [1, 2].Cited by: 9.
The role of mitochondria in insulin resistance and type 2 diabetes mellitus In rodent models, insulin resistance can develop in increased triglyceride accumulation and oxidative stress Cited by: oxidative stress is one mechanism by which LA improves insulin action.
However, the potential effect of LA on oxida-tive stress in muscle cells has not been evaluated. In the present report, we investigated the effects of LA on cultured rat L6 muscle cells that had undergone oxidative stress.
To improve both the responsiveness and sensitivity to. A Novel Mechanism to Reduce both Oxidative Stress and Insulin Resistance by Adiponectin in Skeletal Muscle Cells Abstract Adiponect Abstract Adiponectin is an adipocyte-derived serum protein, which acts to reduce insulin resistance in the liver and muscles and also inhibits atherosclerosis by reducing oxidative stress.
Oxidative stress due to enhanced production or reduced scavenging of reactive oxygen species (ROS) has been associated with diet (dyslipidemia) induced obesity and insulin resistance (IR).
Inflammation plays a critical role in the pathology of obesity-linked insulin resistance and is mechanistically linked to the effects of macrophage-derived cytokines on adipocyte energy metabolism, particularly that of the mitochondrial branched chain amino acid (BCAA) and tricarboxylic acid (TCA) by: 1.
We develop mathematical models of feedback between reactive oxygen species production and dysfunction in mitochondria to provide insight into the role of oxidative stress in insulin resistance. A coculture system previously showed the impact of adipocytes on muscle cell insulin resistance and oxidative capacity (18) (19)(20).
However, the impact of VAT adipocytes on muscle structural. Oxidative Stress and Insulin Resistance. Both insulin resistance and decreased insulin secretion are major features of the pathophysiology of type 2 diabetes [1,32,33,34].Insulin resistance most.
Mechanisms of Diabetes-Induced Liver Damage: The role of oxidative stress and inflammation Hyperglycemia induces oxidative stress and insulin resistance plays a crucial role. Dr. Doni discusses how oxidative stress can lead to diabetes types 1 & 2, with 6 simple steps to prevent the onset of diabetes.
Part 2 of Dr. Doni’s Series on Oxidative Stress. In the first article in this series, I introduced how oxidative stress can affect your it, I mentioned that elevated blood sugar levels are one of the key causes of oxidative stress and. OXIDATIVE STRESS AND INSULIN RESISTANCE. Both insulin resistance and decreased insulin secretion are major features of the pathophysiology of type 2 diabetes (1,32–34).Insulin resistance most often precedes the onset of type 2 diabetes by many years, is present in a large segment of the general population, and is multifactorial (1,32).It is clear that insulin resistance Cited by: In the context of diabetes, the health benefit of antioxidant treatment has been widely debated.
In this study, we investigated the effect of antioxidant treatment during the development of insulin resistance and hyperphagia in obesity and partial lipodystrophy.
We studied the role of antioxidants in the regulation of insulin resistance using the tamoxifen-inducible fat-specific insulin Cited by: 1. Insulin induces apoptosis in brown adipocytes after long-term treatment There are many published data about the role of insulin as a survival signal in different cell types (13 – 15).
However, insulin did not protect from apoptosis induced by TNF-α plus cycloheximide in brown adipocytes from mice (16).Cited by: Oxidative stress plays an important role on the patho - genesis of insulin resistance by disrupting the release of adipokines by adipose tissue such as TNF-α and IL-6, which can trigger inflammation, a mechanism already described above.
Thus, it seems that obesity and MetS are factors associated to inflammation and oxidative by: However, isolated insulin resistance in transgenic mice does not alter expression of oxidative metabolism genes or PGC1α (V.
Yechoor, personal communication), and family history of DM, rather than insulin resistance, was the predominant covariate for both PGC1α and -β expression in our human cohort. oxidative stress is thought to play a causative role in the pathogenesis of type 2 diabetes and its complications and has been shown to increase insulin resistance both in animal models and in human patients with type 2 diabetes (3, 13, 14, 29).Once generated, reactive oxygen species (ROS) can act as second messengers and can activate a number of serine/threonine and Cited by: Oxidative stress is also central to the development of insulin resistanceEndoplasmic reticulum stress.
In response to insulin resistance, β-cells dramatically increase insulin by: Oxidative stress has been implicated implicated in insulin resistance, and a new study by Hoehn et al.
(1) adds some convincing evidence that one specific radical, superoxide generated in the mitochondria, may be a unifying cause. But the findings suggest that we may need to reconsider how we treat it.
The authors begin by suggesting that the failure of. Fatty acids acutely enhance insulin-induced oxidative stress and cause insulin resistance by increasing mitochondrial reactive oxygen species (ROS) generation and nuclear factor-κB inhibitor (IκB)–nuclear factor-κB (NFκB) activation in rat muscle, in the absence of mitochondrial dysfunctionCited by: Free radical theory, oxidative stress theory and mitochondrial theory of aging.
Denham Harman was first to propose the free radical theory of aging in the s, and extended the idea to implicate mitochondrial production of reactive oxygen species in s, .According to this theory, enhanced and unopposed metabolism-driven oxidative stress has a major role in Cited by:.
Atorvastatin but Not Pravastatin Impairs Mitochondrial Function in Human Pancreatic Islets and Rat β-Cells. the role of oxidative stress in our model, we tested the effect of a co-treatment Cited by: Obesity is associated with insulin resistance (IR) and increased oxidative stress.
Thus, the present study aimed to evaluate anthropometric parameters, IR, and oxidative stress in obese individuals subjected to two types of concurrent training at the same intensity but differing in frequency.
Accordingly, 25 individuals were divided into two groups: concurrent training 1 Cited by: 8.Insulin resistance induced by fatty acids.
Model for how excess free fatty acids (FFAs) lead to insulin resistance and enhanced inflammatory responses, predominantly in cells such as skeletal muscle and adipose tissue but also in the liver. Only the major pathways regulated by insulin relative to glucose and lipid homeostasis are shown.