scholarly journals Attenuation of age- and sucrose-induced insulin resistance and syndrome X by a synergistic antioxidant cocktail: the AMIS syndrome and HISS hypothesisThis article is one of a selection of papers published in a Special Issue on Oxidative Stress in Health and Disease.

2010 ◽  
Vol 88 (3) ◽  
pp. 313-323 ◽  
Author(s):  
W. Wayne Lautt ◽  
Zhi Ming ◽  
Dallas J. Legare
Keyword(s):  
Oxidative Stress ◽  
Negative Impact ◽  
Bioelectrical Impedance ◽  
Postprandial Hyperglycemia ◽  
Whole Body ◽  
Syndrome X ◽  
Body Adiposity ◽  
Slow Development ◽  
Health And Disease ◽  
One Year

Absence of meal-induced insulin sensitization (AMIS) results in a predictable progression of dysfunctions, including postprandial hyperglycemia, compensatory hyperinsulinemia, resultant hyperlipidemia, increased oxidative stress, and obesity, progressing to syndrome X and diabetes. To one year of age, rats show a slow development of AMIS, but this can be potentiated by addition of a low-dose sucrose supplement to the diet. Provision of a synergistic antioxidant cocktail consisting of S-adenosylmethionine, vitamin E, and vitamin C (Samec) attenuates the rate and extent of development of AMIS in both normal aging animals and in aging animals on the sucrose diet. Adiposity, assessed from weighed regional fat masses and from bioelectrical impedance to estimate whole-body adiposity, correlated strongly with AMIS (r2 = 0.7–0.8). Rats given the sucrose supplement had accelerated AMIS and developed fasting hyperinsulinemia and postprandial hyperglycemia, hyperlipidemia, hyperinsulinemia, and adiposity. Samec completely compensated for the negative impact of this sucrose supplement and attenuated development of the associated dysfunctions. AMIS is explained by the HISS (hepatic insulin-sensitizing substance) hypothesis, which is outlined in the paper.

Obesity, syndrome X, and diabetes: the role of HISS-dependent insulin resistance altered by sucrose, an antioxidant cocktail, and ageThis article is one of a selection of papers published in a special issue celebrating the 125th anniversary of the Faculty of Medicine at the University of Manitoba.

2009 ◽  
Vol 87 (10) ◽  
pp. 873-882 ◽  
Author(s):  
Zhi Ming ◽  
Dallas J. Legare ◽  
W. Wayne Lautt
Keyword(s):  
Bioelectrical Impedance ◽  
Nutrient Status ◽  
Postprandial Hyperglycemia ◽  
Syndrome X ◽  
Slow Development ◽  
125Th Anniversary ◽  
University Of Manitoba ◽  
The University

Absence of meal-induced insulin sensitization (AMIS) results in a predictable progression of dysfunctions, including postprandial hyperglycemia, compensatory hyperinsulinemia, resultant hyperlipidemia, increased oxidative stress, and obesity, progressing to syndrome X and diabetes. To test the ‘AMIS syndrome’ hypothesis we used 3 known means of producing graded and progressive changes in meal-induced insulin sensitization in rats. We used an aging model (9, 26, and 52 weeks), associated with a slow development of AMIS; a low-dose sucrose supplement model to accelerate the development of AMIS; and an antioxidant cocktail (S-adenosylmethionine, vitamin E, and vitamin C) to protect against the effect of the sucrose on meal-induced insulin sensitization. Adiposity was assessed from weighed regional fat masses and bioelectrical impedance. AMIS developed with age, was increased by sucrose supplementation, and was inhibited by the antioxidant cocktail. AMIS correlated with postprandial hyperglycemia, hyperinsulinemia, hyperlipidemia, and with adiposity (r2 = 0.7–0.8) regardless of age or nutrient status. The range of degrees of AMIS, established over time with these models, afforded the tool with which to test the AMIS syndrome and further the argument that AMIS is the first metabolic defect that cumulatively leads to a predictable series of homeostatic disturbances and dysfunctions, including obesity and type 2 diabetes.

Oxidative stress and aging: Is methylglyoxal the hidden enemy?This review is one of a selection of papers published in a Special Issue on Oxidative Stress in Health and Disease.

2010 ◽  
Vol 88 (3) ◽  
pp. 273-284 ◽  
Author(s):  
Kaushik M. Desai ◽  
Tuanjie Chang ◽  
Hui Wang ◽  
Ali Banigesh ◽  
Arti Dhar ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Aging Process ◽  
Cellular Tissue ◽  
Cardiovascular Complications ◽  
Whole Body ◽  
Age Related ◽  
Transport Chain ◽  
Glycation End Products ◽  
Health And Disease

Aging is a multifactorial process that involves changes at the cellular, tissue, organ and the whole body levels resulting in decreased functioning, development of diseases, and ultimately death. Oxidative stress is believed to be a very important factor in causing aging and age-related diseases. Oxidative stress is caused by an imbalance between oxidants such as reactive oxygen species (ROS) and antioxidants. ROS are produced from the mitochondrial electron transport chain and many oxidative reactions. Methylglyoxal (MG) is a highly reactive dicarbonyl metabolite formed during glucose, protein and fatty acid metabolism. MG levels are elevated in hyperglycemia and other conditions. An excess of MG formation can increase ROS production and cause oxidative stress. MG reacts with proteins, DNA and other biomolecules, and is a major precursor of advanced glycation end products (AGEs). AGEs are also associated with the aging process and age-related diseases such as cardiovascular complications of diabetes, neurodegenerative diseases and connective tissue disorders. AGEs also increase oxidative stress. In this review we discuss the potential role of MG in the aging process through increasing oxidative stress besides causing AGEs formation. Specific and effective scavengers and crosslink breakers of MG and AGEs are being developed and can become potential treatments to slow the aging process and prevent many diseases.

scholarly journals Making the choice between bioelectrical impedance measures for body hydration status assessment

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Dmitry M. Davydov ◽  
Andrey Boev ◽  
Stas Gorbunov
Keyword(s):  
Body Schema ◽  
Bioelectrical Impedance ◽  
Information Criterion ◽  
The Body ◽  
Whole Body ◽  
Hydration Status ◽  
Status Assessment ◽  
Best Fitting ◽  
Body Compartments ◽  
Fitting In

AbstractSituational or persistent body fluid deficit (i.e., de- or hypo-hydration) is considered a significant health risk factor. Bioimpedance analysis (BIA) has been suggested as an alternative to less reliable subjective and biochemical indicators of hydration status. The present study aimed to compare various BIA models in the prediction of direct measures of body compartments associated with hydration/osmolality. Fish (n = 20) was selected as a biological model for physicochemically measuring proximate body compartments associated with hydration such as water, dissolved proteins, and non-osseous minerals as the references or criterion points. Whole-body and segmental/local impedance measures were used to investigate a pool of BIA models, which were compared by Akaike Information Criterion in their ability to accurately predict the body components. Statistical models showed that ‘volumetric-based’ BIA measures obtained in parallel, such as distance2/Rp, could be the best approach in predicting percent of body moisture, proteins, and minerals in the whole-body schema. However, serially-obtained BIA measures, such as the ratio of the reactance to resistance and the resistance adjusted for distance between electrodes, were the best fitting in predicting the compartments in the segmental schema. Validity of these results should be confirmed on humans before implementation in practice.

Effect of an interval rehabilitation program with home-based, vibration-assisted training on the development of muscle and bone in children with cerebral palsy – an observational study

2020 ◽  
Vol 33 (8) ◽  
pp. 1083-1092 ◽  
Author(s):  
Ibrahim Duran ◽  
Kyriakos Martakis ◽  
Christina Stark ◽  
Leonie Schafmeyer ◽  
Mirko Rehberg ◽  
...  
Keyword(s):  
Cerebral Palsy ◽  
Bone Growth ◽  
Muscle Growth ◽  
Rehabilitation Program ◽  
Whole Body ◽  
Cross Sectional ◽  
Home Based ◽  
Children With Cerebral Palsy ◽  
One Year ◽  
Intensive Rehabilitation

AbstractObjectivesIn children with cerebral palsy (CP), the most common cause of physical impairment in childhood, less muscle and bone growth has been reported, when compared with typically developing children. The aim of this study was to evaluate the effect of an intensive rehabilitation program including physiotherapy in combination with 6 months of home-based, vibration-assisted training on muscle and bone growth in children with CP.MethodsWe included children with CP, who participated in a rehabilitation program utilizing whole-body vibration (WBV). Muscle mass was quantified by appendicular lean mass index (App-LMI) and bone mass by total-body-less-head bone mineral content (TBLH-BMC) assessed by Dual-energy X-ray absorptiometry (DXA) at the beginning of rehabilitation and one year later. To assess the functional muscle-bone unit, the relation of TBLH-BMC to TBLH lean body mass (TBLH-LBM) was used.ResultsThe study population included 128 children (52 females, mean age 11.9 ± 2.7). App-LMI assessed in kg/m2 increased significantly after rehabilitation. The age-adjusted Z-score for App-LMI showed no significant change. TBLH-BMC assessed in gram increased significantly. The Z-scores for TBLH-BMC decreased lesser than expected by the evaluation of the cross-sectional data at the beginning of rehabilitation. The parameter $\frac{TBLH-BMC}{TBLH-LBM}$ did not change relevantly after 12 months.ConclusionsMuscle growth and to a lesser extent bone growth could be increased in children with CP. The intensive rehabilitation program including WBV seemed to have no direct effect on the bone, but the observed anabolic effect on the bone, may only been mediated through the muscle.

scholarly journals Systemic oxidative stress is associated with lower aerobic capacity and impaired skeletal muscle energy metabolism in heart failure patients

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Takashi Yokota ◽  
Shintaro Kinugawa ◽  
Kagami Hirabayashi ◽  
Mayumi Yamato ◽  
Shingo Takada ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Heart Failure ◽  
Skeletal Muscle ◽  
Energy Metabolism ◽  
Aerobic Capacity ◽  
Plantar Flexion ◽  
Exercise Intolerance ◽  
Whole Body ◽  
Resonance Spectroscopy ◽  
Systemic Oxidative Stress

AbstractOxidative stress plays a role in the progression of chronic heart failure (CHF). We investigated whether systemic oxidative stress is linked to exercise intolerance and skeletal muscle abnormalities in patients with CHF. We recruited 30 males: 17 CHF patients, 13 healthy controls. All participants underwent blood testing, cardiopulmonary exercise testing, and magnetic resonance spectroscopy (MRS). The serum thiobarbituric acid reactive substances (TBARS; lipid peroxides) were significantly higher (5.1 ± 1.1 vs. 3.4 ± 0.7 μmol/L, p < 0.01) and the serum activities of superoxide dismutase (SOD), an antioxidant, were significantly lower (9.2 ± 7.1 vs. 29.4 ± 9.7 units/L, p < 0.01) in the CHF cohort versus the controls. The oxygen uptake (VO2) at both peak exercise and anaerobic threshold was significantly depressed in the CHF patients; the parameters of aerobic capacity were inversely correlated with serum TBARS and positively correlated with serum SOD activity. The phosphocreatine loss during plantar-flexion exercise and intramyocellular lipid content in the participants' leg muscle measured by 31phosphorus- and 1proton-MRS, respectively, were significantly elevated in the CHF patients, indicating abnormal intramuscular energy metabolism. Notably, the skeletal muscle abnormalities were related to the enhanced systemic oxidative stress. Our analyses revealed that systemic oxidative stress is related to lowered whole-body aerobic capacity and skeletal muscle dysfunction in CHF patients.

scholarly journals Contribution of Adipose Tissue Oxidative Stress to Obesity-Associated Diabetes Risk and Ethnic Differences: Focus on Women of African Ancestry

Antioxidants ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 622
Author(s):  
Pamela A. Nono Nankam ◽  
Télesphore B. Nguelefack ◽  
Julia H. Goedecke ◽  
Matthias Blüher
Keyword(s):  
Oxidative Stress ◽  
Adipose Tissue ◽  
Metabolic Diseases ◽  
African Ancestry ◽  
Fat Distribution ◽  
African Women ◽  
European Ancestry ◽  
Whole Body ◽  
Redox Equilibrium ◽  
Systemic Oxidative Stress

Adipose tissue (AT) storage capacity is central in the maintenance of whole-body homeostasis, especially in obesity states. However, sustained nutrients overflow may dysregulate this function resulting in adipocytes hypertrophy, AT hypoxia, inflammation and oxidative stress. Systemic inflammation may also contribute to the disruption of AT redox equilibrium. AT and systemic oxidative stress have been involved in the development of obesity-associated insulin resistance (IR) and type 2 diabetes (T2D) through several mechanisms. Interestingly, fat accumulation, body fat distribution and the degree of how adiposity translates into cardio-metabolic diseases differ between ethnicities. Populations of African ancestry have a higher prevalence of obesity and higher T2D risk than populations of European ancestry, mainly driven by higher rates among African women. Considering the reported ethnic-specific differences in AT distribution and function and higher levels of systemic oxidative stress markers, oxidative stress is a potential contributor to the higher susceptibility for metabolic diseases in African women. This review summarizes existing evidence supporting this hypothesis while acknowledging a lack of data on AT oxidative stress in relation to IR in Africans, and the potential influence of other ethnicity-related modulators (e.g., genetic-environment interplay, socioeconomic factors) for consideration in future studies with different ethnicities.

scholarly journals Developmental Origins of Kidney Disease: Why Oxidative Stress Matters?

Antioxidants ◽  
2020 ◽  
Vol 10 (1) ◽  
pp. 33
Author(s):  
Chien-Ning Hsu ◽  
You-Lin Tain
Keyword(s):  
Oxidative Stress ◽  
Kidney Disease ◽  
Current Knowledge ◽  
Future Research ◽  
Antioxidant Systems ◽  
Developmental Origins ◽  
Adult Onset ◽  
Functional Changes ◽  
Health And Disease ◽  
Developing Kidney

The “developmental origins of health and disease” theory indicates that many adult-onset diseases can originate in the earliest stages of life. The developing kidney has emerged as being particularly vulnerable to adverse in utero conditions leading to morphological and functional changes, namely renal programming. Emerging evidence indicates oxidative stress, an imbalance between reactive oxygen/nitrogen species (ROS/RNS) and antioxidant systems, plays a pathogenetic role in the developmental programming of kidney disease. Conversely, perinatal use of antioxidants has been implemented to reverse programming processes and prevent adult-onset diseases. We have termed this reprogramming. The focus of this review is twofold: (1) To summarize the current knowledge on oxidative stress implicated in renal programming and kidney disease of developmental origins; and (2) to provide an overview of reprogramming effects of perinatal antioxidant therapy on renal programming and how this may prevent adult-onset kidney disease. Although early-life oxidative stress is implicated in mediating renal programming and adverse offspring renal outcomes, and animal models provide promising results to allow perinatal antioxidants applied as potential reprogramming interventions, it is still awaiting clinical translation. This presents exciting new challenges and areas for future research.

scholarly journals Plasma membrane integrity: implications for health and disease

BMC Biology ◽  
2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Dustin A. Ammendolia ◽  
William M. Bement ◽  
John H. Brumell
Keyword(s):  
Plasma Membrane ◽  
Membrane Damage ◽  
Membrane Integrity ◽  
Whole Body ◽  
Plasma Membrane Integrity ◽  
Plasma Membrane Damage ◽  
Cellular Environment ◽  
Health And Disease ◽  
Repair Pathways ◽  
The Impact

AbstractPlasma membrane integrity is essential for cellular homeostasis. In vivo, cells experience plasma membrane damage from a multitude of stressors in the extra- and intra-cellular environment. To avoid lethal consequences, cells are equipped with repair pathways to restore membrane integrity. Here, we assess plasma membrane damage and repair from a whole-body perspective. We highlight the role of tissue-specific stressors in health and disease and examine membrane repair pathways across diverse cell types. Furthermore, we outline the impact of genetic and environmental factors on plasma membrane integrity and how these contribute to disease pathogenesis in different tissues.

Sign in / Sign up

Export Citation Format

Share Document