The Impact of Oxidative Stress on Adipose Tissue Energy Balance

Diabetes is a major health problem that is usually associated with obesity, together with hyperglycemia and increased advanced glycation endproducts (AGEs) formation. Elevated AGEs elicit severe downstream consequences via their binding to receptors of AGEs (RAGE). This includes oxidative stress and oxidative modifications of biological compounds together with heightened inflammation. For example, albumin (major circulating protein) undergoes increased glycoxidation with diabetes and may represent an important biomarker for monitoring diabetic pathophysiology. Despite the central role of adipose tissue in many physiologic/pathologic processes, recognition of the effects of greater AGEs formation in this tissue is quite recent within the obesity/diabetes context. This review provides a brief background of AGEs formation and adipose tissue biology and thereafter discusses the impact of AGEs-adipocyte interactions in pathology progression. Novel data are included showing how AGEs (especially glycated albumin) may be involved in hyperglycemia-induced oxidative damage in adipocytes and its potential links to diabetes progression.

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Diet, obesity and diabetes: a current update

Clinical Science ◽

10.1042/cs20060150 ◽

2006 ◽

Vol 112 (2) ◽

pp. 93-111 ◽

Cited By ~ 34

Author(s):

Celia G. Walker ◽

M. Gulrez Zariwala ◽

Mark J. Holness ◽

Mary C. SUGDEN

Keyword(s):

Type 2 Diabetes ◽

Adipose Tissue ◽

Energy Balance ◽

Whole Body ◽

Primary Defect ◽

Obesity And Diabetes ◽

Tissue Factors ◽

Metabolic Conditions ◽

The Impact

The prevalence of obesity has been increasing at a rapid rate over the last few decades. Although the primary defect can be attributed to an imbalance of energy intake over energy expenditure, the regulation of energy balance is now recognized to be complex. Adipose-tissue factors play a central role in the control of energy balance and whole-body fuel homoeostasis. The regulation of adipose-tissue function, in particular its secretion of adipokines, is impaired by increases in adipose mass associated with obesity, and with the development of insulin resistance and Type 2 diabetes. This review analyses adipose-regulated energy input and expenditure, together with the impact of dietary macronutrient composition on energy balance in relation to susceptibility to the development of obesity and Type 2 diabetes, and how these metabolic conditions may be exacerbated by the consequences of abnormal adipose function. By gaining a greater understanding of how energy balance is controlled in normal, and in obese and diabetic states, a more practical approach can be employed to prevent and better treat obesity and metabolic disorders.

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Exercise Training Attenuates the Dysregulated Expression of Adipokines and Oxidative Stress in White Adipose Tissue

Oxidative Medicine and Cellular Longevity ◽

10.1155/2017/9410954 ◽

2017 ◽

Vol 2017 ◽

pp. 1-12 ◽

Cited By ~ 23

Author(s):

Takuya Sakurai ◽

Junetsu Ogasawara ◽

Ken Shirato ◽

Tetsuya Izawa ◽

Shuji Oh-ishi ◽

...

Keyword(s):

Oxidative Stress ◽

Adipose Tissue ◽

Exercise Training ◽

White Adipose Tissue ◽

Monocyte Chemoattractant Protein 1 ◽

Enhanced Production ◽

Lifestyle Related Diseases ◽

Inflammatory Changes ◽

The Impact ◽

And Oxidative Stress

Obesity-induced inflammatory changes in white adipose tissue (WAT), which caused dysregulated expression of inflammation-related adipokines involving tumor necrosis factor-αand monocyte chemoattractant protein-1, contribute to the development of insulin resistance. Moreover, current literature reports state that WAT generates reactive oxygen species (ROS), and the enhanced production of ROS in obese WAT has been closely associated with the dysregulated expression of adipokines in WAT. Therefore, the reduction in excess WAT and oxidative stress that results from obesity is thought to be one of the important strategies in preventing and improving lifestyle-related diseases. Exercise training (TR) not only brings about a decrease in WAT mass but also attenuates obesity-induced dysregulated expression of the adipokines in WAT. Furthermore, some reports indicate that TR affects the generation of oxidative stress in WAT. This review outlines the impact of TR on the expression of inflammation-related adipokines and oxidative stress in WAT.

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The Interplay Between Adipose Tissue and Vasculature: Role of Oxidative Stress in Obesity

Frontiers in Cardiovascular Medicine ◽

10.3389/fcvm.2021.650214 ◽

2021 ◽

Vol 8 ◽

Author(s):

Yawen Zhou ◽

Huige Li ◽

Ning Xia

Keyword(s):

Oxidative Stress ◽

Adipose Tissue ◽

Cardiovascular Health ◽

Vascular Endothelial ◽

Adipose Tissues ◽

Pathophysiological Role ◽

The Impact ◽

Vascular Oxidative Stress ◽

The Relationship

Cardiovascular diseases (CVDs) rank the leading cause of morbidity and mortality globally. Obesity and its related metabolic syndrome are well-established risk factors for CVDs. Therefore, understanding the pathophysiological role of adipose tissues is of great importance in maintaining cardiovascular health. Oxidative stress, characterized by excessive formation of reactive oxygen species, is a common cellular stress shared by obesity and CVDs. While plenty of literatures have illustrated the vascular oxidative stress, very few have discussed the impact of oxidative stress in adipose tissues. Adipose tissues can communicate with vascular systems, in an endocrine and paracrine manner, through secreting several adipocytokines, which is largely dysregulated in obesity. The aim of this review is to summarize current understanding of the relationship between oxidative stress in obesity and vascular endothelial dysfunction. In this review, we briefly describe the possible causes of oxidative stress in obesity, and the impact of obesity-induced oxidative stress on adipose tissue function. We also summarize the crosstalk between adipose tissue and vasculature mediated by adipocytokines in vascular oxidative stress. In addition, we highlight the potential target mediating adipose tissue oxidative stress.

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Exercise reduces appetite and traffics excess nutrients away from energetically efficient pathways of lipid deposition during the early stages of weight regain

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00212.2011 ◽

2011 ◽

Vol 301 (3) ◽

pp. R656-R667 ◽

Cited By ~ 26

Author(s):

Amy J. Steig ◽

Matthew R. Jackman ◽

Erin D. Giles ◽

Janine A. Higgins ◽

Ginger C. Johnson ◽

...

Keyword(s):

Adipose Tissue ◽

Energy Balance ◽

Weight Regain ◽

De Novo Lipogenesis ◽

Energetic Cost ◽

Positive Energy ◽

Regular Exercise ◽

Fuel Utilization ◽

Energy Imbalance ◽

The Impact

The impact of regular exercise on energy balance, fuel utilization, and nutrient availability, during weight regain was studied in obese rats, which had lost 17% of their weight by a calorie-restricted, low-fat diet. Weight reduced rats were maintained for 6 wk with and without regular treadmill exercise (1 h/day, 6 days/wk, 15 m/min). In vivo tracers and indirect calorimetry were then used in combination to examine nutrient metabolism during weight maintenance (in energy balance) and during the first day of relapse when allowed to eat ad libitum (relapse). An additional group of relapsing, sedentary rats were provided just enough calories to create the same positive energy imbalance as the relapsing, exercised rats. Exercise attenuated the energy imbalance by 50%, reducing appetite and increasing energy requirements. Expenditure increased beyond the energetic cost of the exercise bout, as exercised rats expended more energy to store the same nutrient excess in sedentary rats with the matched energy imbalance. Compared with sedentary rats with the same energy imbalance, exercised rats exhibited the trafficking of dietary fat toward oxidation and away from storage in adipose tissue, as well as a higher net retention of fuel via de novo lipogenesis in adipose tissue. These metabolic changes in relapse were preceded by an increase in the skeletal muscle expression of genes involved in lipid uptake, mobilization, and oxidation. Our observations reveal a favorable shift in fuel utilization with regular exercise that increases the energetic cost of storing excess nutrients during relapse and alterations in circulating nutrients that may affect appetite. The attenuation of the biological drive to regain weight, involving both central and peripheral aspects of energy homeostasis, may explain, in part, the utility of regular exercise in preventing weight regain after weight loss.

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Weight Loss Induced by Bariatric Surgery Restricts Hepatic GDF15 Expression

Journal of Obesity ◽

10.1155/2018/7108075 ◽

2018 ◽

Vol 2018 ◽

pp. 1-6 ◽

Cited By ~ 1

Author(s):

Timon E. Adolph ◽

Felix Grabherr ◽

Lisa Mayr ◽

Christoph Grander ◽

Barbara Enrich ◽

...

Keyword(s):

Weight Loss ◽

Adipose Tissue ◽

Energy Balance ◽

Tissue Expression ◽

Feedback Mechanism ◽

Obese Patients ◽

Nonalcoholic Fatty Liver ◽

Metabolic Inflammation ◽

Severely Obese ◽

The Impact

Introduction. Obesity and related nonalcoholic fatty liver disease (NAFLD) are an emerging health care issue that imposes substantial morbidity to individuals. Growth and differentiation factor 15 (GDF15) limits food uptake, body weight, and energy balance by modulation of GDNF-family receptor α-like (GFRAL) signalling in the hindbrain. However, the regulation of GDF15 expression in obesity and NAFLD is incompletely understood. We sought to define the impact of weight loss achieved by laparoscopic adjustable gastric banding (LAGB) on hepatic and adipose GDF15 expression in a cohort of severely obese patients. Methods. We analysed GDF15 expression of liver and subcutaneous adipose tissue before and 6 months after LAGB in severely obese patients undergoing LAGB by quantitative real-time PCR. To assess the role of inflammation on GDF15 expression, we analysed Hep G2 hepatocytes stimulated with cytokines such as IL-1β, TNFα, IL-6, LPS, or cellular stressors such as tunicamycin. Results. GDF15 expression was mostly confined to the liver compared to adipose tissue in severely obese patients. Weight loss induced by LAGB was associated with reduced hepatic (but not adipose tissue) expression of GDF15. Stimulation with IL-1β or tunicamycin induced hepatic GDF15 expression in hepatocytes. In line with this, hepatic GDF15 expression directly correlated with IL-1β expression and steatosis severity in NAFLD. These data demonstrated that amelioration of metabolic inflammation and weight loss reduced hepatic GDF15 expression. Conclusion. Based on recent mechanistic findings, our data suggest that hepatic GDF15 may serve as a negative feedback mechanism to control energy balance in NAFLD.

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Gain and loss of subcutaneous and abdominal fat depot mass from late pregnancy to 100 days in milk in German Holsteins

Journal of Dairy Research ◽

10.1017/s0022029919000542 ◽

2019 ◽

Vol 86 (3) ◽

pp. 296-302 ◽

Cited By ~ 4

Author(s):

Lena Ruda ◽

Claudia Raschka ◽

Korinna Huber ◽

Reka Tienken ◽

Ulrich Meyer ◽

...

Keyword(s):

Adipose Tissue ◽

Energy Balance ◽

Energy Density ◽

Negative Energy ◽

Negative Energy Balance ◽

Lactation Period ◽

Dry Period ◽

Gain And Loss ◽

The Impact ◽

Daily Gain

AbstractThis research paper addresses the hypothesis that in times of negative energy balance around parturition in dairy cattle, lipids stored in adipocytes are mobilised in a more intensive manner out of the abdominal depots than out of the subcutaneous adipose tissues. Furthermore, the impact of niacin supplementation and energy density of the ration on adipose tissue mass gain and loss was assessed. Absolute masses of subcutaneous (SCAT), retroperitoneal (RPAT), omental (OMAT), mesenterial (MAT) and abdominal adipose tissue as a whole (AAT) were estimated by ultrasonography at −42, 3, 21 and 100 DIM. Absolute and relative daily gain during dry period (−42 to 3 DIM) and loss in fresh cow period (3 to 21 DIM) and early lactation period (22 to 100 DIM) were calculated. Feeding regime neither by niacin nor by energy density exerted any effect on adipose tissue masses. The AAT was always bigger than SCAT, but RPAT, OMAT and MAT did not differ amongst each other. All depot masses showed similar patterns with an increase during dry period and a decrease after calving. In fresh cow period AAT absolutely and relatively lost more mass than SCAT. This confirms that AAT is more intensively mobilised than SCAT during that time span. Further absolute daily gain during dry period was strongly negatively correlated with absolute daily loss during fresh cow period. This underlines the impact of individual body condition on adipose mobilisation in periparturient dairy cows. According to these results, it has to be taken into account that the largest amount of fat mobilised in the fresh cow period origins from AAT. This might impact the pattern of adipose derived metabolites and metabolic effectors interacting in physiological and deregulated adaptation to negative energy balance.

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Lipid Metabolism in the Cattle in Different Stages of Reproductive Cycle

Asian Journal of Agriculture and Food Sciences ◽

10.24203/ajafs.v9i6.6836 ◽

2021 ◽

Vol 9 (6) ◽

Author(s):

Mihok Tomáš ◽

Bujňák Lukáš ◽

Hreško Šamudovská Alena ◽

Maskaľová Iveta ◽

František Zigo

Keyword(s):

Oxidative Stress ◽

Lipid Metabolism ◽

Energy Balance ◽

Reproductive Cycle ◽

Biochemical Parameters ◽

Negative Energy ◽

Specific Effects ◽

Normal Ranges ◽

Peripartum Period ◽

The Impact

The aim of this study was to evaluate the effect of feeding dairy cows in different stages of reproductive cycle on biochemical parameters and oxidative stress. To evaluate the effect of oxidative stress on lipids and lipid metabolism and to determine the impact of nutrition and energy balance on oxidative stress in peripartum period and in early lactation. Concentrations of different biochemical parameters were measured but for this paper the most important ones were indicators of oxidative stress, cholesterol and triglycerides and also albumin. Factors associated with oxidative stress were period 3 weeks before calving and related to that negative energy balance and also content of nonfiber carbohydrates in the diet in peripartum period. However, further studies will be needed to more precisely determine the specific effects of diet and energy balance on oxidative stress in cows and to establish normal ranges for these biomarkers of oxidative stress.

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Retention of sedentary obese visceral white adipose tissue phenotype with intermittent physical activity despite reduced adiposity

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00042.2015 ◽

2015 ◽

Vol 309 (5) ◽

pp. R594-R602 ◽

Cited By ~ 19

Author(s):

Katherine S. Wainright ◽

Nicholas J. Fleming ◽

Joe L. Rowles ◽

Rebecca J. Welly ◽

Terese M. Zidon ◽

...

Keyword(s):

Oxidative Stress ◽

Physical Activity ◽

Adipose Tissue ◽

White Adipose Tissue ◽

Immune Cell ◽

Regular Physical Activity ◽

Metabolic Phenotype ◽

Running Wheels ◽

The Impact ◽

And Oxidative Stress

Regular physical activity is effective in reducing visceral white adipose tissue (AT) inflammation and oxidative stress, and these changes are commonly associated with reduced adiposity. However, the impact of multiple periods of physical activity, intercalated by periods of inactivity, i.e., intermittent physical activity, on markers of AT inflammation and oxidative stress is unknown. In the present study, 5-wk-old male C57BL/6 mice were randomized into three groups ( n = 10/group): sedentary, regular physical activity, and intermittent physical activity, for 24 wk. All animals were singly housed and fed a diet containing 45% kcal from fat. Regularly active mice had access to voluntary running wheels throughout the study period, whereas intermittently active mice had access to running wheels for 3-wk intervals (i.e., 3 wk on/3 wk off) throughout the study. At death, regular and intermittent physical activity was associated with similar reductions in visceral AT mass (approximately −24%, P < 0.05) relative to sedentary. However, regularly, but not intermittently, active mice exhibited decreased expression of visceral AT genes related to inflammation (e.g., monocyte chemoattractant protein 1), immune cell infiltration (e.g., CD68, CD11c, F4/80, CD11b/CD18), oxidative stress (e.g., p47 phagocyte oxidase), and endoplasmic reticulum stress (e.g., CCAAT enhancer-binding protein homologous protein; all P < 0.05). Furthermore, regular, but not intermittent, physical activity was associated with a trend toward improvement in glucose tolerance ( P = 0.059). Collectively, these findings suggest that intermittent physical activity over a prolonged period of time may lead to a reduction in adiposity but with retention of a sedentary obese white AT and metabolic phenotype.

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The Integrase Inhibitors Dolutegravir and Raltegravir Exert Proadipogenic and Profibrotic Effects and Induce Insulin Resistance in Human/Simian Adipose Tissue and Human Adipocytes

Clinical Infectious Diseases ◽

10.1093/cid/ciaa259 ◽

2020 ◽

Vol 71 (10) ◽

pp. e549-e560 ◽

Cited By ~ 7

Author(s):

Jennifer Gorwood ◽

Christine Bourgeois ◽

Valérie Pourcher ◽

Guillaume Pourcher ◽

Frédéric Charlotte ◽

...

Keyword(s):

Oxidative Stress ◽

Insulin Resistance ◽

Stem Cells ◽

Adipose Tissue ◽

Adipose Stem Cells ◽

Strand Transfer ◽

Adipocyte Size ◽

The Impact

Abstract Background Although some integrase strand transfer inhibitors (INSTIs) promote peripheral and central adipose tissue/weight gain in people with human immunodeficiency virus (PHIV), the underlying mechanism has not been identified. Here, we used human and simian models to assess the impact of INSTIs on adipose tissue phenotype and function. Methods Adipocyte size and fibrosis were determined in biopsies of subcutaneous and visceral adipose tissue (SCAT and VAT, respectively) from 14 noninfected macaques and 19 PHIV treated or not treated with an INSTI. Fibrosis, adipogenesis, oxidative stress, mitochondrial function, and insulin sensitivity were assessed in human proliferating or adipocyte-differentiated adipose stem cells after long-term exposure to dolutegravir or raltegravir. Results We observed elevated fibrosis, adipocyte size, and adipogenic marker expression in SCAT and VAT from INSTI-treated noninfected macaques. Adiponectin expression was low in SCAT. Accordingly, SCAT and VAT samples from INSTI-exposed patients displayed higher levels of fibrosis than those from nonexposed patients. In vitro, dolutegravir and, to a lesser extent, raltegravir were associated with greater extracellular matrix production and lipid accumulation in adipose stem cells and/or adipocytes as observed in vivo. Despite the INSTIs’ proadipogenic and prolipogenic effects, these drugs promoted oxidative stress, mitochondrial dysfunction, and insulin resistance. Conclusions Dolutegravir and raltegravir can directly impact adipocytes and adipose tissue. These INSTIs induced adipogenesis, lipogenesis, oxidative stress, fibrosis, and insulin resistance. The present study is the first to shed light on the fat modifications observed in INSTI-treated PHIV.

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