Mukhopadhyay (2007) found that those living in towns suffered more perceived psychosocial stress and consequently greater prevalence of obesity.
Further potential evidence of a link between insecurity, stress, and obesity is that of the seven nations in which obesity is greatest, five are Anglophonic (U.S., U.K., Australia, New Zealand, and Canada). The non- Anglophonic are Germany (number 3) and Iceland (number 5). Following upon the work of La Porta et. al. (1999), Cutler, Glaeser, and Shapiro point out that “Countries with a common law legal origin (the British model) are much less regulated than are countries with a civil law origin (the French model)… [and that] More regulated countries are 7 percent less obese than are less regulated countries” (2003: 111-112). Less regulated countries enable a more rapid disintegration of the security of traditional social institutions. Anglo-Saxon nations have more readily adopted laissez-faire approaches to their economies, which has generally entailed weaker safety nets and social support systems and hence greater insecurity. The prevalence of obesity in the U.K. is second only to that in the U.S. Yet in the U.K. it has increased faster, starting at a lower level. It is noteworthy that this occurred in the wake of the so- called Thachter revolution in which labor and social protections were shredded (Vlad 2003). Further, between 1984 and 1990, the Gini coefficient for the U.K. rose a striking 10 points, indicating a greater increase in inequality than in any other OECD country (Irvin 2007: 10).
In in vivo studies, it has also been described that ICV injection of saturated fatty acids, in particular arachidonic acid (C20:0), induces ER stress in the hypothalamus of rats  . More recently, elegant studies from Contreras and collaborators have identiﬁed ceramides as another lipotoxic metabolite able to elicit hypothala- mic liptoxicity and ER stress  . Central ceramide delivery enhances hypothalamic expression of ER stress markers and causes overweight due to decreased sympathetic tone to BAT and reduced thermogenesis. Genetic over-expression of BIP/GRP78, a chaperone that facilitates the proper protein folding acting upstream the UPR pathways, speciﬁcally in the ventromedial nucleus of the hypotha- lamus (VMH) reversed ceramide-induced ER stress and metabolic alterations. Opposite biological effects were observed in experi- ments in which BIP/GRP78 was inactivated in the VMH using dominant negative adenovirus. Interestingly, obese Zucker rats exhibited increased levels of ceramides and increased UPR response in the VMH. Overexpression of BIP/GRP78 in the VMH of obese Zucker rats was able to ameliorate their metabolic pheno- type and enhance leptin (pSTAT3) signaling in this hypothalamic region. Overall, these data identiﬁed ceramide accumulation in the VMH as a novel lipotoxic process that eventually leads to ER stress and obesity  ( Table 1 ).
obesity and found that the number of parental stressors (as operationalized by physical health, mental health, financial strain, and family structure) was directly positively related to child obesity (Parks et al., 2012). This particularly held true for ethnic minority groups. Other variables that may play a role in understanding the relations between stress, parental feeding style, and pediatric obesity include (a) whether or not the child lives in a single parent home, (b) the amount of time a parent has to prepare meals and implement mealtime, (c) whether or not a parent is able to be present for meals on a consistent basis, (d) the behaviors of the child, (e) the presence of other children during the meal itself, and (f) the amount of work stress a parent may experience. All of these factors can affect the manner in which a parent behaves during mealtime as well as the level of his or her stress, and may have added uncontrolled variance to the current study’s analyses. The multitude of potential interactive effects these variables may have on parenting stress and child BMI suggest that parental feeding style may have had a smaller influence than hypothesized in the relationship between stress and obesity.
Chapter 5: Discussions, Recommendations, Conclusion and Summary The purpose of this research was to investigate the relationship between age, gender, SES, lifestyle indicators (diet, physical activity), psychosocial indicators
(acculturation, perceived stress) and obesity in the Meskhetian Turk (Ahiska) immigrant population. The quantitative methodology used to determine the study outcome in consideration of these predictor variables and obesity. The findings of this study were important to see if there was an interaction between variables and obesity in this sample group. As mentioned, obesity is a chronic health problem that may trigger different health issues in immigrant populations including heart diseases, stroke, diabetes, stress, high cholesterol and high blood pressure (Adedoyin et al., 2010; Ade et al., 2011; Albrecht & Gordon-Larsen, 2013; Gele & Mbalilaki, 2013; Jamil et al., 2014; Ike-Chinaka, 2013; Kaholokula et al., 2012; Kirby et al., 2012; Krueger et al., 2014). Many studies showed that immigrant populations are vulnerable to obesity and they need to have a better understanding of obesity and its health implications (Ade et al., 2011; Gele & Mbalilaki, 2013; Ike-Chinaka, 2013). Due to negative health implications of obesity in different immigrant populations (Obisesan, 2015), there was a need to examine the association between different variables and obesity.
Methylglyoxal is the precursor of the major quantitative ad- vanced glycation endproducts in physiological systems - argi- nine-derived hydroimidazolones and deoxyguanosine-derived imidazopurinones. Glyoxalase 1 of the glyoxalase system was linked to anthropometric measurements of obesity in human subjects and to body weight in strains of mice. Recent confer- ence reports described increased weight gain on high fat diet- fed mouse with lifelong deficiency of glyoxalase 1 deficiency, compared to wild-type controls, and decreased weight gain in glyoxalase 1-overexpressing transgenic mice, suggesting a functional role of glyoxalase 1 and dicarbonyl stress in obesi- ty. Increased methylglyoxal, dicarbonyl stress, in white adi- pose tissue and liver may be a mediator of obesity and insulin resistance and thereby a risk factor for development of type 2 diabetes and non-alcoholic fatty liver disease. Increased methylglyoxal formation from glyceroneogenesis on adipose tissue and liver and decreased glyoxalase 1 activity in obesity likely drives dicarbonyl stress in white adipose tissue increas- ing the dicarbonyl proteome and related dysfunction. The clin- ical significance will likely emerge from on-going clinical
3 University of Novi Sad, Faculty of Science
Obesity is a serious medical condition, defined as excessive accumulation of fat. Abdominal fat is recognized as the major risk for obesity related diseases such as: hypertension, dyslipidemia, type 2 diabetes mellitus, coronary heart disease, stroke, non-alcoholic fatty liver disease etc. Fat accu- mulation is also related to pro-oxidant and pro-inflammatory states. Recently published articles suggest that oxidative stress may be a link between obesity and related complications. Adiposity leads to increased oxidative stress via several multiple biochemical processes such as superoxide generation through the action of NADPH oxidase, glyceraldehyde auto-oxidation, oxidative phos- phorylation, protein kinase C (PKC) activation, and polyol and hexosamine pathways. On the other hand, oxidative stress plays a causative role in the development of obesity, by stimulating the deposition of adipose tissue, including preadipocyte proliferation, adipocyte differentiation and growth. Exercise-induced weight loss can improve the redox state by modulating both oxidative stress and antioxidant promoters, which reduce endothelial dysfunction and inflammation.
It is therefore necessary to assess the potential importance of intervention strategies to reduce obesity in the population 48 . In general, the serum levels of antioxidant status are significantly higher (p < 0.05) in men than in women; it comes to the percentage of physical inactivity;
93.88% of women do not practice any physical activity. Then it should be noted that the practice of moderate physical activity reduces oxidative stress, while a sustained exercise leads to an overproduction of reactive oxygen species (ROS), not offset by the increase in defense systems, this is therefore not a desirable approach 49 . We found that serum antioxidant vitamins in hypertensive individuals is in the standards However the study of 50,51 in patients suffering from hypertension, oxidative stress has been shown, there may be a deficit of antioxidant defenses 50 as an excess of ROS production 51 . Our result may be explained by adaptation developed by these individuals to oxidative stress and / or diet varied.
larly, obese individuals and parents of obese children tend to underreport the intake of high-fat and high-sugar foods 43 – 45 and would make our re- sults for child fast-food consumption conservative. The effect of parent- report measures on meeting fruit and vegetable and activity guidelines, however, is unknown. Additionally, parent-reported heights and weights were used and have been shown to be accurate in estimating BMI in children . 13 years, even though adolescents themselves underestimate BMI. 46 – 48 Parents, however, overestimate the prevalence of overweight and un- derestimate obesity prevalence in preschool-aged children and school- children. 46,47 To account for potential overestimation of the overweight cat- egory, we dichotomized our outcome to $ 95th percentile or # 95th percen- tile. Thus, although some truly obese TABLE 4 Results of Logistic Regression Analyses of Parent Perception of Stress Level and Covariates on Obesity, Fast-Food Consumption, Fruit and
Obesity is a principal causative factor in the development of metabolic syndrome. Here we report that increased oxidative stress in accumulated fat is an important pathogenic mechanism of obesity-associated metabolic syndrome. Fat accumulation correlated with systemic oxidative stress in humans and mice. Production of ROS increased selectively in adipose tissue of obese mice, accompanied by augmented expression of NADPH oxidase and decreased expression of antioxidative enzymes. In cultured adipocytes, elevated levels of fatty acids increased oxidative stress via NADPH oxidase activation, and oxidative stress caused dysregulated produc- tion of adipocytokines (fat-derived hormones), including adiponectin, plasminogen activator inhibitor–1, IL-6, and monocyte chemotactic protein–1. Finally, in obese mice, treatment with NADPH oxidase inhibitor reduced ROS production in adipose tissue, attenuated the dysregulation of adipocytokines, and improved diabetes, hyperlipidemia, and hepatic steatosis. Collectively, our results suggest that increased oxidative stress in accumulated fat is an early instigator of metabolic syndrome and that the redox state in adipose tissue is a potentially useful therapeutic target for obesity-associated metabolic syndrome.
Basil S. Karam 1 , Alejandro Chavez‑Moreno 1 , Wonjoon Koh 1 , Joseph G. Akar 2 and Fadi G. Akar 1*
Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia in humans. Several risk factors promote AF, among which diabetes mellitus has emerged as one of the most important. The growing recognition that obesity, diabetes and AF are closely intertwined disorders has spurred major interest in uncovering their mechanistic links. In this article we provide an update on the growing evidence linking oxidative stress and inflammation to adverse atrial structural and electrical remodeling that leads to the onset and maintenance of AF in the diabetic heart. We then discuss several therapeutic strategies to improve atrial excitability by targeting pathways that control oxidative stress and inflammation.
KEYWORDS: Type-2 diabetes, Obesity, Adipokines, Leptin, Resistin, Apelin, Oxidative stress, Malondialdehyde.
During the last twenty years the prevalence of diabetes has increased dramatically in many parts of the world. As of 2014, an estimated 387 million people have diabetes worldwide with type 2 diabetes making up about 90% of the cases.  The number of people with diabetes is expected to rise to 592 million by 2035, this is equal to 8.3% of the adult population,  The disease is now a worldwide public health problem. 
(Alaimo, Olson & Frongillo, 2001; Drewnowski & Specter, 2004). Food insecurity may be especially influential among low-income minority groups in the development of obesity and other obesity related diseases (Winkleby, Robinson, Sundquist, & Kraemer, 1999; Casey et al., 2006.) As such, food insecurity was examined as a possible moderator of the relations among stress, hair cortisol and zBMI. The current study found that food insecurity moderated the relation between hair cortisol levels and zBMI such that children with the highest hair cortisol levels and the highest food insecurity had the highest zBMI. This finding supports previous research indicating that food insecurity is related to excess adipose among children. However, this finding expands upon previous findings: children with increased levels of hair cortisol due to chronic stress and food insecurity may be more likely to overconsume high calorie and low nutrient foods. For highly stressed low income Mexican-origin children, fearing that there will not be enough food to eat may accelerate the fat-storing biological processes responsible for obesity.
CL is a polyglycerophospholipid exclusively localized in the mitochondria, where it regulates mitochondrial function and oxida- tive stress in species from yeast to mammals ( Chen et al., 2008; Chicco and Sparagna, 2007 ). This role is mediated by the acyl composition of the side chains of CL, which is dominated by lino- leic acid in insulin-sensitive tissues ( Schlame et al., 2000 ). This unique acyl composition is not derived from de novo synthesis of CL, but rather from a remodeling process that involves phospho- lipases and acyltransferase-transacylases ( Cao et al., 2004; Taylor and Hatch, 2009; Xu et al., 2003 ). Additionally, CL remodeling is believed to replace damaged acyl chains under normal conditions. However, this remodeling process is also capable of generating CL species that are highly sensitive to oxidative damage by ROS under pathological conditions, further exacerbating CL peroxida- tion and oxidative stress. CL is highly sensitive to damage of its double bonds by oxidative stress due to its rich content in linoleic acid and its location near the site of ROS production in the inner mitochondrial membrane. Consequently, CL has been shown to be the only phospholipid in mitochondria that undergoes early oxidation during apoptosis ( Kagan et al., 2005 ). Therefore, patho- logical CL remodeling has been implicated in the etiology of mito- chondrial dysfunction associated with a host of pathophysiolog- ical conditions, including diabetes, obesity, cardiovascular diseases, and aging, all of which are characterized by increased oxidative stress, CL deficiency, and enrichment of docosahexae- noic acid (DHA) content in CL ( Han et al., 2007; Sparagna and Les- nefsky, 2009 ). However, little is known about the molecular mech- anisms governing the pathological remodeling of CL and its relevance to mitochondrial dysfunction in metabolic diseases.
We have therefore chosen to focus on IL-1 β as a potential link between repeated stress and the development of vis- ceral obesity. Within this framework, the data presented in Figure 2 lead to two important questions: 1) what is the functional significance of a regionally specific increase in subcutaneous IL-1β following acute stressor exposure and 2) how might repeated activation of this response play a role in the development of visceral obesity? Whereas the acute activation of this response likely serves beneficial functions, we hypothesize that repeated induction of this depot specific response may dampen the ability of non- visceral adipose tissue to absorb, retain lipids and/or ex- pand via hyperplasia. Consequently visceral adipose depos- ition is increased, thus yielding potential mechanisms whereby stress-induced IL-1 β signaling may affect body fat distribution. These hypotheses are further discussed in the final sections of this review.
scores, uncontrolled eating scores, and cognitive restraint scores provide an avenue to evaluate the potential effectiveness of yoga to improve self-regulation of food intake in addition to changes in weight.
The following chapters describe three studies that have added to the current knowledge about eating behaviors, stress, sleep, physical activity, food insecurity and obesity. Chapter Two provides results from a study in which college students in multiple sections of a general education class completed a survey that assessed eating behaviors, perceived stress, sleep, amount of physical activity, food insecurity, and other self- reported variables. Chapter Three presents results from analysis of baseline data from participants in a weight loss program that were dually enrolled in an intervention
Our study is cross-sectional, so we may miss longtime dietary behaviors that contribute to weight gain. Thus, the direct association between perceived stress and se- vere obesity may reflect confounding by unmeasured longtime obesogenic dietary behaviors. In contrast, other non-diet-related factors may be associated with high levels of stress and severe obesity. For example, low- income women with high levels of stress may not have time for physical activity. In this case, the direct associ- ation between high levels of perceived stress and severe obesity may reflect confounding associations with a lack of physical activity that we were not able to include in our model. Low-income women who are stressed be- cause of a lack of financial resources may also lack physical activity time, which would increase obesity risk.
Saroha, Vivek and Dellschaft, Neele S. and Keisler,
Duane H. and Gardner, David S. and Budge, Helen and Sebert, Sylvain P. and Symonds, Michael E. (2017)
Tissue cell stress response to obesity and its interaction with late gestational diet. Reproduction, Fertility and Development . ISSN 1448-5990
Siburex10 TM shows weight reducing effect which in turn helped reduce oxidative stress.
The present study shows that obesity induction had caused an increase in lipid peroxidation and consequent decrease in superoxide dismutase, catalase and glutathione at both durations. Triphala, trikatu, and their combination were effective in restoring the above parameters. Ayurslim seems to be more effective in restoring lipid peroxidation and SOD activities. Siburex10 TM was effective in restoring catalase and glutathione. Our results suggest that the amelioration of obesity induced cardiotoxicity by Triphala and Trikatu may be related to its antioxidant property and therefore represents a potential therapeutic strategy for obesity With the exception of Orlistat and Sibutramine (Food and Drug Administration (FDA) approved drugs) most of the conventional drugs produce side effects and there is relapse of obesity after cessation of treatment. From this perspective botanicals have been screened for anti – obesity property. Triphala and Trikatu may be helpful in mitigating this particular side effect of such drugs. However, the effectiveness of the active components of Triphala and Trikatu in obesity and mechanisms involved require further investigation.
GSH enzyme activity is much lower than that of the positive control group. GSH enzyme works to convert H 2 O 2 to H 2 O and O 2 , but with hypoxia, the availability of O 2 is reduced. This is probably because the H 2 O 2 stack cannot be converted to O 2 perfectly, due to the low activity of the enzyme. The condition of obesity is independently correlated with high oxidative stress and inflammatory markers. Increased oxidative stress and inflammation in obesity play an important role in the initiation and progression of vascular disease, or it may also lead to the initiation of carcinogenesis in obesity  . The mechanisms responsible for the high state of oxidative stress in obesity are not yet known, but clearly, adipose tissue is one of the important oxidative and inflammatory stress mediators as it contributes to the production of free radicals and proinflammatory cytokines, including IL-6, and TNF alpha.