Oxidative Stress In Obesity Research Articles

Literature Review: The effect of modification diet and antioxidant on inflammatory and oxidative stress concentration in obesity

Obesity is also associated with increased inflammation and oxidative stress. Mediterranean and dash diets, as well as antioxidants, can reduce inflammation and oxidative stress levels in obesity. This study aimed to determine the effects of dietary modifications and antioxidants on inflammatory and oxidative stress levels in obesity. This study was carried out using the literature review method using PubMed, Science Direct, and Google Scholar databases with the keywords Mediterranean Diet, DASH Diet, Antioxidant, Obesity, Inflammation, and Oxidative Stress. The inclusion criteria in this literature are articles published in the last 5 years (2018-2023) using RCT, in English, subjects >18 years old with obesity, interventions providing Mediterranean and dash diet, antioxidants derived from natural ingredients, and articles that can be accessed online. Articles were selected individually through a double process, considering the three main research quality criteria. This study showed that a modified diet and antioxidants can reduce inflammatory biomarkers and oxidative stress in obesity by suppressing NF-κB signaling and protecting against DNA damage. In conclusion, a modified diet and antioxidants can reduce inflammatory and oxidative stress in obesity.

The role of polymorphism of redox-sensitive genes in the mechanisms of oxidative stress in obesity and metabolic diseases

The review summarizes ideas about the role of polymorphic variants of redox-sensitive genes that regulate the development of oxidative stress in obesity and associated metabolic diseases. The concept of oxidative stress, activated oxygen metabolites (AOM), which include reactive forms of oxygen, nitrogen, and chlorine, is considered, and an idea of the antioxidant system and its enzymatic link is given. The important role of gene polymorphism of AOM-producing enzymes — CYBA, CYBB, MT-ND1/2/4L, MT-CO1/3, XOR, CYP, NOS2/3, MPO — in the induction of oxidative stress in obesity has been shown. The dualism of AOM in obesity is emphasized: on the one hand, they are necessary for normal adipogenesis and signaling, and, on the other hand, they play a trigger role in the development of oxidative stress. It has been demonstrated that an imbalance in antioxidant system in obesity and metabolic disorders may be associated with variability in the genes of key antioxidant enzymes and proteins — SOD1/2/3, CAT, GPX1-8, GSR, GSTP1, GSTM1, GSTT1, PRDX3, TXNIP, HMOX1, NQO1, NFE2L2, KEAP1. The critical role of polymorphism in the Nrf2 transcription factor gene, the main regulator of redox homeostasis under physiological conditions and in obesity, has been demonstrated. It has been demonstrated that disruption of redox homeostasis due to genetic variability of the prooxidant-antioxidant system contributes to the development of the pathological obesity phenotype. Understanding the genetic mechanisms underlying oxidative stress in obesity and metabolic diseases is necessary to expand knowledge about the mechanisms of pathogenesis of these diseases and to develop effective methods for their correction.

Perivascular Adipose Tissue Oxidative Stress in Obesity.

Perivascular adipose tissue (PVAT) adheres to most systemic blood vessels in the body. Healthy PVAT exerts anticontractile effects on blood vessels and further protects against cardiovascular and metabolic diseases. Healthy PVAT regulates vascular homeostasis via secreting an array of adipokine, hormones, and growth factors. Normally, homeostatic reactive oxygen species (ROS) in PVAT act as secondary messengers in various signalling pathways and contribute to vascular tone regulation. Excessive ROS are eliminated by the antioxidant defence system in PVAT. Oxidative stress occurs when the production of ROS exceeds the endogenous antioxidant defence, leading to a redox imbalance. Oxidative stress is a pivotal pathophysiological process in cardiovascular and metabolic complications. In obesity, PVAT becomes dysfunctional and exerts detrimental effects on the blood vessels. Therefore, redox balance in PVAT emerges as a potential pathophysiological mechanism underlying obesity-induced cardiovascular diseases. In this review, we summarise new findings describing different ROS, the major sources of ROS and antioxidant defence in PVAT, as well as potential pharmacological intervention of PVAT oxidative stress in obesity.

The Influence of Antioxidants on Oxidative Stress-Induced Vascular Aging in Obesity.

Obesity is a worldwide trend that is growing in incidence very fast. Adipose tissue dysfunction caused by obesity is associated with the generation of oxidative stress. Obesity-induced oxidative stress and inflammation play a key role in the pathogenesis of vascular diseases. Vascular aging is one of the main pathogenesis mechanisms. The aim of this study is to review the effect of antioxidants on vascular aging caused by oxidative stress in obesity. In order to achieve this aim, this paper is designed to review obesity-caused adipose tissue remodeling, vascular aging generated by high levels of oxidative stress, and the effects of antioxidants on obesity, redox balance, and vascular aging. It seems that vascular diseases in obese individuals are complex networks of pathological mechanisms. In order to develop a proper therapeutic tool, first, there is a need for a better understanding of interactions between obesity, oxidative stress, and aging. Based on these interactions, this review suggests different lines of strategies that include change in lifestyle to prevent and control obesity, strategies for adipose tissue remodelling, oxidant-antioxidant balance, inflammation suppression, and strategies against vascular aging. Some antioxidants support different lines of these strategies, making them appropriate for complex conditions such as oxidative stress-induced vascular diseases in obese individuals.

Semaglutide ameliorates obesity-induced cardiac inflammation and oxidative stress mediated via reduction of neutrophil Cxcl2, S100a8, and S100a9 expression.

Obesity, which is driven by inflammation and oxidative stress, is a risk factor for cardiovascular disease. Semaglutide, a glucagon-like peptide-1 receptor agonist, is an antidiabetic drug with major effects on weight loss. In this study, single-cell transcriptomics was used to examine non-cardiomyocytes to uncover the mechanism of obesity-induced myocardial damage and the cardioprotective impact of semaglutide. We constructed obese mouse models and measured Tumor Necrosis Factor-α (TNF-α), Interleukin-6 (IL-6), Reactive Oxygen Species (ROS), and Malonic dialdehyde (MDA) levels in serum and heart tissue to determine the levels of inflammation and oxidative stress in obesity and the effect of semaglutide on these levels. Then, utilizing single-cell transcriptomes to screen for key cell populations and differentially expressed genes (DEGs), we assessed the effects of obesity and semaglutide on non-cardiac cells. Finally, a DEG localization analysis was performed to explore DEGs as well as cell types associated with inflammation and oxidative stress. Semaglutide reduced increased TNF-α, IL-6, ROS, and MDA levels in serum and cardiac tissues in obese mouse. Several genes are closely associated with inflammation and oxidative stress. Chemokine (C-X-C motif) ligand 2 (Cxcl2), S100 calcium binding protein A8 (S100a8), and S100 calcium binding protein A9 (S100a9), which were elevated in obesity but decreased following semaglutide treatment, were also expressed particularly in neutrophils. Finally, by decreasing neutrophil Cxcl2, S100a8, and S100a9 expressions, semaglutide may help to reduce cardiac inflammation and oxidative stress. Semaglutide significantly reduced body weight in obese mice as well as exerted anti-inflammatory and antioxidant effects possibly by inhibiting the expression of S100a8, S100a9, and Cxcl2 in neutrophils. These discoveries are expected to reveal new molecular mechanisms underlying obesity-related heart damage and semaglutide's cardioprotective properties.

Angiotensin II type 2 receptor as a novel activator of brown adipose tissue in obesity.

The angiotensin II type 2 receptor (AT2R) exerts vasorelaxant, anti-inflammatory, and antioxidant properties. In obesity, its activation counterbalances the adverse cardiovascular effects of angiotensin II mediated by the AT1R. Preliminary results indicate that it also promotes brown adipocyte differentiation in vitro. Our hypothesis is that AT2R activation could increase BAT mass and activity in obesity. Five-week-old male C57BL/6J mice were fed a standard or a high-fat (HF) diet for 6 weeks. Half of the animals were treated with compound 21 (C21), a selective AT2R agonist, (1 mg/kg/day) in the drinking water. Electron transport chain (ETC), oxidative phosphorylation, and UCP1 proteins were measured in the interscapular BAT (iBAT) and thoracic perivascular adipose tissue (tPVAT) as well as inflammatory and oxidative parameters. Differentiation and oxygen consumption rate (OCR) in the presence of C21 was tested in brown preadipocytes. In vitro, C21-differentiated brown adipocytes showed an AT2R-dependent increase of differentiation markers (Ucp1, Cidea, Pparg) and increased basal and H+ leak-linked OCR. In vivo, HF-C21 mice showed increased iBAT mass compared to HF animals. Both their iBAT and tPVAT showed higher protein levels of the ETC protein complexes and UCP1, together with a reduction of inflammatory and oxidative markers. The activation of the AT2R increases BAT mass, mitochondrial activity, and reduces markers of tissue inflammation and oxidative stress in obesity. Therefore, insulin reduction and better vascular responses are achieved. Thus, the activation of the protective arm of the renin-angiotensin system arises as a promising tool in the treatment of obesity.

Oxidative stress-related impairment of endothelial function in uncomplicated obesity

Purpose: Visceral obesity is associated with vascular oxidative stress and development of hypertension. Therefore, we tested the hypothesis that suppression of vascular oxidative stress in adults with visceral obesity would improve endothelium-dependent dilation. Methods: IV infusion of a water-soluble antioxidant (ascorbic acid) was performed in 15 middle-age obese adults (3 men/12 women) without diabetes or hypertension in a placebo-controlled, double-blinded, crossover study design. Ascorbic acid was infused at 0.06g/kg fat free mass in 100 ml saline at 5 mL/min over 20 min (bolus) followed by a drip infusion at 0.02 g/kg fat-free mass in 30 ml saline at 0.5 mL/min over 60 min. Endothelium-dependent dilation was assessed via brachial artery flow-mediated dilation (FMD) and expressed as % increase in diameter from baseline before forearm occlusion. Results: Android fat distribution in the visceral cavity (VAT%) was 39 ± 10% and body mass index (BMI) was 37 ± 6 kg/m2. IV infusion significantly increased plasma ascorbic acid concentrations (Baseline: 42 ± 2 vs. Bolus: 66 ± 6 vs. End: 62 ± 4 μmol/L, P<0.001). Compared with baseline, bolus infusion of ascorbic acid significantly increased FMD (Baseline: 5.8 ± 2.5 vs. Bolus: 9.0 ± 4.0 vs. End: 8.0 ± 4.2 %, P=0.01), which remained after statistically adjusting for the stimulus (shear rate area under the curve) via analysis of covariance (P=0.04). No significant change in FMD was observed following placebo (saline) during a separate study visit (Baseline: 8.0 ± 4.4 vs. Bolus: 8.3 ± 3.9 vs. End: 8.6 ± 2.9 %, P=0.86). Conclusions: These preliminary findings suggest that acute elevations in plasma ascorbic acid concentrations improve endothelium-dependent dilation in middle-aged adults with visceral obesity. Future studies should target mechanisms by which mediators of oxidative stress in obesity (e.g., hyperlipidemia, hyperinsulinemia) inhibit nitric oxide-mediated vasodilation. Funding and support: R01HL159370-01 (S.W.H.). This work was also supported by a CTSA grant from NCATS awarded to the University of Kansas for Frontiers: University of Kansas Clinical and Translational Science Institute (# UL1TR002366). The contents are solely the responsibility of the authors and do not necessarily represent the official views of the NIH or CTSA. This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

N-Acetylcysteine Decreases Myocardial Content of Inflammatory Mediators Preventing the Development of Inflammation State and Oxidative Stress in Rats Subjected to a High-Fat Diet.

Arachidonic acid (AA) is a key precursor for proinflammatory and anti-inflammatory derivatives that regulate the inflammatory response. The modulation of AA metabolism is a target for searching a therapeutic agent with potent anti-inflammatory action in cardiovascular disorders. Therefore, our study aims to determine the potential preventive impact of N-acetylcysteine (NAC) supplementation on myocardial inflammation and the occurrence of oxidative stress in obesity induced by high-fat feeding. The experiment was conducted for eight weeks on male Wistar rats fed a standard chow or a high-fat diet (HFD) with intragastric NAC supplementation. The Gas-Liquid Chromatography (GLC) method was used to quantify the plasma and myocardial AA levels in the selected lipid fraction. The expression of proteins included in the inflammation pathway was measured by the Western blot technique. The concentrations of arachidonic acid derivatives, cytokines and chemokines, and oxidative stress parameters were determined by the ELISA, colorimetric, and multiplex immunoassay kits. We established that in the left ventricle tissue NAC reduced AA concentration, especially in the phospholipid fraction. NAC administration ameliorated the COX-2 and 5-LOX expression, leading to a decrease in the PGE2 and LTC4 contents, respectively, and augmented the 12/15-LOX expression, increasing the LXA4 content. In obese rats, NAC ameliorated NF-κB expression, inhibiting the secretion of proinflammatory cytokines. NAC also affected the antioxidant levels in HFD rats through an increase in GSH and CAT contents with a simultaneous decrease in the levels of 4-HNE and MDA. We concluded that NAC treatment weakens the NF-κB signaling pathway, limiting the development of myocardial low-grade inflammation, and increasing the antioxidant content that may protect against the development of oxidative stress in rats with obesity induced by an HFD.

Potential Role of Oxidative Stress in the Production of Volatile Organic Compounds in Obesity.

Obesity is associated with numerous health issues such as sleep disorders, asthma, hepatic dysfunction, cancer, renal dysfunction, diabetes, cardiovascular complications, and infertility. Previous research has shown that the distribution of excess body fat, rather than excess body weight, determines obesity-related risk factors. It is widely accepted that abdominal fat is a serious risk factor for illnesses associated with obesity and the accumulation of visceral fat promotes the release of pro-oxidants, pro-inflammatory, and reactive oxygen species (ROS). The metabolic process in the human body produces several volatile organic compounds (VOCs) via urine, saliva, breath, blood, skin secretions, milk, and feces. Several studies have shown that VOCs are released by the interaction of ROS with underlying cellular components leading to increased protein oxidation, lipid peroxidation, or DNA damage. These VOCs released via oxidative stress in obese individuals may serves as a biomarker for obesity-related metabolic alterations and disease. In this review, we focus on the relationship between oxidative stress and VOCs in obesity.

Oxidative Stress in Non-Obese & Obese Young Healthy Adults

Introduction: Obesity causes various diseases due to systemic oxidative stress. Young healthy obese are unaware of oxidative burden in their body. Total oxidant status (TOS) is a marker of oxidative stress in obesity.
 Aims & Objectives: This study was planned to determine and compare levels of TOS in young healthy non obese and obese, males and females and individuals with active versus sedentary lifestyle.
 Place and duration of study: This study was conducted over one month duration at six women and co-ed colleges of Lahore.
 Material & Methods: This cross-sectional comparative study was conducted on samples collected within one month from 160 healthy males and females, aged 20 to 40 years at APWA College, Lahore College Womens University, Government College University, Gulberg College, PAC Lahore, Ameeruddin Medical College Lahore (n=30 each college). The participants were divided into two groups based on the respondents BMI. TOS was measured colorimetrically. Data was analyzed using IBM-SPSS version 25. Mann Whitney U test compared TOS levels between non obese and obese subjects.
 Results: Fifty percent of the subjects had a normal BMI while 50% were obese according to the Asian Pacific criteria for BMI.Fifty-two percent of the population were males while forty-eight percent of the population was females. Group I (non obese) consisted of 55% males and 45% females with a significant difference in the levels of TOS. The population in Group II (obese) comprised of 50% males and females each also showing significant difference. Thirty-six percent (n=58) of the total population had active lifestyle while sixty-four percent (n=102) of the population had a sedentary lifestyle. While in Group 1(non obese) (64%) had an active lifestyle whereas the rest were sedentary. In comparison only 9% of group II subjects (obese) had an active lifestyle while the remainder were sedentary. A significant difference in level of TOS were seen when compared between subjects with active versus sedentary lifestyle in respective groups. A significant difference (p=0.03) was seen when TOS was compared between subjects with Active lifestyle 4.15(3.17- 5.42) µmol/lversus subjects with sedentary lifestyle 4.9(3.70-7.22) µmol/l.
 Conclusion: Increased levels of TOS were seen in young healthy obese as compared to non-obese. Both non obese and obese females had higher levels of TOS in comparison to males due to greater levels of body fat percentage. Subjects with a sedentary lifestyle have raised levels of TOS in comparison to subjects with active lifestyle.

The Benefits of High-Resistant Starch and Beta-Carotene Snack in Ameliorating Atherogenic Index and Inflammation in Obesity

BACKGROUND: In obesity, lipid abnormalities may be related to the higher risk of cardiovascular diseases associated with increased oxidation of lipids and inflammation. Resistant starch and beta-carotene reduce atherosclerosis risk related to low-grade inflammation and oxidative stress in obesity. AIM: This study aimed to evaluate the benefits of a snack containing high-resistant starch and beta-carotene in improving the atherogenic index of plasma (AIP) and inflammation in obesity. METHODS: This study used a single-blinded and randomized controlled design. Fifty subjects received 42 g of snacks per day for 6 weeks, either tested snacks or standard snacks. Anthropometry, body composition, lipid profile, tumor necrosis factor-alpha (TNF-α), and oxidized low-density lipoprotein (ox-LDL) were measured before and after intervention. RESULTS: The snack containing high-resistant starch and beta-carotene significantly decreased LDL, AIP, and TNF-α (p < 0.05). Positive correlations were found between AIP and triglycerides in both snacks (p < 0.05), LDL or TNF-α in the standard snack (p < 0.05), and TNF-α and ox-LDL in both snacks (p < 0.05). A negative correlation was found between AIP and HDL in both snacks (p < 0.05). CONCLUSIONS: A snack containing high-resistant starch and beta-carotene reduced AIP and inflammation by preventing LDL oxidation.

Monoamine oxidase is a source of cardiac oxidative stress in obese rats: the beneficial role of metformin.

Diet-induced metabolic diseases, such as obesity, metabolic syndrome, and type 2 diabetes (T2DM) are the global threatening epidemics that share cardiovascular oxidative stress as common denominator. Monoamine oxidase (MAO) has recently emerged as a constant source of reactive oxygen species (ROS) in DM. Metformin, the first-line drug in T2DM, elicits cardiovascular protection via pleiotropic effects. The present study was aimed to assess the contribution of MAO to the early cardiac oxidative stress in a rat model of high-calorie junk food (HCJF) diet-induced obesity and prediabetes and whether metformin can alleviate it. After 6months of HCJF, rats developed obesity and hyperglycemia. Hearts were isolated and used for the evaluation of MAO expression and ROS production. Experiments were performed in the presence vs absence of metformin (10µM) and MAO-A and B inhibitors (clorgyline and selegiline, 10µM), respectively. Both MAO isoforms were overexpressed and led to increased ROS generation in cardiac samples harvested from the obese animals. Acute treatment with metformin and MAO inhibitors was able to mitigate oxidative stress. More important, metformin downregulated MAO expression in the diseased samples. In conclusion, MAO contributes to oxidative stress in experimental obesity and can be targeted with metformin.

Pengaruh Proporsi Rumput Laut dan Sawo Mentega terhadap Serat Pangan, Aktivitas Antioksidan, Overrun, dan Sifat Organoleptik Sorbet

Lack of fiber and antioxidants can increase the risk of obesity which lead to oxidative stress. Eucheuma cottonii seaweed contains dietary fiber which provide anti-obesity effects. Beside dietary fiber, antioxidant is also needed to prevent oxidative stress in obesity. Canistel fruit (Pouteria campechiana) contains antioxidants such as vitamin C, beta carotene and polyphenols. The purpose of this study was to determine the effect of the proportion of seaweed and canistel on the content of dietary fiber, antioxidant activity, physical properties, and organoleptic properties of sorbet. This research method used a one-factor completely randomized design (CRD) with two repetitions. These factors are the proportion of seaweed and canistel, namely F1 (20%:80%), F2 (30%:70%), and F3 (40%:60%). The ANOVA test results showed that the proportion of seaweed and canistel had a significant effect (p< 0.05) on the dietary fiber and overrun, while the antioxidant activity and organoleptic properties of sorbet had no significant effect (p >0.05). The selected formula by using Exponential Comparison Method (ECM) results the F1 formula with the proportion of 20%:80%. The selected formula products contained 5.19% dietary fiber, 48% w / v antioxidant activity, and 34.32% overrun.

Efecto antioxidante de Ganoderma lucidum sobre la obesidad

The change in eating patterns has contributed
 to the suffering of one of the main public health problems.
 Obesity is defined as an energy imbalance, where there is
 excessive storage of energy. Oxidative stress originates
 when the redox state of the cell is affected because they are
 exposed to a pro-oxidant environment and the antioxidant
 mechanisms are overwhelmed. Dietary antioxidants are
 substances present in food and have a function of protecting
 the organism from the adverse effects of reactive oxygen
 species. In addition, oxidative stress in obesity can be
 counteracted through physical activity and by modifying the
 diet through functional foods with a high content of bioactive
 compounds with an antioxidant effect. Ganoderma lucidum is
 a medicinal mushroom with various bioactive compounds,
 among which phenolic compounds, polysaccharides and
 triterpenoids stand out, which are largely responsible for
 the antioxidant activity of this species. In the present work,
 a bibliographic review was carried out on the antioxidant
 effect of G. lucidum on obesity.

Oxidative stress in obesity and insulin resistance

Since obesity is one of the main factors in the development of insulin resistance (IR) and is also associated with increased oxidative stress (OxS) rate, this study aims to review the published literature to collate and provide a comprehensive summary of the studies related to the status of the OxS in the pathogenesis of obesity and related IR. OxS represents an imbalance between the production of reactive oxygen and nitrogen species (RONS) and the capacity of the antioxidant defense system (AOS) to neutralize RONS. A steady-state of RONS level is maintained through endogenous enzymatic and non-enzymatic AOS components. Three crucial enzymes, which suppress the formation of free radicals, are superoxide dismutases, catalases, and glutathione peroxidases. The second line of AOS includes non-enzymatic components such as vitamins C and E, coenzyme Q, and glutathione which neutralizes free radicals by donating electrons to RONS. Emerging evidence suggests that high RONS levels contribute to the progression of OxS in obesity by activating inflammatory pathways and thus leading to the development of pathological states, including IR. In addition, decreased level of AOS components in obesity increases the susceptibility to oxidative tissue damage and further progression of its comorbidities. Increased OxS in accumulated adipose tissue should be an imperative target for developing new therapies in obesity-related IR.

Differential contribution of renal cytochrome P450 enzymes to kidney endothelial dysfunction and vascular oxidative stress in obesity

Arachidonic acid (AA)-derived cytochrome P450 (CYP) derivatives, epoxyeicosatrienoic acids (EETs) and 20-hidroxyeicosatetranoic acid (20-HETE), play a key role in kidney tubular and vascular functions and blood pressure. Altered metabolism of CYP epoxygenases and CYP hydroxylases has differentially been involved in the pathogenesis of metabolic disease-associated vascular complications, although the mechanisms responsible for the vascular injury are unclear. The present study aimed to assess whether obesity-induced changes in CYP enzymes may contribute to oxidative stress and endothelial dysfunction in kidney preglomerular arteries. Endothelial function and reactive oxygen species (ROS) production were assessed in interlobar arteries of obese Zucker rats (OZR) and their lean counterparts lean Zucker rats (LZR) and the effects of CYP2C and CYP4A inhibitors sulfaphenazole and HET0016, respectively, were examined on the endothelium-dependent relaxations and O2− and H2O2 levels of preglomerular arteries. Non-nitric oxide (NO) non-prostanoid endothelium-derived hyperpolarization (EDH)-type responses were preserved but resistant to the CYP epoxygenase blocker sulfaphenazole in OZR in contrast to those in LZR. Sulfaphenazole did not further inhibit reduced arterial H2O2 levels, and CYP2C11/CYP2C23 enzymes were downregulated in intrarenal arteries from OZR. Renal EDH-mediated relaxations were preserved in obese rats by the enhanced activity and expression of endothelial calcium-activated potassium channels (KCa). CYP4A blockade restored impaired NO-mediated dilatation and inhibited augmented O2− production in kidney arteries from OZR. The current data demonstrate that both decreased endothelial CYP2C11/ CYP2C23-derived vasodilator H2O2 and augmented CYP4A-derived 20-HETE contribute to endothelial dysfunction and vascular oxidative stress in obesity. CYP4A inhibitors ameliorate arterial oxidative stress and restore endothelial function which suggests its therapeutic potential for the vascular complications of obesity-associated kidney injury.

Effect of Antioxidant-rich Nutraceuticals in the Management of High Fat Diet-induced Obesity in Albino Rats

Background: Obesity, a metabolic disorder caused by an imbalance in energy intake and energy expenditure, is a major risk factor for chronic diseases such as type 2 diabetes, hypertension, cardiovascular heart diseases (CHD) and some types of cancer. This research was designed to investigate the effect of antioxidant rich- nutraceuticals in the management of high fat diet-induced obesity in rats.
 Method: Induction of obesity was achieved by feeding rats with a formulated high fat diet (HFD) for ten (10) weeks. Rats were subsequently group administered 250mg/kg body weight and 500mg/kg body weight of the nutraceutical respectively while apple cider vinegar of 5ml/kg body weight was administered to the standard group. 
 Result: Supplementation showed significant (P<0.05) decrease in the glucose, total cholesterol, triglyceride, low density lipoprotein- cholesterol, malondialdehyde and increased in high density lipoprotein-cholesterol and antioxidant status as compared with untreated high fat diet groups. However, there was no significant difference between supplementation of 500mg/kg and the standard group treated with 5ml/kg of Apple cider vinegar.
 Conclusion: Antioxidant rich nutraceuticals could provide a protective effect against oxidative stress in obesity and remedy complications associated with obesity by reversing the damage to near normal.

Lgals9 deficiency ameliorates obesity by modulating redox state of PRDX2

The adipose tissue is regarded as an endocrine organ and secretes bioactive adipokines modulating chronic inflammation and oxidative stress in obesity. Gal-9 is secreted out upon cell injuries, interacts with T-cell immunoglobulin-3 (Tim-3) and induces apoptosis in activated Th1 cells. Gal-9 also binds to protein disulfide isomerase (PDI), maintains PDI on surface of T cells, and increases free thiols in the disulfide/thiol cycles. To explore the molecular mechanism of obesity, we investigated Gal-9−/− and Gal-9wt/wt C57BL/6J mice fed with high fat-high sucrose (HFHS) chow. Gal-9−/− mice were resistant to diet-induced obesity associated with reduction of epididymal and mesenteric fat tissues and improved glucose tolerance compared with Gal-9wt/wt mice. However, the number of M1, M2 macrophages, and M1/M2 ratio in epididymal fat were unaltered. Under HFHS chow, Gal-9−/− mice receiving Gal-9−/− or Gal-9wt/wt bone marrow-derived cells (BMCs) demonstrated significantly lower body weight compared with Gal-9wt/wt mice receiving Gal-9−/− BMCs. We identified the binding between Gal-9 and peroxiredoxin-2 (PRDX2) in sugar chain-independent manner by nanoLC-MS/MS, immunoprecipitation, and pull-down assay. In 3T3L1 adipocytes, Gal-9 knockdown shifts PRDX2 monomer (reduced form) dominant from PRDX2 dimer (oxidized form) under oxidative stress with H2O2. The inhibition of Gal-9 in adipocytes may be a new therapeutic approach targeting the oxidative stress and subsequent glucose intolerance in obesity.

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

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.

Oxidative Stress, Plant Natural Antioxidants, and Obesity.

Oxidative stress is important in the pathophysiology of obesity, altering regulatory factors of mitochondrial activity, modifying the concentration of inflammation mediators associated with a large number and size of adipocytes, promoting lipogenesis, stimulating differentiation of preadipocytes to mature adipocytes, and regulating the energy balance in hypothalamic neurons that control appetite. This review discusses the participation of oxidative stress in obesity and the important groups of compounds found in plants with antioxidant properties, which include (a) polyphenols such as phenolic acids, stilbenes, flavonoids (flavonols, flavanols, anthocyanins, flavanones, flavones, flavanonols, and isoflavones), and curcuminoids (b) carotenoids, (c) capsaicinoids and casinoids, (d) isothiocyanates, (e) catechins, and (f) vitamins. Examples are analyzed, such as resveratrol, quercetin, curcumin, ferulic acid, phloretin, green tea, Hibiscus Sabdariffa, and garlic. The antioxidant activities of these compounds depend on their activities as reactive oxygen species (ROS) scavengers and on their capacity to prevent the activation of NF-κB (nuclear factor κ-light-chain-enhancer of activated B cells), and reduce the expression of target genes, including those participating in inflammation. We conclude that natural compounds have therapeutic potential for diseases mediated by oxidative stress, particularly obesity. Controlled and well-designed clinical trials are still necessary to better know the effects of these compounds.