scholarly journals Anti-TNF-α Agent Tamarind Kunitz Trypsin Inhibitor Improves Lipid Profile of Wistar Rats Presenting Dyslipidemia and Diet-induced Obesity Regardless of PPAR-γ Induction

Nutrients ◽  
2019 ◽  
Vol 11 (3) ◽  
pp. 512 ◽  
Author(s):  
Fabiana M. C. Carvalho ◽  
Vanessa C. O. Lima ◽  
Izael S. Costa ◽  
Anna B. S. Luz ◽  
Fernando V. L. Ladd ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Food Intake ◽  
Visceral Adipose Tissue ◽  
Trypsin Inhibitor ◽  
Wistar Rats ◽  
Standard Diet ◽  
Ppar Γ ◽  
Tnf Α ◽  
High Glycemic Index ◽  
Visceral Adipose

: The increasing prevalence of obesity and, consequently, chronic inflammation and its complications has increased the search for new treatment methods. The effect of the purified tamarind seed trypsin inhibitor (TTIp) on metabolic alterations in Wistar rats with obesity and dyslipidemia was evaluated. Three groups of animals with obesity and dyslipidemia were formed, consuming a high glycemic index and glycemic load (HGLI) diet, for 10 days: Obese/HGLI diet; Obese/standard diet; Obese/HGLI diet + TTIp (730 μg/kg); and one eutrophic group of animals was fed a standard diet. Rats were evaluated daily for food intake and weight gain. On the 11th day, animals were anesthetized and sacrificed for blood and visceral adipose tissue collection. TTIp treated animals presented significantly lower food intake than the untreated group (p = 0.0065), TG (76.20 ± 18.73 mg/dL) and VLDL-C (15.24 ± 3.75 mg/dL). Plasma concentrations and TNF-α mRNA expression in visceral adipose tissue also decreased in obese animals treated with TTIp (p < 0.05 and p = 0.025, respectively) with a negative immunostaining. We conclude that TTIp presented anti-TNF-α activity and an improved lipid profile of Wistar rats with dyslipidemia and obesity induced by a high glycemic index and load diet regardless of PPAR-γ induction.

scholarly journals Adipocytes and intestinal epithelium dysfunctions linking obesity to inflammation induced by high glycemic index pellet-diet in Wistar rats

2018 ◽  
Vol 38 (3) ◽  
Author(s):  
Anna Beatriz Santana Luz ◽  
Júlia Braga dos Santos Figueredo ◽  
Bianca Damásio Pereira Dantas Salviano ◽  
Ana Júlia Felipe Camelo Aguiar ◽  
Luiza Gabriella Soares Dantas Pinheiro ◽  
...  
Keyword(s):  
Gene Expression ◽  
Adipose Tissue ◽  
Visceral Adipose Tissue ◽  
Glycemic Index ◽  
Wistar Rats ◽  
Standard Diet ◽  
Tnf Α ◽  
Liver And Pancreas ◽  
High Glycemic Index ◽  
Visceral Adipose

We investigated the inflammatory effect of a pellet-diet with high glycemic index and load (HGLI) on the histological organization of adipocytes, intestinal epithelium, and fat in liver and pancreas in adult male Wistar rats. Two groups (n=10) received for 17 weeks: (1) HGLI diet or (2) Standard diet (Labina®). Histological analyses of adipose tissue, jejunum, liver, and pancreas were performed. Stereology analysis, visceral adiposity index, gene expression, and immunohistochemistry of tumor necrosis factor-α (TNF-α) in visceral adipose tissue and plasma TNF-α were also assessed. The HGLI diet-induced hypertrophy of adipocytes with adipocyte volume density equal to 97.0%, cross-sectional area of adipocytes equivalent to 1387 µm² and a total volume of adipocytes of 6.97 cm³ an elevation of 8%, 25%, and 58%, respectively. Furthermore, the HGLI diet increased liver and pancreatic fat deposition, altered and inflamed the intestinal epithelia, and increased TNF-α gene expression (P=0.014) with a positive immunostaining in visceral adipose tissue and high plasma TNF-α in comparison with standard diet. The results suggest that this diet was able to generate changes commonly caused to solid diets with high fat or fructose-rich beverages. To the best of our knowledge, this is the first report in the literature concerning the properties of low-cost, sucrose-rich pellet-diet presenting high glycemic index and high glycemic load efficient on the development of obesity complications in Wistar rats that were subjected to diet-induced obesity. Therefore, the HGLI pellet-diet may be considered an effective tool to be used by the scientific community in experimental research.

Correction of morphofunctional disorders with grapes polyphenols in rats with experimental metabolic syndrome

2018 ◽  
pp. 43-48
Author(s):  
Ю.И. Шрамко ◽  
А.В. Кубышкин ◽  
А.А. Давыдова ◽  
И.И. Фомочкина ◽  
Л.Л. Алиев ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Adipose Tissue ◽  
Visceral Adipose Tissue ◽  
Normal Structure ◽  
Hepatic Tissue ◽  
Standard Diet ◽  
Grape Polyphenols ◽  
Morphological Studies ◽  
Visceral Adipose ◽  
Experimental Group

Цель работы состояла в изучении влияния полифенолов винограда на органы-мишени при экспериментальном метаболическом синдроме у крыс. Методы. В течение 12 недель полифенолы винограда применялись у крыс линии Вистар. Все крысы находились на стандартном рационе. Животные были разделены на 6 групп: 1-я контрольная получала питьевую воду; 2-я контрольная и все 4 экспериментальные - 2,5% раствор фруктозы в качестве питья. 1-я экспериментальная группа дополнительно получала препарат «Фэнокор» с суммарным содержанием полифенолов 181,53 г/дм, 2-я экспериментальная - виноматериал с суммарным содержанием полифенолов 1,73 г/дм; 3-я экспериментальная - виноматериал с суммарным содержанием полифенолов 4,33 г/дм и 4-я экспериментальная - виноматериал с суммарным содержанием полифенолов 8,58 г/дм. После окончания опыта у крыс проводили морфологические исследования висцеральной жировой ткани, тканей миокарда и печени. Результаты. Анализ результатов показал, что применение полифенольных продуктов переработки винограда в концентрациях 181,53 г/дм при моделировании метаболического синдрома приводило к минимизации морфофункциональных нарушений в висцеральной жировой ткани (уменьшение интенсивности лимфоплазмоцитарной инфильтрации), миокарде (мышечные волокна имели типичное строение и адипоциты между ними встречались лишь очагово) и печени (имелись лишь слабые очаговые дистрофические изменения гепатоцитов). Заключение. Результаты работы свидетельствуют о возможности применения виноматериалов с наибольшей концентрацией полифенолов и препарата «Фэнокор» в коррекции и профилактике поражений при метаболическом синдроме. The aim of this work was to study the effect of grape polyphenols on target organs in rats with experimental metabolic syndrome. Methods. Grape polyphenols were used in Wistar rats for 12 weeks. All rats received a standard diet. The animals were divided into 6 groups: group 1, control, received drinking water; group 2, the second control, and four experimental groups received a 2.5% fructose solution for drinking. The first experimental group additionally received a drug, Fenocor, containing polyphenols at 181.53 g/dm; the second experimental group - wine material containing polyphenols at 1,73 g/dm; the third experimental group - wine material containing polyphenols at 4,33 g/dm; and the fourth experimental group - wine material containing polyphenols at 8,58 g/dm. At the end of experiment, morphological studies of visceral adipose tissue, myocardial tissue, and hepatic tissue were performed. Results. The treatment of rats with experimental metabolic syndrome with grape polyphenolic products at a concentration of 181.53 g/dm minimized morphological and functional disorders in visceral adipose tissue (intensity of lymphoplasmocytic infiltration was decreased), myocardium (muscle fibers had normal structure with only occasional adipocytes between them), and liver (only slight focal degenerative changes were observed in hepatocytes). Conclusion. The study indicated a possibility of using wine materials with the highest concentration of polyphenols and the drug Fenocor for correction and prevention of damages in metabolic syndrome.

scholarly journals Vitamin D Promotes Adiposity But Improves Associated Metabolic Derangements In An Obese Rat Model

QJM ◽  
2020 ◽  
Vol 113 (Supplement_1) ◽  
Author(s):  
N A Mohamed ◽  
A A Seif ◽  
M S Abdelhamid ◽  
R S A Eissa
Keyword(s):  
Body Mass Index ◽  
Vitamin D ◽  
Adipose Tissue ◽  
Lipid Profile ◽  
Body Mass ◽  
Visceral Adipose Tissue ◽  
Rat Model ◽  
Dose Group ◽  
Tnf Α ◽  
Visceral Adipose

Abstract Background Obesity is a worldwide problem and is a major risk factor for chronic diseases. The relation between obesity and vitamin D is not completely understood. Obesity is associated with vitamin D insufficiency. Some studies claim that vitamin D may reduce lipogenesis and others claim that vitamin D can promote adipogenesis. Aim of the study This study was planned to evaluate the effect of alteration in vitamin D level on body weight and adipose tissue metabolism in an obese rat model. Methods 32 Female Albino-rats were randomly allocated into: control group (C, n = 8), fed on control diet containing 1000 IU vitamin D/kg diet, and a high caloric diet group (HCD, n = 32). The HCD group was further subdivided into 3 groups according to the vitamin D dose into: standard vitamin D dose group (HCD+SVD) containing 1000 IU vitamin D/kg diet, low vitamin D dose group (HCD+LVD) containing 25 IU vitamin D/kg diet and high vitamin D dose group (HCD+HVD) containing 5169 IU vitamin D/kg diet. Body mass index, serum vitamin D, glucose, lipid profile, TNF-α and adipose tissue UCP-1 were measured. Different fat depots were weighed and histopathologically assessed. Results HCD+HVD group showed a significant increase in the final body mass index and in the different fat depot weights compared to all groups. Compared to the HCD+SVD group, the HCD+HVD group showed significantly lower serum total cholesterol and LDL-c levels, while it showed a non-significant change in serum glucose, TNF-α and visceral adipose tissue UCP-1. A significant negative correlation was found between serum 25(OH)D and visceral adipose tissue UCP-1. HCD+LVD showed the highest visceral adipose tissue UCP-1 compared to all groups. Conclusion Vitamin D promoted adiposity and decreased visceral adipose tissue UCP-1 but improved the associated derangements in lipid profile.

scholarly journals Adipose Inflammation in Obesity: Relationship With Circulating Levels of Inflammatory Markers and Association With Surgery-Induced Weight Loss

2014 ◽  
Vol 99 (1) ◽  
pp. E53-E61 ◽  
Author(s):  
Julie Lasselin ◽  
Eric Magne ◽  
Cédric Beau ◽  
Patrick Ledaguenel ◽  
Sandra Dexpert ◽  
...  
Keyword(s):  
Gene Expression ◽  
Bariatric Surgery ◽  
Weight Loss ◽  
Adipose Tissue ◽  
Visceral Adipose Tissue ◽  
Inflammatory Markers ◽  
Tnf Α ◽  
Inflammatory State ◽  
Adipose Inflammation ◽  
Visceral Adipose

Context: The inflammatory state of the adipose tissue is believed to contribute to systemic low-grade inflammation in obesity. Objective: This study assessed the relationship between adipose and circulating inflammatory markers as well as the influence of adipose inflammation on bariatric surgery-induced weight reduction. Design: This was a cross-sectional and longitudinal study (up to 14 mo). Setting: The study was conducted in the digestive/bariatric surgery department of the Tivoli and Jean Villar clinics, Bordeaux, France. Patients: Thirty-seven obese patients [body mass index (BMI) &gt; 35–40 kg/m2)] seeking bariatric surgery were included. Twenty-eight of them were successively followed up at 1–3 months after surgery and 25 between 6 and 14 months after surgery. Main Outcome Measures: Fasting serum samples were collected before surgery to assess concentrations of inflammatory markers. Samples of visceral adipose tissue were extracted during surgery and gene expression of cytokines and immune cell markers were evaluated using quantitative RT-PCR. Pre- and postsurgery weight and BMI were collected. Results: Gene expression of several cytokines were strongly intercorrelated in the visceral adipose tissue. Adipose expression of macrophage and T cell markers were related to adipose expression of TNF-α and IL-1 receptor antagonist (P &lt; .01) and to systemic levels of TNF-α (P &lt; .01) and IL-6 (P &lt; .05). A higher inflammatory state of the adipose tissue predicted a lower BMI reduction after surgery (P &lt; .05), notably at early stages after surgery. Conclusions: These findings support the involvement of macrophages and T cells in adipose inflammation and provide new information regarding the role of the visceral adipose tissue in the inflammatory state of obesity and its impact on obesity treatment outcomes, such as surgery-induced weight loss.

scholarly journals Visceral Obesity and Plasma Glucose-Insulin Homeostasis: Contributions of Interleukin-6 and Tumor Necrosis Factor-α in Men

2008 ◽  
Vol 93 (5) ◽  
pp. 1931-1938 ◽  
Author(s):  
Amélie Cartier ◽  
Isabelle Lemieux ◽  
Natalie Alméras ◽  
Angelo Tremblay ◽  
Jean Bergeron ◽  
...  
Keyword(s):  
Body Mass Index ◽  
Adipose Tissue ◽  
Body Mass ◽  
Visceral Adipose Tissue ◽  
Plasma Glucose ◽  
Visceral Adiposity ◽  
Oral Glucose ◽  
Tnf Α ◽  
Insulin Homeostasis ◽  
Visceral Adipose

Abstract Objective: This study examined the relationships of two inflammatory cytokines, IL-6 and TNF-α, to visceral adiposity and indices of plasma glucose-insulin homeostasis. Research Design and Methods: Plasma levels of IL-6 and TNF-α were measured in 189 untreated asymptomatic men (aged 43.7 ± 7.8 yr; body mass index 29.0 ± 4.3 kg/m2; waist girth 98.6 ± 10.3 cm). Results: Significant and positive associations were found between both cytokines with adiposity and adipose tissue distribution indices (0.15 ≤ r &lt; 0.32; P &lt; 0.05) as well as plasma glucose-insulin homeostasis variables (0.22 ≤ r &lt; 0.28; P &lt;0.05). Comparison of two subgroups, each composed of 32 overweight men (≥25 kg/m2) with similar body mass index values (28.7 kg/m2 in both groups) but with markedly different levels of visceral adipose tissue (&lt; vs. ≥ 130 cm2), revealed significant differences only for IL-6 levels (1.42 ± 1.15 vs. 0.86 ± 0.52 pg/ml; P &lt; 0.02 for men with high vs. low visceral adipose tissue, respectively). Finally, when subjects were stratified on the basis of their respective concentrations of IL-6 and TNF-α (using the 50th percentile of their overall distribution), an ANOVA revealed an independent contribution of IL-6 to the variation of fasting insulin (P &lt; 0.01) and each of these two cytokines to the variation of insulin levels measured after a 75-g oral glucose challenge (P &lt;0.01 for IL-6 and P &lt; 0.05 for TNF-α). Conclusions: Because IL-6 appeared to be clearly associated with visceral adiposity, TNF-α rather showed associations with indices of total body fatness. Thus, TNF-α may contribute to the insulin resistance of overall obesity, whereas IL-6 may be one of the mediators of the hyperinsulinemic state specifically related to excess visceral adiposity.

P4462Atorvastatin and fenofibrate exert opposite effects on the vascularization and characteristics of visceral adipose tissue

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
O Perez-Mendez ◽  
M Luna-Luna ◽  
A Mondragon-Garcia ◽  
A Aranda-Fraustro
Keyword(s):  
Gene Expression ◽  
Adipose Tissue ◽  
New Zealand ◽  
High Risk ◽  
Visceral Adipose Tissue ◽  
Control Group ◽  
Increased Risk ◽  
Tnf Α ◽  
New Zealand White Rabbits ◽  
Visceral Adipose

Abstract Background Statins may precipitate the onset of type 2 diabetes (T2D) in high-risk patients. In contrast, only the subset of individuals with insulin resistance (IR) and/or diabetes receives cardiovascular benefits with fibrates. The mechanism responsible of such effects may be related with visceral adipose tissue (VAT). In this context, previous observations have suggested that atorvastatin induced an increase of VAT whereas fenofibrate had the opposite effects in rabbits. Purpose To determine the mass, morphology and vascularization of VAT in New Zealand white rabbits that received of atorvastatin or fenofibrate during two months. Methods New Zealand white rabbits (n=6 per group) received by oral gavage during 2 months, 0.33 mg/kg of atorvastatin or 2.6 mg/kg fenofibrate. The control group received 0.5 mL of vehicle. Plasma lipids were monitored. The visceral adipose tissue (VAT) was dissected and quantified. The expression of genes related with vascularization, VEGF-A and TGF-β, FGF2 as well as TNF-α were determined by qPCR in VAT. Histological slices were stained by hematoxilin and eosin to determine the size of adipocytes. The marker of angiogenesis, PECAM-1, was determined by immunohistochemistry. Results As expected, the cholesterol from atorvastatin was lower after treatment while triglycerides decreased in fenofibrate group. The mass of VAT from fenofibrate group was 46% lower compared with the controls meanwhile atorvastatin was associated with a larger diameter of adipocytes (+65%) than that of the control and fenofibrate groups. FGF2 gene expression was lower in fenofibrate than in control group (−54%). By contrast, VEGF-A gene expression in fenofibrate-treated rabbits was 110% higher than in control group. TGF-β and TNF-α remained comparable among groups. In agreement with the gene expression, the marker of angiogenesis PECAM-1 was slightly but significantly higher (+10%) in rabbits treated with fenofibrate than in controls, as determined by immunohistochemistry. Conclusion Fenofibrate enhanced the VEGF-A gene expression, PCAM-1 in VAT whereas decreased its total mass. In contrast, atorvastatin increased the adipocyte size without any effect on vascularization markers. These results suggest that fenofibrate is associated with a favorable remodeling of VAT, in contrast with atorvastatin, which induced a non-favorable remodeling of VAT. These results may be related with the cardiovascular benefits of fenofibrate and the increased risk of T2D in high-risk subjects induced by atorvastatin.

scholarly journals Role of Gut Microbiome on Metabolic Disorders

2020 ◽  
pp. 21-35
Author(s):  
Ifeanyi O. Oshim ◽  
Nneka R. Agbakoba ◽  
Evelyn U. Urama ◽  
Oluwayemisi Odeyemi ◽  
Nkechi A. Olise ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Adipose Tissue ◽  
Intestinal Permeability ◽  
Visceral Adipose Tissue ◽  
Gut Microbiome ◽  
Metabolic Disorders ◽  
Ppar Γ ◽  
Visceral Adipose

Microbiome that reside in the human gut are key contributors to host metabolism and are considered potential sources of novel therapeutics in metabolic disorders. This review discusses the role of gut microbiome in the pathogenesis of obesity, type 2 diabetes mellitus (T2DM), chronic kidney disease and cardiovascular disease. Gut microbiome remains quite stable, although changes take place between birth and adulthood due to external influences, such as diet, disease and environment. Understanding these changes is important to predict diseases and develop therapies. In gut heamostasis, Gut microbiome converts high fibres intake into short-chain fatty acids like butyrate, propionate and acetate which normalize intestinal permeability and alter de novo lipogenesis and gluconeogenesis through reduction of free fatty acid production by visceral adipose tissue. This effect contributes to reduce food intake and to improve glucose metabolism. Propionate can also bind to G protein coupled receptors (GPR)-43 expressed on lymphocytes in order to maintain appropriate immune defence. Butyrate activates peroxisome proliferator-activated receptor-γ (PPAR-γ) leading to beta-oxidation and oxygen consumption, a phenomenon contributing to maintain anaerobic condition in the gut lumen. In contrast, diets most especially western diet consisting among others of high fat and high salt content has been reported to cause gut dysbiosis. This alteration of gut microbiome result to chronic bacterial translocation and increased intestinal permeability that can drive a systemic inflammation leading to macrophage influx into visceral adipose tissue, activation of hepatic kuffer cells and insulin resistance in type 2 diabetes. This effect contributes to lower mucus thickness, decrease butyrate and propionate producing bacteria, L-cells secrete less gut peptides, lack of PPAR-γ activation lead to higher oxygen available for the microbiome at the proximity of the mucosa and increases the proliferation of Enterobacteriaceae with commensurate increase in opportunistic pathogens. However, Gut microbiome are major biomarker for early prognosis of diabetes and other metabolic disorders.

scholarly journals Effect of an office-based intervention on visceral adipose tissue: the WorkACTIVE-P randomized controlled trial

2021 ◽  
Vol 46 (2) ◽  
pp. 117-125
Author(s):  
James L. Dorling ◽  
Christoph Höchsmann ◽  
Catrine Tudor-Locke ◽  
Robbie Beyl ◽  
Corby K. Martin
Keyword(s):  
Adipose Tissue ◽  
Food Intake ◽  
Visceral Adipose Tissue ◽  
Disease Risk ◽  
Office Workers ◽  
Cardiometabolic Disease ◽  
Risk Markers ◽  
Randomized Controlled ◽  
Visceral Adipose ◽  
Cardiometabolic Disease Risk

Office-based activity reduces sedentariness, yet no randomized controlled trials (RCTs) have assessed how such activity influences visceral adipose tissue (VAT). This study examined the effect of an office-based, multicomponent activity intervention on VAT. The WorkACTIVE-P RCT enrolled sedentary office workers (body mass index: 31.4 (standard deviation (SD) 4.4) kg/m2) to an intervention (n = 20) or control (n = 20) group. For 3 months, the intervention group received an office-based pedal desk, further to an intervention promoting its use and increased walking. The control group maintained habitual activity. At baseline and follow-up, VAT, cardiometabolic disease risk markers, physical activity, and food intake were measured. Steps/day were not altered relative to control (P ≥ 0.51), but the pedal desk was utilized for 127 (SD 61) min/day. The intervention reduced VAT relative to control (−0.15 kg; 95% confidence interval (CI) = −0.29 to −0.01; P = 0.04). Moreover, the intervention decreased fasting glucose compared with control (−0.29 mmol/L; 95% CI = −0.51 to −0.06; P = 0.01), but no differences in other cardiometabolic disease markers or food intake were revealed (P ≥ 0.11). A multicomponent intervention decreased VAT in office workers who were overweight or obese. Though longer-term studies are needed, office-based, multicomponent activity regimens may lower cardiometabolic disease risk. Trial registered at ClinicalTrials.gov (NCT02561611). Novelty: In WorkACTIVE-P, a multicomponent activity intervention decreased visceral adipose tissue relative to control in office workers. The intervention also reduced glucose compared with control, though other metabolic risk markers and food intake were not altered. Such multicomponent interventions could help reduce cardiometabolic disease risk, but longer studies are needed.

scholarly journals The Effect of Vitamin D Administration on Leptin, Adiponectin and mRNA MCP-1 Levels in Adipose Tissue of Obese Female Wistar Rats

2020 ◽  
pp. 541-549
Author(s):  
Luh Putu Ratna Sundari ◽  
Made Bakta ◽  
Nyoman Mantik Astawa ◽  
Putu Gede Adiatmika ◽  
Gusti Kamasan Nyoman Arijana ◽  
...  
Keyword(s):  
Vitamin D ◽  
Adipose Tissue ◽  
Visceral Adipose Tissue ◽  
Wistar Rats ◽  
Control Group ◽  
Group Design ◽  
Obese Female ◽  
Female Wistar Rats ◽  
Group A ◽  
Visceral Adipose

In obesity, there is an accumulation of adipocytes which produces adipokine that are pro-inflammatory substance, such as leptin and MCP-1 and anti-inflammatory substance, such as adiponectin, while the bioavailability of vitamin D is decreased. This research aimed to study the effect of vitamin D administration on leptin, MCP-1, and adiponectin levels in adipose tissue rats with obesity. Vitamin D was administered to the obese model of 6-9 months old female Wistar rats. This experiment was a randomized control group design with a post-test group design only. Twenty-seven (27) female obese Wistar rats were included in this study. The animals were divided randomly into 3 groups: 9 rats were given 2400 IU vitamin D (group A), 9 rats were given 800 IU vitamin D (group B) and 9 rats were given a placebo as control (group C). The administration of Vitamin D was given once daily for 8 weeks. The visceral adipose tissue was taken to measure the level of leptin, adiponectin and mRNA MCP-1. Data among groups was analyzed by using one-way ANOVA and followed by LSD test, at a significance level of p <0.05. The lowest level of leptin (1059.15+135.20 pg/ml) and mRNA MCP-1 (2.36 + 0.75 fg/ml) and the highest adiponectin level (3.43 + 0.47 ng/ml) were found in group A. In conclusion, oral administration of vitamin D (2400 IU) decreased pro-inflammatory substances, such as leptin and mRNA MCP-1 and increased anti-inflammatory substances, such as adiponectin, in visceral adipose tissue of obese female Wistar rats.

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