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 ◽  
...  

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.

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 ◽  
...  

: 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.


2014 ◽  
Vol 99 (1) ◽  
pp. E53-E61 ◽  
Author(s):  
Julie Lasselin ◽  
Eric Magne ◽  
Cédric Beau ◽  
Patrick Ledaguenel ◽  
Sandra Dexpert ◽  
...  

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.


2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
O Perez-Mendez ◽  
M Luna-Luna ◽  
A Mondragon-Garcia ◽  
A Aranda-Fraustro

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.


Author(s):  
Ю.И. Шрамко ◽  
А.В. Кубышкин ◽  
А.А. Давыдова ◽  
И.И. Фомочкина ◽  
Л.Л. Алиев ◽  
...  

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.


Author(s):  
Gabriel Wagner ◽  
Anna Fenzl ◽  
Josefine Lindroos-Christensen ◽  
Elisa Einwallner ◽  
Julia Husa ◽  
...  

Abstract Obesity and body fat distribution are important risk factors for the development of type 2 diabetes and metabolic syndrome. Evidence has accumulated that this risk is related to intrinsic differences in behavior of adipocytes in different fat depots. We recently identified LIM domain only 3 (LMO3) in human mature visceral adipocytes; however, its function in these cells is currently unknown. The aim of this study was to determine the potential involvement of LMO3-dependent pathways in the modulation of key functions of mature adipocytes during obesity. Based on a recently engineered hybrid rAAV serotype Rec2 shown to efficiently transduce both brown adipose tissue (BAT) and white adipose tissue (WAT), we delivered YFP or Lmo3 to epididymal WAT (eWAT) of C57Bl6/J mice on a high-fat diet (HFD). The effects of eWAT transduction on metabolic parameters were evaluated 10 weeks later. To further define the role of LMO3 in insulin-stimulated glucose uptake, insulin signaling, adipocyte bioenergetics, as well as endocrine function, experiments were conducted in 3T3-L1 adipocytes and newly differentiated human primary mature adipocytes, engineered for transient gain or loss of LMO3 expression, respectively. AAV transduction of eWAT results in strong and stable Lmo3 expression specifically in the adipocyte fraction over a course of 10 weeks with HFD feeding. LMO3 expression in eWAT significantly improved insulin sensitivity and healthy visceral adipose tissue expansion in diet-induced obesity, paralleled by increased serum adiponectin. In vitro, LMO3 expression in 3T3-L1 adipocytes increased PPARγ transcriptional activity, insulin-stimulated GLUT4 translocation and glucose uptake, as well as mitochondrial oxidative capacity in addition to fatty acid oxidation. Mechanistically, LMO3 induced the PPARγ coregulator Ncoa1, which was required for LMO3 to enhance glucose uptake and mitochondrial oxidative gene expression. In human mature adipocytes, LMO3 overexpression promoted, while silencing of LMO3 suppressed mitochondrial oxidative capacity. LMO3 expression in visceral adipose tissue regulates multiple genes that preserve adipose tissue functionality during obesity, such as glucose metabolism, insulin sensitivity, mitochondrial function, and adiponectin secretion. Together with increased PPARγ activity and Ncoa1 expression, these gene expression changes promote insulin-induced GLUT4 translocation, glucose uptake in addition to increased mitochondrial oxidative capacity, limiting HFD-induced adipose dysfunction. These data add LMO3 as a novel regulator improving visceral adipose tissue function during obesity. Key messages LMO3 increases beneficial visceral adipose tissue expansion and insulin sensitivity in vivo. LMO3 increases glucose uptake and oxidative mitochondrial activity in adipocytes. LMO3 increases nuclear coactivator 1 (Ncoa1). LMO3-enhanced glucose uptake and mitochondrial gene expression requires Ncoa1.


2021 ◽  
Vol 4 (Supplement_1) ◽  
pp. 245-247
Author(s):  
S Keshavjee ◽  
J Yadav ◽  
K Schwenger ◽  
S Fischer ◽  
T D Jackson ◽  
...  

Abstract Background Non-alcoholic fatty liver disease (NAFLD) includes simple steatosis (SS) and nonalcoholic steatohepatitis (NASH). It affects 74–98% of individuals with morbid obesity undergoing bariatric surgery (BSX). Among several factors contributing to NAFLD pathogenesis, adipokines secreted by visceral adipose tissue (VAT) can play a role by regulating glucose/lipid metabolism and inflammation. Aims This study aims to determine if visceral adipose tissue adipokine and cytokine gene expression are associated with NAFLD (SS and NASH) at the time of BSX. Methods Patients were recruited from the Toronto Western Hospital Bariatric Clinic. Demographic data was recorded. The VAT and liver biopsies were collected at the time of bariatric surgery. VAT adipokines and other mediators were assessed by RT-PCR and included markers of thermogenic capacity, inflammation, fibrosis, adipokines, and others. Liver histology was assessed by a pathologist using the Brunt system and individuals were diagnosed as either SS, NASH, or having a healthy liver (HL). Blood samples were collected pre-BSX to measure liver and metabolic syndrome related parameters, including HOMA-IR, HbA1c, liver enzymes, and lipid profile. Anthropometry was also assessed. Groups were compared using Kruskal-Wallis test followed by Wilcoxon ranked sum, or chi-square and Fisher’s exact test as necessary. Data was considered to be statistically significant with a p-value less than 0.05. Results We are presenting data on 126 patients, 80.2% females with a median age of 49 and a body mass index (BMI) of 46.9. Fifty-seven patients had SS, 34 had NASH and 35 had a healthy liver (HL). BMI, age, and sex did not differ between the three groups. First, we found that those with NASH had significantly higher VAT expression of fibrosis (Loxl2), inflammation (CCL4 and TGFb1) and proliferation markers (E2F1) and significantly lower expression of adipokines (TNFa and resistin) compared to HL. Also, we found that SS had significantly higher fibrosis (Col3a1, Col6a1, Loxl2, CD9 and Acta2), inflammation (Nox2, TGFb1, IFNg and Clec10a), browning (PPARa, PPARg and Glut1) and proliferation (E2F1) marker expression compared to HL. Conclusions Results show that there is a significant difference in the expression pattern of VAT fibrotic and inflammatory markers between HL, SS and NASH patients. The observed increase of inflammatory markers in NAFLD is in line with prior research outlining the ability of inflammatory mediators from VAT to contribute to liver pathology via portal circulation. The relationship between VAT characteristics and NAFLD are important in understanding the widespread metabolic effects of obesity. Funding Agencies CIHRCanadian Liver foundation


2000 ◽  
Vol 83 (04) ◽  
pp. 545-548 ◽  
Author(s):  
Vanessa Van Harmelen ◽  
Johan Hoffstedt ◽  
Per Lundquist ◽  
Hubert Vidal ◽  
Veronika Stemme ◽  
...  

SummaryHigh plasma plasminogen activator inhibitor-1 (PAI-1) activity is a frequent finding in obesity and adipose tissue has recently been suggested to be a source of circulating PAI-1 in humans. In the present study, differences in adipose tissue gene expression and protein secretion rate of PAI-1 between subcutaneous and visceral adipose tissue was analysed in specimens obtained from 22 obese individuals. The secretion rate of PAI-1 was two-fold higher in subcutaneous adipose tissue than in visceral adipose tissue (292 ± 50 vs 138 ± 24 ng PAI-1/107 cells, P <0.05). In accordance with the secretion data, subcutaneous adipose tissue contained about three-fold higher levels of PAI-1 mRNA than visceral adipose tissue (2.43 ± 0.37 vs 0.81 ± 0.12 attomole PAI-1 mRNA/µg total RNA, P <0.001). PAI-1 secretion from subcutaneous but not from visceral adipose tissue correlated significantly with cell size (r = 0.43, P <0.05). In summary, subcutaneous adipose tissue secreted greater amounts of PAI-1 and had a higher PAI-1 gene expression than visceral adipose tissue from the same obese individuals. Bearing in mind that subcutaneous adipose tissue is the largest fat depot these finding may be important for the coagulation abnormalities associated with obesity.


QJM ◽  
2020 ◽  
Vol 113 (Supplement_1) ◽  
Author(s):  
N A Mohamed ◽  
A A Seif ◽  
M S Abdelhamid ◽  
R S A Eissa

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.


Diabetologia ◽  
2008 ◽  
Vol 51 (4) ◽  
pp. 641-647 ◽  
Author(s):  
N. Klöting ◽  
D. Schleinitz ◽  
K. Ruschke ◽  
J. Berndt ◽  
M. Fasshauer ◽  
...  

2019 ◽  
Vol 91 (3) ◽  
pp. 400-410 ◽  
Author(s):  
Judith Brock ◽  
Andreas Schmid ◽  
Thomas Karrasch ◽  
Petra Pfefferle ◽  
Jutta Schlegel ◽  
...  

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