scholarly journals Tamarind Multifunctional Protein: Safety and Anti-Inflammatory Potential in Intestinal Mucosa and Adipose Tissue in a Preclinical Model of Diet-Induced Obesity

Obesity Facts ◽  
2021 ◽  
pp. 1-13
Author(s):  
Vanessa C.O. Lima ◽  
Anna B.S. Luz ◽  
Maria do Socorro M. Amarante ◽  
Maíra C.J.S. Lima ◽  
Fabiana M.C. Carvalho ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Intestinal Mucosa ◽  
Liver Enzymes ◽  
Glycemic Load ◽  
Preclinical Model ◽  
Low Grade ◽  
Perirenal Adipose Tissue ◽  
Diet Induced Obesity ◽  
Chronic Inflammatory Condition ◽  
Anti Inflammatory

<b><i>Introduction:</i></b> Obesity has emerged as one of the main public health problems. This condition triggers a series of hormonal and metabolic changes related to a low-grade chronic inflammatory condition. The trypsin inhibitor purified from tamarind (TTIp) seeds is a promising anti-inflammatory molecule, but its safety needs to be evaluated. This study aimed to evaluate TTIp bioactive dose effects on organs involved in its metabolism (liver and pancreas) and affected tissues (small intestine and perirenal adipose tissue) in an obesity model. <b><i>Methods:</i></b> Three groups of adult male Wistar rats were used (n = 5). Two of these groups had diet-induced obesity, and a third group was eutrophic. TTIp was administered by gavage in one of the obese groups for 10 days, while the remaining groups received a vehicle. The chromatographic profile and the inhibition assay corroded the purification of the inhibitor. Physical and behavioral changes, liver enzymes, and stereological and histopathological analyses of tissues were evaluated. <b><i>Results:</i></b> TTIp did not cause visible signs of toxicity, nor caused changes in liver enzymes, the liver, and pancreatic tissues. TTIp did not cause changes in the intestinal mucosa, showing improvement in the villi’s histopathological characteristics compared to the group of animals with obesity without treatment with TTIp (<i>p</i> = 0.004). The analysis of perirenal adipose tissue showed that the average sectional area of animals with obesity that received TTIp did not differ from the control. There was a difference between the high glycemic load diet group and the group treated with the inhibitor (351.8 ± 55.5) (<i>p</i> = 0.016). In addition, the group that received TTIp had no inflammatory infiltrates. <b><i>Conclusion:</i></b> Based on histological and stereological analysis, the use of TTIp is potentially safe and anti-inflammatory in the evaluated obesity model and can be investigated as a possible adjuvant in obesity therapy.

scholarly journals Decreased TLR3 in Hyperplastic Adipose Tissue, Blood and Inflamed Adipocytes is Related to Metabolic Inflammation

2018 ◽  
Vol 51 (3) ◽  
pp. 1051-1068 ◽  
Author(s):  
Jèssica Latorre ◽  
José M. Moreno-Navarrete ◽  
Mónica Sabater ◽  
Maria Buxo ◽  
José I. Rodriguez-Hermosa ◽  
...  
Keyword(s):  
Weight Loss ◽  
Adipose Tissue ◽  
Low Grade ◽  
Metabolic Inflammation ◽  
Fat Depots ◽  
Acute Surgery ◽  
Obese Subjects ◽  
Anti Inflammatory ◽  
The Impact

Background/Aims: Obesity is characterized by the immune activation that eventually dampens insulin sensitivity and changes metabolism. This study explores the impact of different inflammatory/ anti-inflammatory paradigms on the expression of toll-like receptors (TLR) found in adipocyte cultures, adipose tissue, and blood. Methods: We evaluated by real time PCR the impact of acute surgery stress in vivo (adipose tissue) and macrophages (MCM) in vitro (adipocytes). Weight loss was chosen as an anti-inflammatory model, so TLR were analyzed in fat samples collected before and after bariatric surgery-induced weight loss. Associations with inflammatory and metabolic parameters were analyzed in non-obese and obese subjects, in parallel with gene expression measures taken in blood and isolated adipocytes/ stromal-vascular cells (SVC). Treatments with an agonist of TLR3 were conducted in human adipocyte cultures under normal conditions and upon conditions that simulated the chronic low-grade inflammatory state of obesity. Results: Surgery stress raised TLR1 and TLR8 in subcutaneous (SAT), and TLR2 in SAT and visceral (VAT) adipose tissue, while decreasing VAT TLR3 and TLR4. MCM led to increased TLR2 and diminished TLR3, TLR4, and TLR5 expressions in human adipocytes. The anti-inflammatory impact of weight loss was concomitant with decreased TLR1, TLR3, and TLR8 in SAT. Cross-sectional associations confirmed increased V/ SAT TLR1 and TLR8, and decreased TLR3 in obese patients, as compared with non-obese subjects. As expected, TLR were predominant in SVC and adipocyte precursor cells, even though expression of all of them but TLR8 (very low levels) was also found in ex vivo isolated and in vitro differentiated adipocytes. Among SVC, CD14+ macrophages showed increased TLR1, TLR2, and TLR7, but decreased TLR3 mRNA. The opposite patterns shown for TLR2 and TLR3 in V/ SAT, SVC, and inflamed adipocytes were observed in blood as well, being TLR3 more likely linked to lymphocyte instead of neutrophil counts. On the other hand, decreased TLR3 in adipocytes challenged with MCM dampened lipogenesis and the inflammatory response to Poly(I:C). Conclusion: Functional variations in the expression of TLR found in blood and hypertrophied fat depots, namely decreased TLR3 in lymphocytes and inflamed adipocytes, are linked to metabolic inflammation.

scholarly journals Modulation of the inflammatory response to LPS by the recruitment and activation of brown and brite adipocytes in mice

2020 ◽  
Vol 319 (5) ◽  
pp. E912-E922
Author(s):  
Patrick Munro ◽  
Océane Dufies ◽  
Samah Rekima ◽  
Agnès Loubat ◽  
Christophe Duranton ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Inflammatory Response ◽  
Low Grade ◽  
Inflammatory Phenotype ◽  
Anti Inflammatory ◽  
And Function

Recruitment and activation of brown and brite adipocytes in the adipose tissue of mice lead to a local low-grade anti-inflammatory phenotype in response to acute endotoxemia without alteration of adipocyte phenotype and function.

scholarly journals Differential effects of EPA and DHA on plasma and adipose tissue lipid mediators: the ComparED study

2020 ◽  
Vol 79 (OCE2) ◽  
Author(s):  
Cécile Vors ◽  
Fabiana Piscitelli ◽  
Roberta Verde ◽  
Sofia Laforest ◽  
Janie Allaire ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Plasma Levels ◽  
Corn Oil ◽  
Lipid Mediators ◽  
High Dose ◽  
Low Grade ◽  
Double Blind ◽  
Epa And Dha ◽  
Anti Inflammatory ◽  
The Individual

AbstractOxylipins and endocannabinoids (eCBs) both belong to superclasses of lipid mediators with potent inflammation modulatory activities. The adipose tissue (AT) plays a key role in metabolic syndrome-related inflammation, via altered adipocyte physiology, infiltrated macrophages and altered profile of eCBs. We previously reported that DHA is more potent than EPA at modulating systemic inflammation, but the underlying mechanisms remain unclear. The objective of this study was to compare the individual effect of high-dose DHA and of EPA on circulating lipid mediators, i.e. plasma oxylipins and eCBs, and AT-related inflammation. In a randomized double-blind crossover trial, 154 volunteers with abdominal obesity and low-grade inflammation were subjected to three 10-wk supplementation phases: 1- EPA (2.7 g/d); 2- DHA (2.7 g/d); 3- corn oil (control), each separated by a 9-wk washout. Supplements were provided as re-esterified triacylglycerols. Profiling of plasma oxylipins and eCBs was performed on 58 subjects after each phase. Abdominal subcutaneous AT biopsies were also obtained from 13 individuals after each phase. Plasma DHA-, EPA-, arachidonic acid-derived oxylipins were analyzed by LC-MS. eCBs and some of their bioactive congeners were analyzed in plasma and AT by LC-APCI-MS. Adipocyte diameter was determined by histological analysis and AT macrophage infiltration was quantified by double immunofluorescence. Compared with EPA, DHA increased plasma levels of hydroxy-docosahexaenoic acids (7-, 11-, 14-, 4-, 17-HDOHE; P < 0.0001) and palmitoylethanolamide (PEA; P = 0.04). Compared with DHA, EPA led to higher plasma level of hydroxy-eicosapentaenoic acids (12-, 15-, 5-HEPE; P < 0.0001). In the AT, EPA increased the level of oleoylethanolamide (OEA; P = 0.01) compared with DHA, but no other difference was observed between treatments in adipose eCBs and eCB-related lipids. DHA and EPA did not differentially modify adipocyte size distributions (P > 0.50) and proportions of M1-type and M2-type macrophages (P > 0.30). In conclusion, increased plasma levels of anti-inflammatory DHA-derived oxylipins and plasma PEA may be responsible, at least to some extent, for the more potent anti-inflammatory effects of DHA compared with EPA observed in the ComparED study. Conversely, subcutaneous AT does not seem to be involved in explaining such differences between EPA and DHA.

scholarly journals Mechanisms Mediating Dose-Dependent Effects of Eicosapentaenoic Acid in White Adipose Tissue From High Fat Diet-Induced Obese Mice

2021 ◽  
Vol 5 (Supplement_2) ◽  
pp. 1209-1209
Author(s):  
Hanna Davis ◽  
Mandana Pahlavani ◽  
Yujiao Zu ◽  
Latha Ramalingam ◽  
Shane Scoggin ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Eicosapentaenoic Acid ◽  
White Adipose Tissue ◽  
Macrophage Infiltration ◽  
Low Grade ◽  
Mrna Levels ◽  
Obese Mice ◽  
Adipocyte Size ◽  
M1 Macrophage ◽  
Anti Inflammatory

Abstract Objectives Obesity is a global epidemic and complex disease associated with an expansion of white adipose tissue (WAT). Obesity is accompanied by chronic low-grade inflammation, characterized by elevated levels of secreted pro-inflammatory cytokines and M1 macrophage infiltration into WAT. Eicosapentaenoic acid (EPA), a long-chain omega-3 polyunsaturated fatty acid, has been reported to have anti-obesity and anti-inflammatory properties. Moreover, we previously showed that EPA dose-dependently improved glucose intolerance, and inflammation in diet-induced obese mice. The objective of this study is to further determine mechanisms underlying these metabolic protective effects of EPA in epididymal WAT (e-WAT). Methods Male B6 mice were fed a HF diet (45% kcal fat) or a HF diet supplemented with 9, 18, or 36 g/kg of EPA-enriched fish oil (EPA 9, 18 or 36) for 14 weeks. We performed histological assessments in eWAT to determine adipocyte size; and measure macrophage infiltration by immunohistochemistry using galectin-3. RNA was isolated from eWAT for RNA sequencing and gene expression analyses. Data were analyzed using GraphPad Prism software. Results EPA36-fed mice had significantly lower body weight and fat percentage, compared to HF (P &lt; 0.05). In addition, EPA18 and 36 significantly decreased weight of e-WAT (P &lt; 0.05) and increased glucose clearance compared to HF (P &lt; 0.05). Moreover, all EPA doses had smaller adipocytes (P &lt; 0.05). Compared to HF, EPA18 and 36 significantly reduced macrophage infiltration in e-7.43 fold, respectively. Consistent with these changes, EPA18 and 36 reduced the mRNA levels of HF-induced inflammatory markers, including arachidonate 5-lipoxygenase (Alox5) and leukotriene B4 receptor (Ltb4r) compared to HF (P &lt; 0.05). RNA Seq analyses revealed that EPA18 attenuated HF-induced inflammation in part by up-regulating cyclic AMP (cAMP)-dependent protein kinase A (PKA) signaling pathways and down-regulating triggering receptor expressed on myeloid cells 1 (TREM1) signaling. Conclusions EPA dose-dependently ameliorated HF-induced obesity and inflammation by reducing adipocyte size and macrophage infiltration and modulating pro- and anti-inflammatory pathways in e-WAT. These effects were achieved at human equivalent doses, that are currently prescribed for reducing triglycerides. Funding Sources USDA NIFA NIH.

scholarly journals Rice Bran Oil Attenuates Chronic Inflammation by Inducing M2 Macrophage Switching in High-Fat Diet-Fed Obese Mice

Foods ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 359
Author(s):  
Hyejeong Park ◽  
Seungmin Yu ◽  
Wooki Kim
Keyword(s):  
Adipose Tissue ◽  
Rice Bran ◽  
Rice Bran Oil ◽  
Macrophage Polarization ◽  
M2 Macrophage ◽  
Low Grade ◽  
Obese Mice ◽  
Anti Inflammatory ◽  
Low Grade Inflammation ◽  
Inflammatory Effect

Macrophages are involved in all inflammatory processes from killing pathogens to repairing damaged tissue. In the obese state, macrophages infiltrate into enlarged adipose tissue and polarize into pro-inflammatory M1 macrophages, resulting in chronic low-grade inflammation due to the secretion of inflammatory mediators. Rice bran oil (RBO) is an edible oil containing tocopherols, tocotrienols, and γ-oryzanol. Previous research in normal diet-fed mice suggested that RBO mitigates inflammatory responses by modulating mitochondrial respiration of macrophages. Therefore, we investigated if RBO had an anti-inflammatory effect in diet-induced obese mice by assessing the expression of inflammatory markers in epididymal white adipose tissue (eWAT) and polarization of bone marrow-derived macrophages (BMDMs). Rice bran oil exerted a local anti-inflammatory effect in white adipose tissue by suppressing the production of inflammatory mediators and upregulating transcription of anti-inflammatory genes. Rice bran oil also promoted anti-inflammatory M2 macrophage polarization in BMDMs thereby affecting systemic inflammation. Overall, our in vivo and ex vivo results highlight the potential of RBO as a dietary mediator that can ameliorate obesity-induced chronic low-grade inflammation by mediating the expression of inflammation-related factors and macrophage polarization.

scholarly journals Mechanisms and Effect of Coptidis Rhizoma on Obesity-Induced Inflammation: In Silico and In Vivo Approaches

2021 ◽  
Vol 22 (15) ◽  
pp. 8075
Author(s):  
Oh-Jun Kwon ◽  
Ji-Won Noh ◽  
Byung-Cheol Lee
Keyword(s):  
Adipose Tissue ◽  
Inflammatory Cytokines ◽  
Tolerance Test ◽  
Control Group ◽  
Low Grade ◽  
Cytokines And Chemokines ◽  
Epididymal Fat ◽  
Coptidis Rhizoma ◽  
Anti Inflammatory

Obesity is characterized as a chronic, low-grade inflammation state accompanied by the infiltration of immune cells into adipose tissue and higher levels of inflammatory cytokines and chemokines. This study aimed to investigate the mechanisms and effects of Coptidis Rhizoma (CR) on obesity and its associated inflammation. First, we applied a network pharmacology strategy to search the target genes and pathways regulated by CR in obesity. Next, we performed in vivo experiments to confirm the antiobesity and anti-inflammatory effects of CR. Mice were assigned to five groups: normal chow (NC), control (high-fat diet (HFD)), HFD + CR 200 mg/kg, HFD + CR 400 mg/kg, and HFD + metformin 200 mg/kg. After 16 weeks of the experimental period, CR administration significantly reduced the weight of the body, epididymal fat, and liver; it also decreased insulin resistance, as well as the area under the curve of glucose in the oral glucose tolerance test and triglyceride in the oral fat tolerance test. We observed a decrease in adipose tissue macrophages (ATMs) and inflammatory M1 ATMs, as well as an increase in anti-inflammatory M2 ATMs. Gene expression levels of inflammatory cytokines and chemokines, including tumor necrosis factor-α, F4/80, and C-C motif chemokine (CCL)-2, CCL4, and CCL5, were suppressed in adipose tissue in the CR groups than levels in the control group. Additionally, histological analyses suggested decreased fat accumulation in the epididymal fat pad and liver in the CR groups than that in the control group. Taken together, these results suggest that CR has a therapeutic effect on obesity-induced inflammation, and it functions through the inhibition of macrophage-mediated inflammation in adipose tissue.

scholarly journals Physical Activity and Inflammation Phenotype Conversion

2019 ◽  
Vol 8 (2) ◽  
pp. 64-73 ◽  
Author(s):  
Mary P. Miles ◽  
Stephanie Wilson ◽  
Carl J. Yeoman
Keyword(s):  
Physical Activity ◽  
Adipose Tissue ◽  
Gut Microbiota ◽  
Acute Exercise ◽  
The Body ◽  
Low Grade ◽  
M1 Macrophages ◽  
Gut Barrier Function ◽  
Anti Inflammatory ◽  
Low Grade Inflammation

ABSTRACT Inflammation is a protective response to infection or injury; however, persistent microtraumas at the tissue level may result in chronic low-grade inflammation that plays both direct and indirect roles in the development of many diseases and aging. The purpose of this review is to describe the underlying physiology of low-grade inflammation and highlight potential inflammation lowering effects of physical activity (PA). Unique contributions of this review are to introduce the concept of inflammation phenotype flexibility in contrast to the low-grade inflammation state and describe how PA influences inflammation phenotype by altering muscle, gut, adipose, and postprandial metabolism. Pro-inflammatory M1 macrophages and cytokines—such as tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6—contribute to low-grade inflammation. Among the mechanisms that commonly contribute to low-grade inflammation are dysfunctional adipose tissue, a leaky gut, gut microbiota that promotes inflammation, and large postprandial glycemic and lipidemic responses. Physical activity may lower inflammation by decreasing M1 macrophages in visceral adipose tissue, decreasing adipose tissue volume, production of anti-inflammatory myokines, promotion of butyrate-producing members of the gut microbiota, improved gut barrier function, and lowering of postprandial glycemic and lipidemic responses. While exercise has many anti-inflammatory mechanisms, phenotype conversion is complex, multifaceted, and difficult to achieve. Our understanding of how PA influences inflammation must include acute exercise-induced anti-inflammatory effects, contribution to the inflammation state from multiple sources in the body, and phenotypic shifts underpinning low-grade inflammation.

scholarly journals Inflammation features of brown adipose tissue of rats with diet-induced obesity development after different regimes of melatonin administration

2021 ◽  
Vol 86 (3) ◽  
pp. 28-33
Author(s):  
O. Kalmukova ◽  
Y. Leonova ◽  
O. Savchuk ◽  
N. Skrypnyk ◽  
M. Dzerzhynsky
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Signal Pathways ◽  
Standard Diet ◽  
Low Grade ◽  
Leukocyte Infiltration ◽  
Diet Induced Obesity ◽  
Brown Adipose ◽  
Wide Range ◽  
Obese Rats

One of the prominent obesity-related changes is the development of systemic low-grade proinflammatory state. Brown adipose tissue (BAT) may serve as a potential target for activation by melatonin to facilitate heat production and simultaneously stimulate lipolysis during obesity development. At the same time, melatonin is known to have immunomodulatory properties, which are performed via endocrine and paracrine signal pathways in variety cell types (including brown adipocytes)and change significantly during the day. Therefore, it can be used in a wide range of doses and at different times of the day (chronotherapeutic approach). Thus, the main goal of our research was to analyze the inflammation state of brown adipose tissue of rats during high-calorie diet induced-obesity development after different daily melatonin application in different regimes. Melatonin was administered by gavage for 7 weeks in dose 30 mg/kg 1 h before lights-off (HCD ZT11, M ZT11, evening), or 1 h after lights-on (HCD ZT01, M ZT01, morning). Tissue collagen content and leukocyte infiltration levels in BAT, detected by Van Gieson trichrome staining, were used as markers for the assessment of BAT inflammation state BAT. Propagation of obesity resulted in the increase of BATfibrosis level (the relative area occupied by collagen fibers) and tissue leukocyte infiltration in comparison to control rats. BAT fibrosis level after melatonin administrations to obese rats of HCD ZT01 and HCD ZT11 groups decreased to control values. Similar effects were observedinBAT tissue leukocyte infiltration after both regimes (HCD ZT01 and HCD ZT11 groups) of melatonin intake: this parameter decreased significantly, comparing to obese rats, but was still elevated, comparing to controls. At the same time, melatonin treatmentin morning or evening regimes did not have any impact on BAT fibrosis propagation and leukocyte infiltration in animals that consumed standard diet (M ZT01 and M ZT11 groups). To sum up, we suggest corrective properties of melatonin in context of chronic low-grade inflammation in obese rats BAT and suppose its wide potential for the therapeutic use combined with virtually absent side effects on BAT histophysiology of non-obese rats.

Abstract 295: Microsomal Prostaglandin E Synthase 1 Deficiency Attenuates Diet-Induced Obesity and Promotes the Formation of Brite Adipose Tissue

2012 ◽  
Vol 32 (suppl_1) ◽  
Author(s):  
Natalie J Moretz ◽  
Nicholas Hatch ◽  
Sarah Srodulski ◽  
Victoria L King
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Weight Gain ◽  
Marked Reduction ◽  
Body Weight Gain ◽  
Prostaglandin E ◽  
Low Grade ◽  
Prostaglandin E Synthase ◽  
Diet Induced Obesity ◽  
Microsomal Prostaglandin E Synthase

Mice deficient in adipocyte specific phospholipases A2 have a marked reduction in prostaglandin E2 (PGE2) levels and are resistant to the development of diet-induced obesity. Clinical data suggest that obesity is a chronic low grade inflammatory disease, characterized by the influx of inflammatory cells into the adipose tissue. During a chronic inflammatory state, microsomal prostaglandin E synthase-1 (mPGES-1) is the primary source of PGE2. We have previously demonstrated that mice deficient in mPGES-1 (KO) have a marked reduction in body weight gain and adiposity compared to littermate controls (WT) fed a high fat (HF) diet with a concomitant reduction in urinary PGE2 concentrations and an increase in urinary PGI2 concentrations. The reduction in weight gain is not for accounted by alterations in food intake or locomotor activity. However, resting metabolic rate, measured by indirect calorimetry, was increased in KO mice compared to WT fed a HF diet. Moreover, body temperature was also increased in KO mice compared to WT mice (37.0 ± 0.2 vs 35.8 ± 0.2; P < 0.05) fed a HF diet. Taken together these data suggest that mPGES-1 deficiency increases energy expenditure in response to feeding a HF diet. Analysis of white adipose tissue (WAT) depots demonstrated an increase in number of smaller adipocytes per unit area in the KO mice compared to WT mice. The WAT from KO mice also had a marked decrease in triglyceride content, F4/80 staining and CD86 staining with a concomitant increase in CD206 staining suggesting an attenuation in macrophage recruitment into the WAT as well as an M2 phenotype. Additionally, COX-2 and UCP-1 and PPAR-γ expression were increased in WAT depots with a concomitant localization of multi-locular adipocytes in WAT depots, demonstrating the presence of brown adipocytes in WAT depots in KO mice fed a HF diet. These data suggest that the reduction in body weight gain in the KO mice may be due an increase in thermogenesis mediated by the formation of brite adipose tissue in WAT depots.

scholarly journals Resolution of Adipose Tissue Inflammation

2010 ◽  
Vol 10 ◽  
pp. 832-856 ◽  
Author(s):  
Ana González-Périz ◽  
Joan Clària
Keyword(s):  
Adipose Tissue ◽  
Lipid Mediators ◽  
Current Status ◽  
Critical Event ◽  
Low Grade ◽  
Adipose Tissue Inflammation ◽  
Nonalcoholic Fatty Liver ◽  
Tissue Inflammation ◽  
Inflammatory State ◽  
Anti Inflammatory

The presence of the so-called “low-grade” inflammatory state is recognized as a critical event in adipose tissue dysfunction in obesity. This chronic “low-grade” inflammation in white adipose tissue is powerfully augmented through the infiltration of macrophages, which, together with adipocytes, perpetuate a vicious cycle of macrophage recruitment and secretion of free fatty acids and deleterious adipokines that predispose the development of obesity-related comorbidities, such as insulin resistance and nonalcoholic fatty liver disease. In the last decade, many factors have been identified that contribute to mounting uncontrolled inflammation in obese adipose tissue. Among them, bioactive lipid mediators derived from the cyclooxygenase and 5-lipoxygenase pathways, which convert the ω-6-polyunsaturated fatty acid (PUFA) arachidonic acid into potent proinflammatory eicosanoids (i.e., prostaglandins [PGs] and leukotrienes), have emerged. Interestingly, the same lipid mediators that initially trigger the inflammatory response also signal the termination of inflammation by stimulating the biosynthesis of anti-inflammatory and proresolving lipid autacoids. This review discusses the current status, characteristics, and progress in this class of “stop signals”, including the lipoxins, which were the first identified ω-6 PUFA–derived lipid mediators with potent anti-inflammatory properties; the recently described ω-3 PUFA–derived lipid mediators resolvins and protectins; and the cyclopentenone PGs of the D series. Special emphasis is given to the participation of these bioactive lipid autacoids in the resolution of adipose tissue inflammation and in preventing the development of obesity-related complications.

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