scholarly journals Cadmium: An Emerging Role in Adipose Tissue Dysfunction

2021 ◽  
Author(s):  
Sarra Mohammed Attia ◽  
Kavitha Varadharajan ◽  
Muralitharan Shanmugakonar ◽  
Sandra Concepcion Das ◽  
Hamda A. Al-Naemi
Keyword(s):  
Adipose Tissue ◽  
Inflammatory Markers ◽  
Toxic Heavy Metal ◽  
Cd Accumulation ◽  
Toxic Impact ◽  
Anthropogenic Inputs ◽  
Industrial Sectors ◽  
Adipose Tissue Macrophages ◽  
Anti Inflammatory ◽  
Cd Exposure

AbstractCadmium (Cd) is a toxic heavy metal that is widespread in the environment due to the substantial anthropogenic inputs from the agriculture and industrial sectors. The toxic impact of Cd adversely affects human health and is linked with endocrine disruption, carcinogenicity, diabetes-related diseases, and metabolic disorder. One of the main characterizations of Cd is bioaccumulation where its half-life reaches 40 years with an unknown biological role. Several organs were found to be targets for Cd accumulation such as the liver, kidneys, and adipose tissue. Adipose tissue (AT) is a dynamic organ that plays a significant role in the body’s homeostasis through the maintenance of energy storage. Another vital function for AT is the secretion of adipokines which provides a metabolic cross-talk with the whole body’s organs. Cd is found to adversely impact the function of AT. This includes the disruption of adipogenesis, lipogenesis, and lipolysis. As a consequence, dysfunctional AT has disruptive patterns of adipokines secretions. The main adipokines produced from AT are leptin and adiponectin. Both were found to be significantly declined under the Cd exposure. Additionally, adipose tissue macrophages can produce either anti-inflammatory markers or pro-inflammatory markers depending on the local AT condition. Cadmium exposure was reported to upregulate pro-inflammatory markers and downregulate anti-inflammatory markers. However, the exact mechanisms of Cd’s adverse role on AT structure, function, and secretion patterns of adipokines are not totally clarified. Therefore, in this review, we present the current findings related to Cd detrimental effects on adipose tissues.

scholarly journals Effects of Berries on High-Fat Diet-Induced Inflammation

2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 449-449
Author(s):  
Patricia Perez ◽  
Desiree Wanders ◽  
Hannah Land ◽  
Kathryn Chiang ◽  
Rami Najjar ◽  
...  
Keyword(s):  
Gene Expression ◽  
Adipose Tissue ◽  
Inflammatory Markers ◽  
In Vitro Study ◽  
Vitro Study ◽  
In Vivo Study ◽  
High Fat ◽  
Anti Inflammatory

Abstract Objectives Studies suggest that inflammation mediates the link between obesity and its comorbidities including type 2 diabetes and cardiovascular disease. Hence, there is a demand for effective alternative or complementary approaches to treat obesity-associated inflammation. The objective of this study was to determine whether consumption of blackberries (BL) and raspberries (RB) alone or in combination reduce obesity-induced inflammation. Methods In Vitro Study: RAW 264.7 macrophages were pretreated with either BL, RB, or BL + RB, each at a final concentration of 200 µg/mL for 2 h. LPS (1 ng/mL) was then added to the media for 16 h. mRNA expression of inflammatory cytokines was measured. In Vivo Study: Five-week-old mice were acclimated to a low-fat low-sucrose (LFLS) diet for one week after which mice were randomized 10 per group to one of five groups: 1) LFLS, 2) high-fat high-sucrose (HFHS), 3) HFHS + 10% BL, 4) HFHS + 10% RB, or 5) HFHS + 5% BL + 5% RB. Expression of inflammatory markers was measured in the liver as well as epididymal and inguinal white adipose tissue. Results In Vitro Study: Each berry alone and in combination suppressed the LPS-induced increase in inflammatory markers, with the combination (BL + RB) having the greatest effect. The combination suppressed LPS-induced expression of Ccl2, Tnfa, F4/80, and Il6 by 3.7−, 5.3−, 5.3−, and 4.4-fold, respectively. In Vivo Study: Gene expression analysis indicated that berry consumption had no significant effect on proinflammatory (Ccl2, Il1b, Tnfa, Il6, Itgam) or anti-inflammatory (Adipoq, Arg1, Mgl1) markers in adipose tissue depots or liver. However, relatively low gene expression of inflammatory markers in the tissues indicates that the mice fed the HFHS diet failed to develop a robust inflammatory state. Conclusions BL and RB have direct anti-inflammatory effects on immune cells. Initial analysis indicates that consumption of BL and RB has no significant effects on markers of inflammation in a diet-induced mouse model of obesity. However, it is possible that the relatively low levels of inflammation in these mice masked the anti-inflammatory potential of BL and RB. Ongoing analysis will provide additional insights into the effects of BL and RB on inflammation in these tissues. Funding Sources Lewis Foundation Award.

scholarly journals The Absence of Adiponectin Alters Niacin’s Effects on Adipose Tissue Inflammation in Mice

Nutrients ◽  
2020 ◽  
Vol 12 (8) ◽  
pp. 2427
Author(s):  
Emily C. Graff ◽  
Han Fang ◽  
Desiree Wanders ◽  
Robert L. Judd
Keyword(s):  
Adipose Tissue ◽  
High Fat Diet ◽  
Inflammatory Markers ◽  
Adipose Tissue Inflammation ◽  
High Fat ◽  
Tissue Inflammation ◽  
Low Fat Diet ◽  
Expression Of Genes ◽  
Ccl2 Expression ◽  
Anti Inflammatory

Obesity is an immunometabolic disease associated with chronic inflammation and the dysregulation of pro- and anti-inflammatory cytokines. One hallmark of obesity is reduced concentrations of the anti-inflammatory adipokine, adiponectin. Pharmacologic doses of niacin produce multiple metabolic benefits, including attenuating high-fat diet (HFD)-induced adipose tissue inflammation and increasing adiponectin concentrations. To determine if adiponectin mediates the anti-inflammatory effects of niacin, male C57BL/6J (WT) and adiponectin null (Adipoq-/-) mice were maintained on a low-fat diet (LFD) or HFD for 6 weeks, before being administered either vehicle or niacin (360 mg/kg/day) for 5 weeks. HFD-fed mice had increased expression of genes associated with macrophage recruitment (Ccl2) and number (Cd68), and increased crown-like structure (CLS) number in adipose tissue. While niacin attenuated Ccl2 expression, there were no effects on Cd68 or CLS number. The absence of adiponectin did not hinder the ability of niacin to reduce Ccl2 expression. HFD feeding increased gene expression of inflammatory markers in the adipose tissue of WT and Adipoq-/- mice. While niacin tended to decrease the expression of inflammatory markers in WT mice, niacin increased their expression in HFD-fed Adipoq-/- mice. Therefore, our results indicate that the absence of adiponectin alters the effects of niacin on markers of adipose tissue inflammation in HFD-fed mice, suggesting that the effects of niacin on tissue cytokines may involve adiponectin.

scholarly journals Curcumin Reduces Hepatic and White Adipose Tissue Inflammation and Expression of Specific Zinc Transporters in Diet-Induced Obese Mice

2021 ◽  
Vol 5 (Supplement_2) ◽  
pp. 325-325
Author(s):  
Tariful Islam ◽  
Geetika Katasani ◽  
Iurii Koboziev ◽  
Kembra Albracht-Schulte ◽  
Shane Scoggin ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
White Adipose Tissue ◽  
Inflammatory Markers ◽  
Zinc Homeostasis ◽  
Metabolic Effects ◽  
Zinc Transporters ◽  
Whole Body ◽  
Mrna Levels ◽  
Alcoholic Fatty Liver ◽  
Anti Inflammatory

Abstract Objectives Obesity is a complex metabolic disease, that is often associated with non-alcoholic fatty liver disease (NAFLD). Inflammation is a common feature of both diseases. Curcumin, a traditionally used spice in Asia, exerts anti-inflammatory effects in liver and white adipose tissue (WAT) of diet-induced obese (DIO) mice. However, mechanisms involved in these beneficial effects remain obscure. Zinc is an important micronutrient involved in inflammatory responses. Whole-body zinc homeostasis plays a critical role in decreasing tissue specific inflammation. Zinc homeostasis is maintained mainly by zinc transporters known as ZnT (zinc transporters) and Zip (Zrt and Irt-like proteins) family. We propose that zinc transporters may contribute to curcumin's protective metabolic effects. Thus, the objective of this research was to determine curcumin's effects on inflammatory markers and zinc transporters in liver and WAT from DIO mice. Methods Male B6 mice were fed a HFD (45% kcal fat) or HFD supplemented with 0.4% (w/w) curcumin (HFC) for fourteen weeks. Serum triglycerides (TG) and free fatty acid (FFA) levels were measured. mRNA levels for inflammatory markers and zinc transporters were determined in WAT and liver by qRT-PCR. Results No significant changes were observed in body weight, serum TG and FFA levels with curcumin supplementation. However, gene expression of inflammatory markers, including Stat1, and Nf-KB subunit p65 were significantly reduced in liver and WAT from HFC group compared to HF (P < 0.05). Furthermore, curcumin reduced hepatic zinc transporters Zip10, Zip14, ZnT10 but increased ZnT9 expression. In WAT, curcumin significantly reduced mRNA levels for Zip1, Zip14, ZnT1, and ZnT7 (P < 0.05). Conclusions Our results indicate that zinc transporters may in part mediate the anti-inflammatory properties of curcumin, particularly Zip14, in WAT and liver of DIO mice. Future mechanistic studies are necessary to establish whether zinc transporters are required for curcumin's anti-inflammatory effects in obesity and associated NAFLD. Funding Sources AHA grant# 19AIREA34450279.

scholarly journals Cell-extrinsic autophagy in mature adipocytes regulates anti-inflammatory response to intestinal tissue injury through lipid mobilization

2021 ◽  
Author(s):  
Felix Clemens Richter ◽  
Matthias Friedrich ◽  
Mathilde Pohin ◽  
Ghada Alsaleh ◽  
Irina Guschina ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Intestinal Inflammation ◽  
Inflammatory Responses ◽  
Tissue Injury ◽  
Inflammatory Diseases ◽  
Protective Effects ◽  
Adipose Tissue Macrophages ◽  
Anti Inflammatory ◽  
Major Nutrients

Autophagy is a critical cellular recycling pathway which is genetically linked to the development of intestinal inflammation in humans. Inflammation drives adipose tissue breakdown and provision of major nutrients such as free fatty acids (FFA). However, the effect of autophagy-mediated FFA release by adipocytes in immune-mediated inflammatory diseases remains unexplored. In a mouse model of intestinal inflammation, we found that visceral adipocytes upregulate autophagy at peak inflammation. Adipocyte-specific loss of the key autophagy gene Atg7 (Atg7Ad) resulted in the exacerbation of intestinal inflammation. TNFα-induced lipolysis was impaired in Atg7-deficient adipocytes leading to the reduced availability of several FFA species, and decreased expression of the FFA transporter CD36 on adipose tissue macrophages (ATMs). Visceral adipose tissues from Atg7Ad mice released less IL-10 resulting in lower levels of circulating IL-10 in colitis. ATMs present the main source of adipose tissue-derived IL-10 during colitis. In vitro assays confirmed that FFA restriction from macrophages reduced CD36 expression and diminished IL-10 production. Taken together, our study demonstrates that autophagy-mediated FFA release from adipocytes directs anti-inflammatory responses in ATMs, which in turn conveys protective effects for distant intestinal inflammation.

scholarly journals Human Adipose Tissue Macrophages Are Enhanced but Changed to an Anti-Inflammatory Profile in Obesity

2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Karen Fjeldborg ◽  
Steen B. Pedersen ◽  
Holger J. Møller ◽  
Tore Christiansen ◽  
Marianne Bennetzen ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Human Adipose Tissue ◽  
Multivariate Regression Analysis ◽  
Low Grade ◽  
Macrophage Marker ◽  
Adipose Tissue Macrophages ◽  
Obese Subjects ◽  
Anti Inflammatory ◽  
Inflammatory Profile

Objective. Adipose tissue (AT) macrophages are increased in obesity and associated with low grade inflammation. We aimed to characterize the phenotype of AT macrophages in humans in relation to obesity and insulin resistance.Design. Gene-expression levels of general macrophage markers (CD68 and CD14), proinflammatory markers/M1 (TNF-α, MCP-1, and IL-6), and anti-inflammatory markers/M2 (CD163, CD206, and IL-10) were determined by RT-PCR in subcutaneous AT samples from lean and obese subjects. Insulin resistance was determined by HOMA-IR.Results. All the macrophage markers were elevated in the AT from obese compared to lean subjects (P<0.001). To determine the phenotype of the macrophages the level of CD14 was used to adjust the total number of macrophages. The relative expression of CD163 and IL-10 was elevated, and TNF-αand IL-6 were reduced in AT from obese subjects (allP<0.05). In a multivariate regression analysis CD163 was the only macrophage marker significantly associated with HOMA-IR (β: 0.57;P<0.05). Conclusion. Obesity is associated with elevated numbers of macrophages in the AT. Unexpectedly, the macrophages change phenotype by obesity, with a preponderance of M2 and a decrement of M1 markers in AT from obese subjects. Moreover, CD163 was the only macrophage marker associated with HOMA-IR after multiple adjustments.

scholarly journals Targeting of adipose tissue macrophages by bee venom phospholipase A2 attenuates high-fat diet-induced obesity

2021 ◽  
Author(s):  
Hyunju Jeong ◽  
Chanju Lee ◽  
Chenyu Cheng ◽  
Hung Chun Chou ◽  
HyeJin Yang ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Phospholipase A2 ◽  
High Fat Diet ◽  
Normal Diet ◽  
Bee Venom ◽  
High Fat ◽  
Adipose Tissue Macrophages ◽  
Anti Inflammatory

Abstract Background/objectives Adipose tissue macrophages (ATMs) exist in either the M1 or M2 form. The anti-inflammatory M2 ATMs accumulate in lean individuals, whereas the pro-inflammatory M1 ATMs accumulate in obese individuals. Bee venom phospholipase A2 (bvPLA2), a major component in honeybee (Apis mellifera) venom, exerts potent anti-inflammatory effects via interactions with regulatory T cells (Treg) and macrophages. This study investigated the effects of bvPLA2 on a high-fat diet (HFD)-induced obesity in mice. Subjects/methods For in vivo experiments, male C57BL/6, CD206-deficient, and Treg-depleted mice models were fed either a normal diet 41.86 kJ (ND, 10 kcal% fat) or high-fat diet 251.16 kJ (HFD, 60 kcal% fat). Each group was i.p. injected with PBS or bvPLA2 (0.5 mg/kg) every 3 days for 11 weeks. Body weight and food intake were measured weekly. Histological changes in the white adipose tissue (WAT), liver, and kidney as well as the immune phenotypes of the WAT were examined. Immune cells, cytokines, and lipid profiles were also evaluated. The direct effects of bvPLA2 on 3T3-L1 pre-adipocytes and bone marrow-derived macrophages were measured in vitro. Results bvPLA2 markedly decreased bodyweight in HFD-fed mice. bvPLA2 treatment also decreased lipid accumulation in the liver and reduced kidney inflammation in the mice. It was confirmed that bvPLA2 exerted immunomodulatory effects through the CD206 receptor. In addition, bvPLA2 decreased M1 ATM and alleviated the M1/M2 imbalance in vivo. However, bvPLA2 did not directly inhibit adipogenesis in the 3T3-L1 adipose cells in vitro. Conclusions bvPLA2 is a potential therapeutic strategy for the management of obesity by regulating adipose tissue macrophage homeostasis.

scholarly journals Inhibiting LXRα phosphorylation in hematopoietic cells reduces inflammation and attenuates atherosclerosis and obesity in mice

2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Maud Voisin ◽  
Elina Shrestha ◽  
Claire Rollet ◽  
Cyrus A. Nikain ◽  
Tatjana Josefs ◽  
...  
Keyword(s):  
T Cells ◽  
Adipose Tissue ◽  
Hematopoietic Cells ◽  
Adaptive Immune Cells ◽  
Adipose Tissue Macrophages ◽  
Lower Body Weight ◽  
Inflammatory Phenotype ◽  
Obesity In Mice ◽  
Anti Inflammatory ◽  
Inflammatory Macrophages

AbstractAtherosclerosis and obesity share pathological features including inflammation mediated by innate and adaptive immune cells. LXRα plays a central role in the transcription of inflammatory and metabolic genes. LXRα is modulated by phosphorylation at serine 196 (LXRα pS196), however, the consequences of LXRα pS196 in hematopoietic cell precursors in atherosclerosis and obesity have not been investigated. To assess the importance of LXRα phosphorylation, bone marrow from LXRα WT and S196A mice was transplanted into Ldlr−/− mice, which were fed a western diet prior to evaluation of atherosclerosis and obesity. Plaques from S196A mice showed reduced inflammatory monocyte recruitment, lipid accumulation, and macrophage proliferation. Expression profiling of CD68+ and T cells from S196A mouse plaques revealed downregulation of pro-inflammatory genes and in the case of CD68+ upregulation of mitochondrial genes characteristic of anti-inflammatory macrophages. Furthermore, S196A mice had lower body weight and less visceral adipose tissue; this was associated with transcriptional reprograming of the adipose tissue macrophages and T cells, and resolution of inflammation resulting in less fat accumulation within adipocytes. Thus, reducing LXRα pS196 in hematopoietic cells attenuates atherosclerosis and obesity by reprogramming the transcriptional activity of LXRα in macrophages and T cells to promote an anti-inflammatory phenotype.

scholarly journals JAZF1 Inhibits Adipose Tissue Macrophages and Adipose Tissue Inflammation in Diet-Induced Diabetic Mice

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Fanping Meng ◽  
Yao Lin ◽  
Min Yang ◽  
Minyan Li ◽  
Gangyi Yang ◽  
...  
Keyword(s):  
T Cells ◽  
Adipose Tissue ◽  
Inflammatory Markers ◽  
Treg Cells ◽  
Adipose Tissue Inflammation ◽  
Tissue Inflammation ◽  
Adipose Tissue Macrophages ◽  
Lower Blood ◽  
Macrophage Populations

Background. Juxtaposed with another zinc finger gene 1 (JAZF1) affects gluconeogenesis, insulin sensitivity, lipid metabolism, and inflammation, but its exact role in chronic inflammation remains unclear. This study aimed to examine JAZF1 overexpression in vivo on adipose tissue macrophages (ATMs). Methods. Mouse models of high-fat diet- (HFD-) induced insulin resistance were induced using C57BL/6J and JAZF1-overexpressing (JAZF1-OX) mice. The mice were randomized (8–10/group) to C57BL/6J mice fed regular diet (RD) (NC group), C57BL/6J mice fed HFD (HF group), JAZF1-OX mice fed RD (NJ group), and JAZF1-OX mice fed HFD (HJ group). Adipose tissue was harvested 12 weeks later. ATMs were evaluated by flow cytometry. Inflammatory markers were evaluated by ELISA. Results. JAZF1-OX mice had lower blood lipids, blood glucose, body weight, fat weight, and inflammatory markers compared with HF mice (all P<0.05). JAZF1 overexpression decreased ATM number and secretion of proinflammatory cytokines. JAZF1 overexpression decreased total CD4+ T cells, active T cells, and memory T cells and increased Treg cells. JAZF1 overexpression downregulated IFN-γ and IL-17 levels and upregulated IL-4 levels. JAZF1 overexpression decreased MHCII, CD40, and CD86 in total ATM, CD11c+ ATM, and CD206+ ATM. Conclusions. JAZF1 limits adipose tissue inflammation by limiting macrophage populations and restricting their antigen presentation function.

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