scholarly journals Review: Obesity and COVID-19: A Detrimental Intersection

2021 ◽  
Vol 12 ◽  
Author(s):  
Maria Alessandra Gammone ◽  
Nicolantonio D’Orazio
Keyword(s):  
Adipose Tissue ◽  
Visceral Fat ◽  
Molecular Mechanisms ◽  
Therapeutic Potential ◽  
Fat Distribution ◽  
Low Grade ◽  
Viral Spread ◽  
Obese Subjects ◽  
Adipose Inflammation ◽  
Phenotypic Shift

Obesity has been recognized as an independent risk factor for critical illness and major severity in subjects with coronavirus disease 2019 (COVID-19). The role of fat distribution, particularly visceral fat (often linked to metabolic abnormalities), is still unclear. The adipose tissue represents a direct source of cytokines responsible for the pathological modifications occurring within adipose tissue in obese subjects. Adipokines are a crucial connection between metabolism and immune system: their dysregulation in obesity contributes to chronic low-grade systemic inflammation and metabolic comorbidities. Therefore the increased amount of visceral fat can lead to a proinflammatory phenotypic shift. This review analyzes the interrelation between obesity and COVID-19 severity, as well as the cellular key players and molecular mechanisms implicated in adipose inflammation, investigating if adipose tissue can constitute a reservoir for viral spread, and contribute to immune activation and cytokines storm. Targeting the underlying molecular mechanisms might have therapeutic potential in the management of obesity-related complications in COVID-19 patients.

scholarly journals Follistatin-Like 1: A Potential Mediator of Inflammation in Obesity

2013 ◽  
Vol 2013 ◽  
pp. 1-12 ◽  
Author(s):  
Nengguang Fan ◽  
Haiyan Sun ◽  
Yufan Wang ◽  
Yifei Wang ◽  
Lijuan Zhang ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Molecular Mechanisms ◽  
Inflammatory Responses ◽  
Low Grade ◽  
Dependent Manner ◽  
Proinflammatory Mediators ◽  
Raw264.7 Macrophages ◽  
Potential Mediator ◽  
Obese Subjects

Obesity is associated with a state of chronic low-grade inflammation, which contributes to insulin resistance and type 2 diabetes. However, the molecular mechanisms that link obesity to inflammation are not fully understood. Follistatin-like 1 (FSTL1) is a novel proinflammatory cytokine that is expressed in adipose tissue and secreted by preadipocytes/adipocytes. We aimed to test whether FSTL1 could have a role in obesity-induced inflammation and insulin resistance. It was found that FSTL1 expression was markedly decreased during differentiation of 3T3-L1 preadipocytes but reinduced by TNF-α. Furthermore, a significant increase in FSTL1 levels was observed in adipose tissue of obese ob/ob mice, as well as in serum of overweight/obese subjects. Mechanistic studies revealed that FSTL1 induced inflammatory responses in both 3T3-L1 adipocytes and RAW264.7 macrophages. The expression of proinflammatory mediators including IL-6, TNF-α, and MCP-1 was upregulated by recombinant FSTL1 in a dose-dependent manner, paralleled with activation of the IKKβ-NFκB and JNK signaling pathways in the two cell lines. Moreover, FSTL1 impaired insulin signaling in 3T3-L1 adipocytes, as revealed by attenuated phosphorylation of both Akt and IRS-1 in response to insulin stimulation. Together, our results suggest that FSTL1 is a potential mediator of inflammation and insulin resistance in obesity.

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 Age and sex variation in visceral adipose tissue

2019 ◽  
Vol 6 (1) ◽  
pp. 101
Author(s):  
Pallavi Panchu ◽  
Biju Bahuleyan ◽  
Rose Babu ◽  
Vineetha Vijayan
Keyword(s):  
Adipose Tissue ◽  
Visceral Fat ◽  
Metabolic Disorders ◽  
Age Groups ◽  
Fat Distribution ◽  
Age Group ◽  
Cross Sectional ◽  
Younger Age ◽  
The Difference ◽  
Gender Pattern

Background: Adipose tissue mainly visceral fat is said to be harmful and acts as a harbinger of metabolic disorders. A changing trend is seen in the recent decades with decreasing incidence of metabolic disorders in men even though visceral fat is said to be higher in them. Sex hormones may influence the deposition pattern of adipose tissue. The aim of this study was to observe effects of age on visceral fat and to know if the difference in gender pattern of fat distribution is maintained throughout life or disappears after menopause.Methods: This cross-sectional observational study was conducted in Thrissur on 385 apparently healthy subjects using Omron body composition analyser. Data was analysed using SPSS 20.0 version. The tests employed were NOVA, independent samples t-test.Results: In each age group, men had significantly higher visceral fat than females. As age increased, visceral fat increased significantly in both genders. In each group, except for younger age groups, VF levels were equal in men and women.Conclusions: Visceral fat is higher in men and this difference is seen in all age groups. As age increases, visceral fat levels also increased in men and women. The distribution of visceral fat is such that a greater number of men have high to very high levels at a younger age group, a feature observed in women only in the peri and post-menopausal age. Adoption of an active lifestyle coupled with healthy diet should protect against onset of metabolic disorders.

Exploiting Laboratory Insights to Improve Outcomes of Pediatric Central Nervous System Tumors

2016 ◽  
pp. e540-e546 ◽  
Author(s):  
Giles W. Robinson ◽  
Hendrik Witt ◽  
Adam Resnick
Keyword(s):  
Brain Tumor ◽  
Molecular Mechanisms ◽  
Therapeutic Potential ◽  
Pediatric Brain Tumor ◽  
Pediatric Brain Tumors ◽  
Low Grade ◽  
Short Period ◽  
Tumor Management ◽  
The Impact ◽  
Pediatric Brain

Over a relatively short period of time, owing to improvements in biotechnology, our ability to identify the molecular mechanisms within pediatric brain tumors has dramatically increased. These findings have reshaped the way that we describe these diseases and have provided insights into how to better treat these often devastating diseases. Although still far from reaching the full therapeutic potential these advancements hold, the impact of these findings is steadily taking hold of pediatric brain tumor management. In this article, we summarize the major discoveries within three common pediatric brain tumor categories; medulloblastoma, ependymoma, and low-grade glioma. We discuss the current impact of these findings on treatment and the direction these findings may take the field of pediatric neuro-oncology.

TWEAK prevents TNF-α-induced insulin resistance through PP2A activation in human adipocytes

2013 ◽  
Vol 305 (1) ◽  
pp. E101-E112 ◽  
Author(s):  
Ana Vázquez-Carballo ◽  
Victòria Ceperuelo-Mallafré ◽  
Matilde R. Chacón ◽  
Elsa Maymó-Masip ◽  
Margarita Lorenzo ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Insulin Signaling ◽  
Visceral Fat ◽  
Molecular Mechanisms ◽  
Physiological Role ◽  
Metabolic Effects ◽  
Human Adipocytes ◽  
Fat Depots ◽  
Tnf Α

Visceral fat is strongly associated with insulin resistance. Obesity-associated adipose tissue inflammation and inflammatory cytokine production are considered key mediators of insulin signaling inhibition. TWEAK is a relatively new member of the TNF cytokine superfamily, which can exist as full length membrane-associated (mTWEAK) and soluble (sTWEAK) isoforms. Although TWEAK has been shown to have important functions in chronic inflammatory diseases its physiological role in adipose tissue remains unresolved. In this study, we explore the molecular mechanisms involved in the modulation of TNF-α-induced effects on insulin sensitivity by sTWEAK in a human visceral adipose cell line and also in primary human adipocytes obtained from visceral fat depots. Our data reveal that sTWEAK ameliorates TNF-α-induced insulin resistance on glucose uptake, GLUT4 translocation and insulin signaling without affecting other metabolic effects of TNF-α such as lipolysis or apoptotis. Co-immunoprecipitation experiments in adipose cells revealed that pretreatment with sTWEAK specifically inhibits TRAF2 association with TNFR1, but not with TNFR2, which mediates insulin resistance. However, sTWEAK does not affect other downstream molecules activated by TNF-α, such as TAK1. Rather, sTWEAK abolishes the stimulatory effect of TNF-α on JNK1/2, which is directly involved in the development of insulin resistance. This is associated with an increase in PP2A activity upon sTWEAK treatment. Silencing of the PP2A catalytic subunit gene overcomes the dephosphorylation effect of sTWEAK on JNK1/2, pointing to PP2A as a relevant mediator of sTWEAK-induced JNK inactivation. Overall, our data reveal a protective role of TWEAK in glucose homeostasis and identify PP2A as a new driver in the modulation of TNF-α signaling by sTWEAK.

scholarly journals COVID-19 and Obesity: Role of Ectopic Visceral and Epicardial Adipose Tissues in Myocardial Injury

2021 ◽  
Vol 12 ◽  
Author(s):  
Adèle Lasbleiz ◽  
Bénédicte Gaborit ◽  
Astrid Soghomonian ◽  
Axel Bartoli ◽  
Patricia Ancel ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Intensive Care ◽  
Inflammatory Cytokines ◽  
Visceral Adipose Tissue ◽  
Cardiovascular Events ◽  
Low Grade ◽  
Viral Spread ◽  
Visceral Adipose ◽  
Pro Inflammatory Cytokines

In March 2020, the WHO declared coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a global pandemic. Obesity was soon identified as a risk factor for poor prognosis, with an increased risk of intensive care admissions and mechanical ventilation, but also of adverse cardiovascular events. Obesity is associated with adipose tissue, chronic low-grade inflammation, and immune dysregulation with hypertrophy and hyperplasia of adipocytes and overexpression of pro-inflammatory cytokines. However, to implement appropriate therapeutic strategies, exact mechanisms must be clarified. The role of white visceral adipose tissue, increased in individuals with obesity, seems important, as a viral reservoir for SARS-CoV-2 via angiotensin-converting enzyme 2 (ACE2) receptors. After infection of host cells, the activation of pro-inflammatory cytokines creates a setting conducive to the “cytokine storm” and macrophage activation syndrome associated with progression to acute respiratory distress syndrome. In obesity, systemic viral spread, entry, and prolonged viral shedding in already inflamed adipose tissue may spur immune responses and subsequent amplification of a cytokine cascade, causing worse outcomes. More precisely, visceral adipose tissue, more than subcutaneous fat, could predict intensive care admission; and lower density of epicardial adipose tissue (EAT) could be associated with worse outcome. EAT, an ectopic adipose tissue that surrounds the myocardium, could fuel COVID-19-induced cardiac injury and myocarditis, and extensive pneumopathy, by strong expression of inflammatory mediators that could diffuse paracrinally through the vascular wall. The purpose of this review is to ascertain what mechanisms may be involved in unfavorable prognosis among COVID-19 patients with obesity, especially cardiovascular events, emphasizing the harmful role of excess ectopic adipose tissue, particularly EAT.

scholarly journals Abdominal adipose tissue: Significance and methods of detection

2005 ◽  
Vol 58 (5-6) ◽  
pp. 258-264 ◽  
Author(s):  
Biljana Srdic ◽  
Edita Stokic ◽  
Agneza Polzovic ◽  
Sinisa Babovic
Keyword(s):  
Adipose Tissue ◽  
Body Fat ◽  
Visceral Fat ◽  
Fat Distribution ◽  
Body Fat Distribution ◽  
Abdominal Adipose Tissue ◽  
Fat Depots ◽  
Advantages And Disadvantages ◽  
Increased Risk ◽  
Menopausal Women

Introduction. The presence of excess fat in the abdomen, out of proportion to total body fat, is associated with increased risk for cardiovascular and metabolic diseases and other complications of obesity. Histoanatomical characteristics of the abdominal adipose tissue In regard to subcutaneous fat, accumulation of visceral abdominal adipose tissue is more associated with increased metabolic risk. However, mean have more visceral fat than pre-menopausal women. Compared with pre-menopausal women, postmenopausal women have 49% more intraabdominal fat, regardless of age and total fat mass. Measurement of abdominal fat depots Various anthropometric indicators have been suggested for measuring body fat distribution. All of them have advantages and disadvantages, in relation to their interpretation and use. Many are specified as ratios and are difficult to interpret biologically, whereas a change in body fat distribution may exhibit little or no change in the ratios. Waist circumference and sagittal abdominal diameter are good predictors of visceral fat. But, extreme individual variations in visceral to subcutaneous ratio demonstrate the limitations of external anthropometry. The best methods to estimate the amount of visceral fat are imaging techniques like computed tomography or magnetic resonance, but they are expensive and inconvinient in routine practice. Conclusion. Further investigations should provide a simple and optimal indicator of abdominal obesity which should correlate with the amount of viscelar fat and the risk. .

scholarly journals Mitochondrial function, fatty acid metabolism, and immune system are relevant features of pig adipose tissue development

2012 ◽  
Vol 44 (22) ◽  
pp. 1116-1124 ◽  
Author(s):  
Annie Vincent ◽  
Isabelle Louveau ◽  
Florence Gondret ◽  
Bénédicte Lebret ◽  
Marie Damon
Keyword(s):  
Adipose Tissue ◽  
Fatty Acid ◽  
Molecular Mechanisms ◽  
Expression Patterns ◽  
Enrichment Analysis ◽  
Functional Enrichment Analysis ◽  
Functional Enrichment ◽  
Low Grade ◽  
Large White ◽  
Mitochondrial Energy Metabolism

The molecular mechanisms underlying the genetic control of fat development in humans and livestock species still require characterization. To gain insights on gene expression patterns associated with genetic propensity for adiposity, we compared subcutaneous adipose tissue (SCAT) transcriptomics profiles from two contrasted pig breeds for body fatness. Samples were obtained from Large White (LW; lean phenotype) and Basque pigs (B; low growth and high fat content) at 35 kg ( n = 5 per breed) or 145 kg body weight ( n = 10 per breed). Using a custom adipose tissue microarray, we found 271 genes to be differentially expressed between the two breeds at both stages, out of which 123 were highly expressed in LW pigs and 148 genes were highly expressed in B pigs. Functional enrichment analysis based on gene ontology (GO) terms highlighted gene groups corresponding to the mitochondrial energy metabolism in LW pigs, whereas immune response was found significantly enriched in B pigs. Genes associated with lipid metabolism, such as ELOVL6, a gene involved in fatty acid elongation, had a lower expression in B compared with LW pigs. Furthermore, despite enlarged adipocyte diameters and higher plasma leptin concentration, B pigs displayed reduced lipogenic enzyme activities compared with LW pigs at 145 kg. Altogether, our results suggest that the development of adiposity was associated with a progressive worsening of the metabolic status, leading to a low-grade inflammatory state, and may thus be of significant interest for both livestock production and human health.

P2680Changes in body fat distribution after intensive dietary intervention in patients with stable coronary artery disease

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
J Henzel ◽  
M Makarewicz-Wujec ◽  
L Wardziak ◽  
P Trochimiuk ◽  
C Kepka ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Body Fat ◽  
Visceral Fat ◽  
Dietary Intervention ◽  
Fat Distribution ◽  
Control Group ◽  
Total Body Fat ◽  
Artery Disease ◽  
Stable Cad ◽  
Total Body

Abstract Introduction Contradictory reports are available on the role of adipose tissue in the pathophysiology and progression of coronary artery disease (CAD). It seems accepted that local fat distribution is more relevant than the general amount of body fat. As in the case of visceral fat, pericardial adipose tissue (PEAT) has been postulated an important mediator of metabolic risk, with a special role attributed to epicardial adipose tissue (EAT). Purpose To study the effect of intensive dietary and lifestyle modification on the distribution of body fat in patients diagnosed with stable CAD qualified to conservative treatment. Methods Total body fat mass (TBF), visceral fat area (VFA), PEAT volume, and EAT volume were measured in 67 participants (43% women) of the DISCO-CT trial (Dietary Intervention to Stop COronary Atherosclerosis in Computed Tomography, NCT02571803) who completed the study by the end of 2018. All patients, randomly assigned to either experimental or control arm in a 1:1 fashion, were regularly followed-up at our site, with those in the experimental arm being strictly supervised by a dietitian to stick to Dietary Approaches to Stop Hypertension (DASH) diet and encouraged to lifestyle changes atop optimal medical therapy. Contrast-enhanced coronary computed tomography was performed at baseline and after the median time of 59 weeks (2x192-multislice scanner, temporal resolution 66 ms, Somatom Force, Siemens). PEAT and EAT volumes, expressed in mm3, were measured with a dedicated offline workstation (syngo.via Frontier, Siemens Healthcare) using a semiautomatic segmentation technique (window width range −195 to −45 Hounsfield units). TBF, expressed in kg, and VFA, expressed in cm2, were measured using the InBody S10 Body Water Analyser at baseline and completion of the study. 57% of subjects included into the analysis represented the experimental arm. Results There were no significant between-arm differences in baseline TBF, VFA, PEAT, and EAT volumes. A significant reduction by 3.7±5.0 kg in TBF (p<0.001; 95% CI 2.1, 5.3) and by 19.7±30.1 cm2 in VFA (p<0.001; 95% CI 9.8, 29.6) was observed in the experimental arm, while in the control group both TBF and VFA irrelevantly increased, by 0.6±4.7 kg (p=0.53; 95% CI −2.4, 1.3) and 2.2±27.0 cm2 (p=0.67; 95% CI −12.7, 8.2), respectively. A significant decrease in PEAT volume, by 19.9±43.0 mm3 (p=0.007; 95% CI 5.8, 34.1), was observed in the experimental group, compared to a non-significant PEAT volume reduction by 5.8±3.5.0 mm3 (p=0.38, 95% CI −7.5; 19.2) in the control group. Contrarily, no significant changes in EAT volumes were observed in either experimental (reduction by 3.8±15.2 mm3; p=0.13, 95% CI −1.2, 8.8) or control arm (reduction by 5.1±17.2 mm3; p=0.13, 95% CI −1.5, 11.6). Conclusion Intensive dietary intervention in patients with stable CAD can lead to a significant reduction in total body fat, visceral fat and pericardial fat, this effect, however, may not apply to epicardial fat. Acknowledgement/Funding This study was founded by a grant (2.15/III/15) from the Institute of Cardiology in Warsaw, Poland

scholarly journals Systemic Oxidative Stress and Visceral Adipose Tissue Mediators of NLRP3 Inflammasome and Autophagy Are Reduced in Obese Type 2 Diabetic Patients Treated with Metformin

Antioxidants ◽  
2020 ◽  
Vol 9 (9) ◽  
pp. 892
Author(s):  
Zaida Abad-Jiménez ◽  
Sandra López-Domènech ◽  
Rubén Díaz-Rúa ◽  
Francesca Iannantuoni ◽  
Segundo Ángel Gómez-Abril ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Adipose Tissue ◽  
Visceral Adipose Tissue ◽  
Nlrp3 Inflammasome ◽  
Molecular Mechanisms ◽  
Diabetic Patients ◽  
Low Grade ◽  
Obese Patients ◽  
Visceral Adipose

Obesity is a low-grade inflammatory condition affecting a range of individuals, from metabolically healthy obese (MHO) subjects to type 2 diabetes (T2D) patients. Metformin has been shown to display anti-inflammatory properties, though the underlying molecular mechanisms are unclear. To study whether the effects of metformin are mediated by changes in the inflammasome complex and autophagy in visceral adipose tissue (VAT) of obese patients, a biopsy of VAT was obtained from a total of 68 obese patients undergoing gastric bypass surgery. The patients were clustered into two groups: MHO patients and T2D patients treated with metformin. Patients treated with metformin showed decreased levels of all analyzed serum pro-inflammatory markers (TNFα, IL6, IL1β and MCP1) and a downwards trend in IL18 levels associated with a lower production of oxidative stress markers in leukocytes (mitochondrial ROS and myeloperoxidase (MPO)). A reduction in protein levels of MCP1, NFκB, NLRP3, ASC, ATG5, Beclin1 and CHOP and an increase in p62 were also observed in the VAT of the diabetic group. This downregulation of both the NLRP3 inflammasome and autophagy in VAT may be associated with the improved inflammatory profile and leukocyte homeostasis seen in obese T2D patients treated with metformin with respect to MHO subjects and endorses the cardiometabolic protective effect of this drug.

Sign in / Sign up

Export Citation Format

Share Document