Chronic Inflammation In Obesity Research Articles

The Benefits of the Mediterranean Diet on Inflamm-Aging in Childhood Obesity.

(1) Background: Numerous elements of the Mediterranean diet (MD) have antioxidant and anti-inflammatory qualities. (2) Methods: We present a narrative review of the potential benefits of the Mediterranean dietary pattern (MD) in mitigating aging-related inflammation (inflamm-aging) associated with childhood obesity. The mechanisms underlying chronic inflammation in obesity are also discussed. A total of 130 papers were included after screening abstracts and full texts. (3) Results: A complex interplay between obesity, chronic inflammation, and related comorbidities is documented. The MD emerges as a promising dietary pattern for mitigating inflammation. Studies suggest that the MD may contribute to weight control, improved lipid profiles, insulin sensitivity, and endothelial function, thereby reducing the risk of metabolic syndrome in children and adolescents with obesity. (4) Conclusions: While evidence supporting the anti-inflammatory effects of the MD in pediatric obesity is still evolving, the existing literature underscores its potential as a preventive and therapeutic strategy. However, MD adherence remains low among children and adolescents, necessitating targeted interventions to promote healthier dietary habits. Future high-quality intervention studies are necessary to elucidate the specific impact of the MD on inflammation in diverse pediatric populations with obesity and associated comorbidities.

Influence of cardiorespiratory fitness on obesity-associated inflammation in women and men: The FATCOR study

Background and aimsCardiorespiratory fitness has been postulated to lower chronic inflammation in obesity. We assessed sex-specific associations of inflammation with cardiorespiratory fitness in overweight and obese persons. Methods and resultsPeak oxygen uptake (VO2max) was measured by treadmill in 566 participants (age 48 ± 9 years, 60% women) with body mass index >27.0 kg/m2 in the FAT associated CardiOvasculaR dysfunction (FATCOR) study. Fitness was identified from age- and sex specific reference levels of VO2max. The inflammatory markers C-reactive protein (CRP), serum amyloid A (SAA), kynurenine:tryptophan ratio (KTR) and pyriodoxic acid ratio (PAr) were measured by mass spectrometry. In the total study population 63% had obesity and 74% were cardiorespiratory unfit. Unfit women had the highest fat percentage and the highest serum levels of CRP and SAA (p < 0.05). In multivariable linear regression analyses in women, higher CRP (β −0.15, p = 0.001), SAA (β −0.10, p = 0.03) and PAr (β −0.09, p = 0.03) were associated with lower VO2max after adjusting for confounders. In multivariable analyses in men, higher PAr (β −0.14, p = 0.02) was associated with lower VO2max. In multivariable analyses in obese women, higher CRP and PAr remained associated with lower VO2max (p < 0.05), while in obese men there was no significant association. When normalizing VO2max for fat-free mass (VO2maxFFM) higher CRP, SAA and PAr index were associated with lower VO2maxFFM in women, while only higher PAr index was associated with lower VO2maxFFM in men. ConclusionThe association of inflammation with lower cardiorespiratory fitness was more pronounced in women than men, in particular when obesity was present. Clinical trial registrationURL: http://www.clinicaltrials.gov NCT02805478.

The role of adipose tissue and subsequent liver tissue hypoxia in obesity and early stage metabolic dysfunction associated steatotic liver disease.

Obesity is linked to several health complication, including Metabolic Dysfunction Associated Steatotic Liver Disease (MASLD). Adipose tissue hypoxia has been suggested as an important player in the pathophysiological mechanism leading to chronic inflammation in obesity, and in the progression of MASLD. The study aims to investigate the effect of progressive obesity on adipose and liver tissue hypoxia. Male 8-week-old C57BL/6J mice were fed a high-fat high-fructose diet (HFHFD) or control diet (CD) for 4, 8, 12, 16 and 20 weeks. Serum ALT, AST and lipid levels were determined, and glucose and insulin tolerance testing was performed. Liver, gonadal and subcutaneous adipose tissue was assessed histologically. In vivo tissue pO2 measurements were performed in gonadal adipose tissue and liver under anesthesia. A PCR array for hypoxia responsive genes was performed in liver and adipose tissue. The main findings in the liver were validated in another diet-induced MASLD mice model, the choline-deficient L-amino acid defined high-fat diet (CDAHFD). HFHFD feeding induced a progressive obesity, dyslipidaemia, insulin resistance and MASLD. In vivo pO2 was decreased in gonadal adipose tissue after 8 weeks of HFHFD compared to CD, and decreased further until 20 weeks. Liver pO2 was only significantly decreased after 16 and 20 weeks of HFHFD. Gene expression and histology confirmed the presence of hypoxia in liver and adipose tissue. Hypoxia could not be confirmed in mice fed a CDAHFD. Diet-induced obesity in mice is associated with hypoxia in liver and adipose tissue. Adipose tissue hypoxia develops early in obesity, while liver hypoxia occurs later in the obesity development but still within the early stages of MASLD. Liver hypoxia could not be directly confirmed in a non-obese liver-only MASLD mice model, indicating that obesity-related processes such as adipose tissue hypoxia are important in the pathophysiology of obesity and MASLD.

Potential targets for traditional Chinese medicine treatment of chronic inflammation in obesity: macrophage polarization

Obesity has been identified as a chronic low-grade systemic inflammation and a key risk factor for diseases such as diabetes, hypertension, and malignancies, and has become an urgent global health burden. Adipose tissue macrophages play a significant role in adipose immune homeostasis and inflammatory responses. Under different conditions, they can be polarized into pro-inflammatory M1 phenotype or anti-inflammatory M2 phenotype. In obese individuals, there is abnormal polarization of macrophages in adipose tissue, leading to an imbalance in the M1/M2 phenotype dynamic equilibrium and the development of pathological inflammation. Therefore, restoring the balance of M1/M2 macrophage polarization is an important potential target for the treatment of chronic inflammation in obesity. Studies have shown that traditional Chinese medicine(TCM) can positively modulate macrophage polarization and produce beneficial effects on obesity. Based on existing evidence, this paper systematically reviewed the potential mechanisms of TCM in improving chronic inflammation in obesity from the perspective of macrophage polarization, in order to provide evidence for the clinical diagnosis and treatment of chronic inflammation in obesity with TCM and offer new insights for related research design and the development of new TCM.

Free fatty acids and peripheral blood mononuclear cells (PBMC) are correlated with chronic inflammation in obesity

Obesity-related chronic inflammation is closely related to the ability of immune cells to adapt to the body’s needs, research has shown that excess FAs can further activate pro-inflammatory transcription factors in the nucleus by interacting with various receptors such as CD36 and TLR4, thereby affecting the inflammatory state of cells. However, how the profile of various fatty acids in the blood of obese individuals is associated with chronic inflammation remains unclear.ObjectiveThe biomarkers associated with obesity were identified from 40 fatty acids (FAs) in the blood, and analyze the relationship between the biomarkers and chronic inflammation. Furthermore, by analyzing the difference in the expression of CD36, TLR4 and NF-κB p65 in peripheral blood mononuclear cells (PBMC) between obese and standard weight people, understand that immunophenotype PBMC is associated with chronic inflammation.MethodsThis study is a cross-sectional study. Participants were recruited from the Yangzhou Lipan weight loss training camp from May 2020 to July 2020. The sample size was 52 individuals, including 25 in the normal weight group and 27 in the obesity group. Individuals with obesity and controls of normal weight were recruited to identify biomarkers associated with obesity from 40 fatty acids in the blood; correlation analysis was conducted between the screened potential biomarkers FAs and the chronic inflammation index hs-CRP to identify FA biomarkers associated with chronic inflammation. Changes in the fatty acid receptor CD36, inflammatory receptor TLR4, and inflammatory nuclear transcription factor NF-κB p65 in PBMC subsets were used to further test the relationship between fatty acids and the inflammatory state in individuals with obesity.Results23 potential FA biomarkers for obesity were screened, eleven of the potential obesity biomarkers were also significantly related to hs-CRP. Compared to the control group, in monocytes the obesity group expressed higher TLR4, CD36, and NF-κB p65 in lymphocytes, the obesity group expressed higher TLR4 and CD36; and in granulocytes the obesity group expressed higher CD36.ConclusionBlood FAs are associated with obesity and are associated with chronic inflammation through increased CD36, TLR4, and NF-κB p65 in monocytes.

Dietary pulses as a means to improve the gut microbiome, inflammation, and appetite control in obesity.

A dysbiotic intestinal microbiome has been linked to chronic diseases such as obesity, which may suggest that interventions that target the microbiome may be useful in treating obesity and its complications. Appetite dysregulation and chronic systemic low-grade inflammation, such as that observed in obesity, are possibly linked with the intestinal microbiome and are potential therapeutic targets for the treatment of obesity via the microbiome. Dietary pulses (e.g., common beans) are composed of nutrients and compounds that possess the potential to modulate the gut microbiota composition and function which can in turn improve appetite regulation and chronic inflammation in obesity. This narrative review summarizes the current state of knowledge regarding the connection between the gut microbiome and obesity, appetite regulation, and systemic and adipose tissue inflammation. More specifically, it highlights the efficacy of interventions employing dietary common beans as a means to improve gut microbiota composition and/or function, appetite regulation, and inflammation in both rodent obesity and in humans. Collectively, results presented and discussed herein provide insight on the gaps in knowledge necessary for a comprehensive understanding of the potential of beans as a treatment for obesity while highlighting what further research is required to gain this understanding.

Treatment with bergamot (Citrus bergamia) leaves extract attenuates leptin resistance in obese rats.

Low-grade chronic inflammation in obesity is associated with leptin resistance. In order to alleviate this pathological condition, bioactive compounds capable of attenuating oxidative stress and inflammation have been researched, and bergamot (Citrus bergamia) presents these properties. The aim was to evaluate the effect of bergamot leaves extract on leptin resistance in obese rats. Animals were divided into 2 groups: control diet (C, n=10) and high sugar-fat diet (HSF, n=20) for 20 weeks. After detecting hyperleptinemia, animals were divided to begin the treatment with bergamot leaves extract (BLE) for 10 weeks: C+placebo (n=7), HSF+placebo (n=7), and HSF+BLE (n=7) by gavage (50mg/kg). Evaluations included nutritional, hormonal and metabolic parameters; adipose tissue dysfunction; inflammatory, oxidative markers and hypothalamic leptin pathway. HSF group presented obesity, metabolic syndrome, adipose tissue dysfunction, hyperleptinemia and leptin resistance compared to control group. However, the treated group showed a decrease in caloric consumption and attenuation of insulin resistance. Moreover, dyslipidemia, adipose tissue function, and leptin levels showed an improvement. At the level of the hypothalamus, the treated group showed a reduction of oxidative stress, inflammation and modulation of leptin signaling. In conclusion, BLE properties were able to improve leptin resistance through recovery of the hypothalamic pathway.

β-(1,3)-D-glucan from &lt;em&gt;Pleurotus ostreatus&lt;/em&gt; correlates with lower plasma IL-6, IL-1β, HOMA-IR, and higher pancreatic beta cell count in High-Fat and High-Fructose Diet (HFFD) rats

Introduction: The increasing consumption of high-fat and high-fructose foods contributes to the increasing prevalence of global obesity. Low-grade chronic inflammation in obesity is a significant risk factor for insulin resistance and type 2 diabetes. Therefore, this study aimed to determine the effect of β-(1,3)-D-glucan from oyster mushroom (Pleurotus ostreatus) extract on rats fed with a high-fat and high-fructose diet. Design and Methods: This experimental study was conducted on 35 male Sprague-Dawley rats aged eight weeks. The rats were divided into groups given a normal (N) diet, a high-fat and high-fructose diet (HFFD), D1 (HFFD+125 mg/kg BW β-glucan), D2 (HFFD+250 mg/kg BW β glucan), and D3 (HFFD+375 mg/kg BW β-glucan) with an intervention of 14 weeks. IL-6 and IL-1β levels were measured by the ELISA method, while HOMA-IR (Homeostatic Model Assessment for Insulin Resistance) was calculated by the fasting insulin (ng/mL) x fasting blood glucose (mg/dL)/405 formula. Pancreatic beta-cell counts were measured by hematoxylin and eosin (H&amp;E) staining. Results: The results showed no differences in IL-6 and IL-1β between the treatment groups. However, there were significant differences in HOMA-IR and pancreatic beta-cell counts between groups. There were negative correlations between the dose of β-glucan and IL-6, IL-1β, and HOMA-IR levels. Also, there was a positive correlation between the dose of β-glucan and the number of pancreatic beta cells. Conclusions: Administration of β-(1,3)-D-glucan from oyster mushroom (Pleurotus ostreatus) extract prevented hyperglycemia and insulin resistance, also reduced inflammation in rats fed with HFFD regardless of weight gain.

Anti-Inflammatory Mechanisms of Dietary Flavones: Tapping into Nature to Control Chronic Inflammation in Obesity and Cancer

Flavones are natural phytochemicals broadly distributed in our diet. Their anti-inflammatory properties provide unique opportunities to control the innate immune system and inflammation. Here, we review the role of flavones in chronic inflammation with an emphasis on their impact on the molecular mechanisms underlying inflammatory diseases including obesity and cancer. Flavones can influence the innate immune cell repertoire restoring the immune landscape. Flavones impinge on NF-κB, STAT, COX-2, or NLRP3 inflammasome pathways reestablishing immune homeostasis. Devoid of adverse side effects, flavones could present alternative opportunities for the treatment and prevention of chronic inflammation that contributes to obesity and cancer.

Investigation of the Relationship between IL-6, IL-6R and CXCL5 Polymorphisms and Obesity in Denizli Province of Turkey

Obesity and its effects on increasing morbidity and mortality have reached the level of an epidemic with a high frequency in modern populations. IL-6 released from adipose tissue is known to trigger the chronic inflammation in obesity. CXCL5, which mediates the activation and migration of neutrophils, has been found at high levels in obese subjects. In our study, we aimed to investigate the possible effects of IL-6, IL-6R and CXCL5, polymorphisms and haplotypes on the development of obesity. We studied IL-6, rs2069827 (-1363, G/T), rs1800797 (-597, G/A), rs1800796 (-572, G/C) and rs1800795 (-174, G/C), IL-6R rs4845617 (-183, G/A), rs2228145 (+48892, A/C) and CXCL5 rs352046 (-156, G/C) polymorphic sites in 60 obesity patients and 59 healthy controls. For genotyping we used PCR-RFLP based approach. The IL-6 rs1800796, rs1800795 and IL-6R rs4845617 G allelles could be the possible genetic factors responsible for obesity. We found similar results in female obese group. The results indicated that there was no association between obesity and other SNPs (rs2069827, rs1800797, and rs1800795 and rs2228145) and CXCL5, rs352046. The results of IL-6 and IL-6R haplotype analysis by global differentiation test showed that haplotypes may have different distributions between obese and controls. Our results showed that polymorphisms and possible haplotypes in IL-6 and IL-6R genes, which have an important role in inflammation, may affect the development of obesity. This study points out the necessity of investigating the possible effects of gene polymorphisms of other cytokines and their receptors in the development of obesity in larger populations.

Polycationic PAMAM ameliorates obesity-associated chronic inflammation and focal adiposity

As a surging public health crisis, obesity and overweight predispose individuals to various severe comorbidities contributed by the accompanying chronic inflammation. However, few options exist for tackling chronic inflammation in obesity or inhibiting depot-specific adiposity. Here, we report that polycationic polyamidoamine (PAMAM) treatment can improve both aspects of obesity. With the discovery that the plasma cell-free RNA (cfRNA) level is elevated in obese subjects, we applied the cationic PAMAM generation 3 (P-G3) scavenger to treat diet-induced obese (DIO) mice. Intraperitoneal delivery of P-G3 alleviated the chronic inflammation in DIO mice and reduced their body weight, resulting in improved metabolic functions. To further enhance the applicability of P-G3, we complexed P-G3 with human serum albumin (HSA) to attain a sustained release, which showed consistent benefits in treating DIO mice. Local injection of HSA-PG3 into subcutaneous fat completely restricted the distribution of the complex within the targeted depot and reduced focal adiposity. Our study illuminates a promising cationic strategy to ameliorate chronic inflammation in obesity and target local adiposity.

The Nrf2 in Obesity: A Friend or Foe?

Obesity and its complications have become serious global health concerns recently and increasing work has been carried out to explicate the underlying mechanism of the disease development. The recognized correlations suggest oxidative stress and inflammation in expanding adipose tissue with excessive fat accumulation play important roles in the pathogenesis of obesity, as well as its associated metabolic syndromes. In adipose tissue, obesity-mediated insulin resistance strongly correlates with increased oxidative stress and inflammation. Nuclear factor erythroid 2-related factor 2 (Nrf2) has been described as a key modulator of antioxidant signaling, which regulates the transcription of various genes coding antioxidant enzymes and cytoprotective proteins. Furthermore, an increasing number of studies have demonstrated that Nrf2 is a pivotal target of obesity and its related metabolic disorders. However, its effects are controversial and even contradictory. This review aims to clarify the complicated interplay among Nrf2, oxidative stress, lipid metabolism, insulin signaling and chronic inflammation in obesity. Elucidating the implications of Nrf2 modulation on obesity would provide novel insights for potential therapeutic approaches in obesity and its comorbidities.

Palmitoleic Acid Acts on Adipose-Derived Stromal Cells and Promotes Anti-Hypertrophic and Anti-Inflammatory Effects in Obese Mice

Adipose tissue (AT) secretes adipokines, modulators of low-grade chronic inflammation in obesity. Molecules that induce the emergence of new and functional adipocytes in AT can alleviate or prevent inflammatory and metabolic disorders. The objective of this study was to investigate the role of palmitoleic acid (n7) in 3T3-L1 and primary pre-adipocyte differentiation and AT inflammation. C57BL/6j mice were submitted to a control or high-fat diet (HFD) for 8 weeks, and treated with n7 for 4 weeks. Mice consuming a HFD presented an increase in body weight, epididymal (Epi) fat mass, and Epi adipocytes size. N7 treatment attenuated the body weight gain and completely prevented the hypertrophy of Epi adipocytes, but not the increment in Epi mass induced by the HFD, suggesting a greater adipocytes hyperplasia in animals treated with n7. It was agreed that n7 increased 3T3-L1 proliferation and differentiation, as well as the expression of genes involved in adipogenesis, such as Cebpa, Pparg, aP2, Perilipin, and Scl2a4. Furthermore, n7 decreased the inflammatory cytokines Mcp1, Tnfa, Il6, Cxcl10, and Nos2 genes in Epi vascular stromal cells, but not in the whole AT. These findings show that n7 exerts anti-hypertrophic effects in adipocytes which influence the surrounding cells by attenuating the overexpression of pro-inflammatory cytokines triggered by a HFD.

The Traditional Mongolian Medicine Qiqirigan-8 Effects on Lipid Metabolism and Inflammation in Obesity: Pharmacodynamic Evaluation and Relevant Metabolites.

Objective: Traditional Mongolian Medicine Qiqirigan-8 (MMQ-8) is a Chinese botanical drug with effective pharmacological properties in obesity. However, the pharmacological mechanism of MMQ-8 remains unclear. This study aimed to determine the active metabolites of MMQ-8 and its therapeutic effects on lipid metabolism and inflammation. Methods: The active metabolites of MMQ-8 were identified by ultrahigh-performance liquid chromatograph Q extractive mass spectrometry (UHPLC-QE-MS) assay and network analysis. An obesity rat model induced by high-fat diet was used in the study. Serum levels of lipids and inflammatory factors were detected using biochemical analysis and enzyme-linked immunosorbent assay (ELISA). Pathological analysis of liver tissues and arteries was conducted with hematoxylin and eosin (H&E) staining and immunohistochemistry. Protein expression of the tumor necrosis factor (TNF) signaling pathway was investigated by Western-blot. Simultaneously, bone marrow cells were used for RNA sequencing and relevant results were validated by cell culture and quantitative real-time polymerase chain reaction (RT-qPCR). Results: We identified 69 active metabolites and 551 target genes of MMQ-8. Of these, there are 65 active metabolites and 225 target genes closely related to obesity and inflammation. In vivo, we observed that MMQ-8 had general decreasing effects on body weight, white adipose tissue weight, and serum lipids. MMQ-8 treatment notably decreased the liver function markers and hepatic steatosis, and significantly decreased inflammation. In serum, it notably decreased TNF-α, interleukin (IL)-6, and inducible nitric oxide synthase (INOS), while elevating IL-10 levels. MMQ-8 treatment also significantly inhibited proteins phosphorylation of nuclear factor-kappa B inhibitor alpha (IκBα), mitogen-activated protein kinase (p38), extracellular regulated kinase 1/2(ERK1/2), and stress-activated protein kinase/c-Jun N-terminal kinase (SAPK/JNK), and decreased vascular endothelium damage and macrophage infiltration and polarization to M1. These findings coincide with the RNA-sequencing data of bone marrow cells and results of in vitro experiments. Conclusion: We determined the pharmacological actions and relevant metabolites of MMQ-8 in obesity for the first time. Our study revealed MMQ-8 can optimize lipid metabolism and reduce chronic inflammation in obesity. However, more in-depth research is needed, for example, to understand the principle of compound compatibility and the inhibition effects on hepatic steatosis, T cell differentiation, and inflammatory signal transduction.

Roles of Transmembrane Protein 97 (TMEM97) in Adipose Tissue and Skeletal Muscle.

The combination of sarcopenia and obesity (sarcopenic obesity) is associated with the development of metabolic syndrome and cardiovascular events. The molecular pathways that develop sarcopenic obesity have studied intensively. Transmembrane protein 97 (TMEM97) is 176 amino acids conserved integral membrane protein with four transmembrane domains that is expressed in several types of cancer. Its physiological significance in adipose tissue and skeletal muscle has been unclear. We studied TMEM97-transgenic mice and mice lacking TMEM97, and our findings indicate that TMEM97 expression is regulated in adipose tissue and skeletal muscle from obesity. TMEM97 represses adipogenesis and promotes myogenesis in vitro. Fat-specific TMEM97 transgenic mice showed systemic insulin resistance. Mice overexpressing TMEM97 in skeletal muscle exhibited systemic insulin resistance. Mice lacking TMEM97 were protected against diet-induced obesity and insulin resistance. These phenotypes are associated with the effects of TMEM97 on inflammation genes in adipose tissue and skeletal muscle. Our findings indicates that there is a link between TMEM97 and chronic inflammation in obesity.

Chronic Inflammation in Obesity and Cancer Cachexia.

Chronic inflammation has long been linked to obesity and related conditions such as type 2 diabetes and metabolic syndrome. According to current research, the increased risk of cancer in people with certain metabolic diseases may be due to chronic inflammation. Adipocytokines, which are pro-inflammatory cytokines secreted in excess, are elevated in many chronic metabolic diseases. Cytokines and inflammatory mediators, which are not directly linked to DNA, are important in tumorigenesis. Cachexia, a type of metabolic syndrome linked to the disease, is associated with a dysregulation of metabolic pathways. Obesity and cachexia have distinct metabolic characteristics, such as insulin resistance, increased lipolysis, elevated free fatty acids (FFA), and ceramide levels, which are discussed in this section. The goal of this research project is to create a framework for bringing together our knowledge of inflammation-mediated insulin resistance.

Obesity and COVID-19: Mechanistic Insights From Adipose Tissue.

Obesity is associated with an increase in morbidity and mortality from COVID-19. The risk is related to the cytokine storm, a major contributor to multiorgan failure and a pathological character of COVID-19 patients with obesity. While the exact cause of the cytokine storm remains elusive, disorders in energy metabolism has provided insights into the mechanism. Emerging data suggest that adipose tissue in obesity contributes to the disorders in several ways. First, adipose tissue restricts the pulmonary function by generation of mechanical pressures to promote systemic hypoxia. Second, adipose tissue supplies a base for SARS-CoV-2 entry by overexpression of viral receptors (ACE2 and DPP4). Third, impaired antiviral responses of adipocytes and immune cells result in dysfunction of immunologic surveillance as well as the viral clearance systems. Fourth, chronic inflammation in obesity contributes to the cytokine storm by secreting more pro-inflammatory cytokines. Fifth, abnormal levels of adipokines increase the risk of a hyper-immune response to the virus in the lungs and other organs to enhance the cytokine storm. Mitochondrial dysfunction in adipocytes, immune cells and other cell types (endothelial cells and platelets, etc.) is a common cellular mechanism for the development of cytokine storm, which leads to the progression of mild COVID-19 to severe cases with multiorgan failure and high mortality. Correction of energy surplus through various approaches is recommended in the prevention and treatment of COVID-19 in the obese patients.

Laparoscopic sleeve gastrectomy for morbid obesity improves gut microbiota balance, increases colonic mucosal-associated invariant T cells and decreases circulating regulatory T cells.

Laparoscopic sleeve gastrectomy (LSG) for morbid obesity may improve gut microbiota balance and decrease chronic inflammation. This study examines the changes in gut microbiota and immune environment, including mucosal-associated invariant T cells (MAIT cells) and regulatory T cells (Treg cells) caused by LSG. Ten morbidly obese patients underwent LSG at our institution between December 2018 and March 2020. Flow cytometry for Th1/Th2/Th17 cells, Treg cells and MAIT cells in peripheral blood and colonic mucosa and 16S rRNA analysis of gut microbiota were performed preoperatively and then 12months postoperatively. Twelve months after LSG, the median percent total weight loss was 30.3% and the median percent excess weight loss was 66.9%. According to laboratory data, adiponectin increased, leptin decreased, and chronic inflammation improved after LSG. In the gut microbiota, Bacteroidetes and Fusobacteria increased after LSG, and indices of alpha diversity increased after LSG. In colonic mucosa, the frequency of MAIT cells increased after LSG. In peripheral blood, the frequency of Th1 cells and effector Treg cells decreased after LSG. After LSG for morbid obesity, improvement in chronic inflammation in obesity is suggested by change in the constituent bacterial species, increase in the diversity of gut microbiota, increase in MAIT cells in the colonic mucosa, and decrease in effector Treg cells in the peripheral blood.

Obesity, metabolic syndrome, and inflammation: An update for anaesthetists caring for patients with obesity

Our understanding of chronic inflammation in obesity is evolving. Suggested mechanisms include hypoxia of adipose tissue and a subsequent increase in circulating cytokines. It is now known that adipose tissue, far from being an inert tissue, produces and secretes multiple peptides that influence inflammation and metabolism, including substrates of the renin–angiotensin–aldosterone system (RAAS). RAAS blocking antihypertensive medication and cholesterol-lowering agents are now being evaluated for their metabolic and inflammation–modulating effects. Surgery also has pro-inflammatory effects, which may be exacerbated in patients with obesity. This narrative review will summarise the recent literature surrounding obesity, metabolic syndrome, inflammation, and interplay with the RAAS, with evidence-based recommendations for the optimisation of patients with obesity, prior to surgery and anaesthesia.

Correlation of Waist Circumference with Monocyte Lymphocyte Ratio, Hemoglobin, and Hba1c in Obesity

Background: Obesity is a condition of excessive BMI, accompanied by accumulation of abnormal fat, especially visceral fat. Visceral fat accumulation can be known by measuring waist circumference. Chronic inflammation in obesity, especially central obesity can cause insulin resistance. Monocyte lymphocyte ratio (MLR) is one of the inflammatory markers that is cheap and easy to examine. Anemia can be caused by chronic inflammatory in obesity and interfere by quality of life, activity, and nutrition. HbA1c as one of the glucose parameters can increase because of insulin resistance. Method: Cross-sectional study of 46 obese young adults, based on WHO criteria during May-September 2018 was done. MLR was measured by manual calculation of differential counts hematology analyzer. Hemoglobin was measured by hematology analyzer and HbA1c was measured by high performance liquid chromatography (HPLC). Pearson test was performed for analyzing data with p &lt;0.05 was significant. Results: Waist circumference had significant weak positive correlation with MLR and HbA1c respectively (r = 0.376 p = 0.010 ; r = 0.378 p = 0.010) and waist circumference had significant moderate positive correlation with Hb (r = 0.452, p= 0.002). Conclusions: There was significant weak positive correlation between waist circumference and MLR, and HbA1c. There was significant moderate positive correlation between waist circumference and Hb in obesity. Future examination of inflammatory parameters and anemia is needed for further study Keywords: Waist circumference, MLR, Hb, and HbA1c.