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Intestinal permeability and bacterial translocation are increased in obesity and metabolic syndrome (MS). ILC3 cells contribute to the integrity of intestinal epithelium by producing IL-22 via IL-1ß and IL-23. This study investigates the role of IL-1R1 in inducing ILC3 cells and conferring protection during obesity and MS. For this purpose, C57BL/6 wild-type (WT) and IL-1R1-deficient mice were fed a standard diet (SD) or high-fat diet (HFD) for 16 weeks. Weight and blood glucose levels were monitored, and adipose tissue and blood samples were collected to evaluate obesity and metabolic parameters. The small intestine was collected to assess immunological and junction protein parameters through flow cytometry and RT-PCR, respectively. The intestinal permeability was analyzed using the FITC-dextran assay. The composition of the gut microbiota was also analyzed by qPCR. We found that IL-1R1 deficiency exacerbates MS in HFD-fed mice, increasing body fat and promoting glucose intolerance. A worsening of MS in IL-1R1-deficient mice was associated with a reduction in the ILC3 population in the small intestine. In addition, we found decreased IL-22 expression, increased intestinal permeability and bacterial translocation to the visceral adipose tissue of these mice compared to WT mice. Thus, the IL-1R1 receptor plays a critical role in controlling intestinal homeostasis and obesity-induced MS, possibly through the differentiation or activation of IL-22-secreting ILC3s.
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BACKGROUND: Obesity is associated with low-grade inflammation and increased intestinal permeability (IP). The Brazil nut (BN) (Bertholletia excelsa H.B.K.) appears to be a promising dietary intervention to control inflammation by enhancing antioxidant defenses. OBJECTIVES: We aimed to assess the effect of daily BN consumption on inflammatory biomarkers and IP in the context of an energy-restricted intervention. Furthermore, we evaluated the correlation between the changes in these inflammatory markers and the changes in serum selenium and IP. METHODS: In this 8-wk nonrandomized controlled trial, 56 women with overweight or obesity were allocated into 2 groups, both following an energy-restricted diet (-500 kcal/d). The control group (CO) consumed a nut-free diet, while the BN group consumed 8 g BN/d, providing 347.2 µg selenium (Se). Inflammatory cytokines were analyzed in plasma and Se in serum. IP was assessed using the lactulose/mannitol test (LM ratio). RESULTS: Forty-six women completed the intervention. Both groups achieved similar energy restriction (CO Δ= -253.7 ± 169.4 kcal/d; BN Δ= -265.8 ± 141.8 kcal/d) and weight loss (CO Δ= -2.5 ± 0.5 kg; BN Δ= -3.5 ± 0.5 kg). The BN group showed lower values of C-reactive protein, tumor necrosis factor, interleukin (IL)1-ß, IL-8, percentage lactulose excretion, and LM ratio than the CO group. Additionally, changes in serum Se concentration were predictive of changes in IL-8 concentration (ß: -0.054; adjusted R2: 0.100; 95% confidence interval [CI]: -0.100; -0.007; P = 0.025), and changes in IL-8 were predictive of changes in the LM ratio (ß: 0.006; adjusted R2: 0.101; 95% CI: 0.001, 0.011; P = 0.024). CONCLUSIONS: Regular intake of BNs can be a promising complementary dietary strategy for controlling low-grade inflammation and improving IP in women with overweight/obesity undergoing energy-restricted treatment. However, the effects of BNs seem to be Se status-dependent. This trial was registered at the Brazilian Registry of Clinical Trials (ReBEC: https://ensaiosclinicos.gov.br/rg/RBR-3ntxrm/.
Assuntos
Bertholletia , Biomarcadores , Obesidade , Sobrepeso , Selênio , Humanos , Feminino , Bertholletia/química , Adulto , Obesidade/dietoterapia , Obesidade/sangue , Biomarcadores/sangue , Sobrepeso/dietoterapia , Sobrepeso/sangue , Pessoa de Meia-Idade , Selênio/sangue , Inflamação/sangue , Restrição Calórica , Permeabilidade , Brasil , Nozes , Citocinas/sangue , Função da Barreira IntestinalRESUMO
BACKGROUND AND AIMS: Cardiometabolic diseases refer to a group of interrelated conditions, sharing metabolic dysfunctions like insulin resistance, obesity, dyslipidemia, and hypertension. The gut microbiota has been associated with CMD and related conditions. Alterations in the intestinal epithelium permeability triggered by chronic stress and diet could bridge gut microbiota with inflammation and CMD development. Here, we assessed the relationship between intestinal permeability and circulating SCFAs with cardiometabolic health status (CMHS) and gut microbiota in a sample of 116 Colombian adults. METHODS AND RESULTS: Plasma levels of lipopolysaccharide-binding protein (LBP), intestinal fatty acid-binding protein (I-FABP), claudin-3, and purported zonulin peptides (PZP) were measured by ELISA, whereas plasmatic levels of acetate, propionate, butyrate, isobutyrate, and valerate were measured by gas chromatography/mass spectrometry. In addition, for further statistical analysis, we took data previously published by us on this cohort, including gut microbiota and multiple CMD risk factors that served to categorize subjects as cardiometabolically healthy or cardiometabolically abnormal. From univariate and multivariate statistical analyses, we found the levels of I-FABP, LBP, and PZP increased in the plasma of cardiometabolically abnormal individuals, although only PZP reached statistical significance. CONCLUSIONS: Our results did not confirm the applicability of I-FABP, LBP, claudin-3, or SCFAs as biomarkers for associating intestinal permeability with the cardiometabolic health status in these subjects. On the other hand, the poorly characterized peptides detected with the ELISA kit branded as "zonulin" were inversely associated with cardiometabolic dysfunctions and gut microbiota. Further studies to confirm the true identity of these peptides are warranted.
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Microbioma Gastrointestinal , Hipertensão , Adulto , Humanos , Claudina-3 , Intestinos , PermeabilidadeRESUMO
Metabolic disorders are an increasing concern in the industrialized world. Current research has shown a direct link between the composition of the gut microbiota and the pathogenesis of obesity and diabetes. In only a few weeks, an obesity-inducing diet can lead to increased gut permeability and microbial dysbiosis, which contributes to chronic inflammation in the gut and adipose tissues, and to the development of insulin resistance. In this review, we examine the interplay between gut inflammation, insulin resistance, and the gut microbiota, and discuss how some probiotic species can be used to modulate gut homeostasis. We focus primarily on Faecalibacterium prausnitzii, a highly abundant butyrate-producing bacterium that has been proposed both as a biomarker for the development of different gut pathologies and as a potential treatment due to its production of anti-inflammatory metabolites.
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Obesity is mainly caused by intake of a high-fat diet and sedentarism, and is considered a public health issue worldwide. Increased intestinal permeability may favour endotoxaemia generated by lipopolysaccharides, a substance present in the cell membrane of Gram-negative bacteria, and, consequently, an increase in systemic inflammation and metabolic diseases. In contrast (On the other hand), consumption of a healthy diet can help in the prevention and treatment of metabolic syndrome. In this way, chia seeds (Salvia hispanica L.), rich in polyunsaturated fatty acids, may present an anti-inflammatory role. In addition, chia is rich in antioxidants like caffeic and gallic acid and fiber. However, few studies have investigated the relationship between chia seeds, inflammatory mechanisms and intestinal permeability. Therefore, the aim of this study was to analyse the effects of chia administration on metabolism in obese mice. Swiss mice were fed a hyperlipidic diet either supplemented with or without 3% chia flour for 16â¯weeks. The results showed that supplementation could not reduce the deleterious effects of the lipid-rich diet in terms of body composition, glucose intolerance and activity of antioxidants enzymes in the liver. In addition, supplementation with chia in the control diet decreased the amount of occludin in the intestinal colon. In conclusion, although chia did not improve metabolic parameters it seemed to restore the intestinal barriers integrity. The beneficial effects of chia seem to be dependent of the quantity used, since our data conflict with those in the literature; however, it is important to note that other studies, unlike our protocol, used chia in the form of seeds or oil, and not flour.
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Glicemia/metabolismo , Dieta Hiperlipídica , Farinha/análise , Índice Glicêmico , Salvia/química , Animais , Antioxidantes/análise , Biomarcadores/sangue , Peso Corporal , Ácidos Cafeicos/análise , HDL-Colesterol/sangue , LDL-Colesterol/sangue , Fibras na Dieta/análise , Ácidos Graxos Insaturados/análise , Ácido Gálico/análise , Teste de Tolerância a Glucose , Masculino , Camundongos , Camundongos Obesos , Sementes/química , Triglicerídeos/sangueRESUMO
Fiber fermentation by gut microbiota yields short-chain fatty acids (SCFAs) that are either absorbed by the gut or excreted in feces. Studies are conflicting as to whether SCFAs are beneficial or detrimental to cardiometabolic health, and how gut microbiota associated with SCFAs is unclear. In this study of 441 community-dwelling adults, we examined associations of fecal SCFAs, gut microbiota diversity and composition, gut permeability, and cardiometabolic outcomes, including obesity and hypertension. We assessed fecal microbiota by 16S rRNA gene sequencing, and SCFA concentrations by gas chromatography/mass spectrometry. Fecal SCFA concentrations were inversely associated with microbiota diversity, and 70 unique microbial taxa were differentially associated with at least one SCFA (acetate, butyrate or propionate). Higher SCFA concentrations were associated with a measure of gut permeability, markers of metabolic dysregulation, obesity and hypertension. Microbial diversity showed association with these outcomes in the opposite direction. Associations were significant after adjusting for measured confounders. In conclusion, higher SCFA excretion was associated with evidence of gut dysbiosis, gut permeability, excess adiposity, and cardiometabolic risk factors. Studies assessing both fecal and circulating SCFAs are needed to test the hypothesis that the association of higher fecal SCFAs with obesity and cardiometabolic dysregulation is due to less efficient SCFA absorption.