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-Cardiac cytokines in cardiac tissue. (A) IL-6 (pg protein/g); (B) TNF-α. Results expressed as median and interquartile range. Comparison by Mann-Whitney test. * indicates p < 0.05; n = 8 animals/group.

-Cardiac cytokines in cardiac tissue. (A) IL-6 (pg protein/g); (B) TNF-α. Results expressed as median and interquartile range. Comparison by Mann-Whitney test. * indicates p < 0.05; n = 8 animals/group.

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Background: Obesity is a chronic low-grade inflammation condition related to cardiac disorders. However, the mechanism responsible for obesity-related cardiac inflammation is unclear. The toll-like receptor 4 (TLR-4) belongs to a receptor of the transmembrane family responsible for the immune response whose activation stimulates the production of...

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... the TLR-4 gene and protein expression in cardiac tissue, it is possible to verify that both were increased in the OB group (Figure 1). NF-ĸB phosphorylation in cardiac tissue was also higher in the OB group (Figure 2), resulting in increased cytokines, since this group showed higher TNF-α and IL-6 levels compared to the C group ( Figure 3). ...

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... These changes are associated with the reprogramming of mitochondrial metabolism in adipose tissues. Furthermore, TLRs such as TLR4 and TLR9 contribute to obesity-associated metabolic disorders [82,83]. ...
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Obesity is a chronic disease characterized by the abnormal or excessive accumulation of body fat, affecting more than 1 billion people worldwide. Obesity is commonly associated with other metabolic disorders, such as type 2 diabetes, non-alcoholic fatty liver disease, cardiovascular diseases, chronic kidney disease, and cancers. Factors such as a sedentary lifestyle, overnutrition, socioeconomic status, and other environmental and genetic conditions can cause obesity. Many molecules and signaling pathways are involved in the pathogenesis of obesity, such as nuclear factor (NF)-κB, Toll-like receptors (TLRs), adhesion molecules, G protein-coupled receptors (GPCRs), programmed cell death 1 (PD-1)/programmed death-ligand 1 (PD-L1), and sirtuin 1 (SIRT1). Commonly used strategies of obesity management and treatment include exercise and dietary change or restriction for the early stage of obesity, bariatric surgery for server obesity, and Food and Drug Administration (FDA)-approved medicines such as semaglutide and liraglutide that can be used as monotherapy or as a synergistic treatment. In addition, psychological management, especially for patients with obesity and distress, is a good option. Gut microbiota plays an important role in obesity and its comorbidities, and gut microbial reprogramming by fecal microbiota transplantation (FMT), probiotics, prebiotics, or synbiotics shows promising potential in obesity and metabolic syndrome. Many clinical trials are ongoing to evaluate the therapeutic effects of different treatments. Currently, prevention and early treatment of obesity are the best options to prevent its progression to many comorbidities.
... LPS can also stimulate nonimmune cells and initiate the inflammatory process. The literature reports that an innate LPS-pattern recognition receptor, the Toll-like receptor-4 (TLR-4) is widely expressed in the body, including cardiac tissue 13 . Thus, the innate inflammatory response can be induced in cardiomyocytes by LPS independently of the immune cell involvement 14 . ...
... The obesity-related disorders, such as insulin resistance, diabetes, and dyslipidemia, are considered HF predictors and associate with adipose tissue dysfunction, promoting maladaptive cardiac responses, such as myocyte hypertrophy, contractile dysfunction, and cardiac remodeling, which contribute to their development and chronic HF progression. 40 Alves et al., 41 in an elegant study with Wistar rats, have hypothesized that the activation of the toll-like receptor 4 (TLR-4) participates in the obesity-related cardiac disease by triggering cytokine production via nuclear factor-ĸB (NF-ĸB). The 'obese' group, which was fed a high sugar-fat diet and water plus 25% of sucrose for 30 weeks, showed: obesity, high levels of glucose, triglycerides and uric acid, insulin resistance, high systolic blood pressure, high levels of tumor necrosis factor alpha (TNF-α) in the adipose tissue, in addition to cardiac remodeling and diastolic dysfunction. ...
... The obesity-related disorders, such as insulin resistance, diabetes, and dyslipidemia, are considered HF predictors and associate with adipose tissue dysfunction, promoting maladaptive cardiac responses, such as myocyte hypertrophy, contractile dysfunction, and cardiac remodeling, which contribute to their development and chronic HF progression. 40 Alves et al., 41 in an elegant study with Wistar rats, have hypothesized that the activation of the toll-like receptor 4 (TLR-4) participates in the obesity-related cardiac disease by triggering cytokine production via nuclear factor-ĸB (NF-ĸB). The 'obese' group, which was fed a high sugar-fat diet and water plus 25% of sucrose for 30 weeks, showed: obesity, high levels of glucose, triglycerides and uric acid, insulin resistance, high systolic blood pressure, high levels of tumor necrosis factor alpha (TNF-α) in the adipose tissue, in addition to cardiac remodeling and diastolic dysfunction. ...
Article
1-Octacosanol (Octa) is reported to possess many physiological properties. However, its relative mechanism has not been illustrated yet. Herein, we aimed to investigate the effect of Octa on insulin resistance in mice fed with a high fat diet (HFD) and used an in vitro simulated gastrointestinal tract to analyze its digestive behavior. The effects of Octa on the gut microbiota were verified by in vitro fermentation using the mouse fecal microbiota. As a result, the Octa monomer was digested into shortened saturated and unsaturated fatty acids (C10-C24) in the simulated gastrointestinal tract. Octa improved the fasting blood glucose (FBG), insulin resistance (IR), plasma lipids, and inflammatory response in HFD-fed mice in a dose-dependent manner. This study also suggested that a high-dose of Octa effectively decreased the levels of toll-like receptor 4 (TLR4), nuclear factor kappa-B (NF-κB), tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) in the plasma of HFD-fed mice. Octa improved the oxidative stress induced by a HFD and increased the expression of the Nrf2/ARE signaling pathway. Importantly, Octa reshaped gut microbiota through decreasing Firmicutes content and increasing Bacteroidota and Verrucomicrobiota contents at the phylum level, and the changes of intestinal flora structure caused by Octa were significantly correlated with the changes of inflammatory biomarkers. In conclusion, the effects of Octa on insulin resistance might be attributed to the reconstruction of the gut microbiota structure and inhibition of the TLR4/NF-κB inflammatory pathway in HFD-induced obese individuals.