Figure - available from: Inflammation
This content is subject to copyright. Terms and conditions apply.
Source publication
Obesity, manifested by increased adiposity, represents a main cause of morbidity in the developed countries, causing increased risk of insulin resistance and type 2 diabetes mellitus. Recruitment of macrophages and activation of innate immunity represent the initial insult, which can be further exacerbated through secretion of chemokines and adipoc...
Similar publications
Bone marrow adipocytes may be responsible for cancer progression. Although marrow adipogenesis is suspected to be involved in prostate carcinogenesis, an association between marrow adiposity and prostate cancer risk has not been clearly established in vivo. This work included 115 newly diagnosed cases of histologically confirmed prostate cancer (ra...
Citations
... Numerous studies consistently show that central obesity, characterized by the accumulation of visceral fat, contributes to insulin resistance and the development of IFG [30][31][32][33][34]. This association is mediated through various biomolecular mechanisms, including the release of pro-inflammatory cytokines and adipokines from adipose tissue, which interfere with insulin signalling pathways [35]. Elevated blood pressure is also associated with insulin resistance and impaired glucose metabolism through mechanisms involving endothelial dysfunction and oxidative stress [36]. ...
Introduction
Obesity is associated with concomitant chronic conditions. An early metabolic consequence of obesity is disruption of glucose and insulin homeostasis. One of the consequences is impaired fasting glucose (IFG). Visceral fat is metabolically more harmful than subcutaneous fat, but few information is available regarding the association between the risk of abnormal glucose in increased waist circumference.
Methods
This study is based on a cross sectional of 1,381 population-based from Palembang, Indonesia.
The eligibility requirements subject were to be older than 18 and consent to taking fasting glucose and lipid profile tests as well as physical exams measuring their body weight, height, blood pressure, abdominal circumference, and waist circumference.
Results
The number of subjects consisting of 798 noncentral obesity with normoglycemia, 376 central obesity with normoglycemia, and 207 central obesity with concomitant IFG. The prevalence central obesity with concomitant IFG was 35.51%. In subjects with central obesity, there were significant differences in proportions based on sex, age, marital status, education, and occupation. In multivariate analysis show that the risk factors that contribute to having a significant association with central obesity with concomitant IFG are sex (female), age (>40 years), blood pressure (hypertension), and HDL-C <50 mg/dL (p<0.001). The analysis also founded that there was a significant difference in the dietary pattern of sweet foods (p = 0.018), sweet drinks (p = 0.002), soft drinks (p = 0.001) and smoking habit (p<0.001) between subjects with obesity central and concomitant IFG compared to subjects with noncentral obesity. The majority of subjects with obesity central and concomitant IFG had consuming these risky foods >6 times/week.
Conclusion
The prevalence of central obesity with IFG is quite high. There are significant differences in the characteristics, lipid profile, blood pressure, dietary pattern, and smoking habit of central obesity with concomitant IFG was confirmed in this population-based observational study.
... Nicotine, a major constituent of cigarette smoke, was found to impair insulin sensitivity by activating the sympathetic nervous system and increasing lipolysis, leading to elevated free fatty acids and decreased glucose uptake by skeletal muscles (36). In addition, smoking is associated with increased pro-inflammatory cytokines, such as tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6), which can further contribute to insulin resistance (37). Furthermore, cigarette smoking has been linked to abdominal obesity, another critical component of MetS (35,38). ...
Backgrounds
Habitual substance use, i. e., alcohol, tobacco and betel nut, has been found with an increased risk of metabolic syndrome (MetS) in the general population, whereas the association remains unclear in physically fit military personnel. This study aimed to investigate the combination of these substances use and their associations with new-onset MetS in the military.
Methods
A total of 2,890 military men and women, aged 18–39 years, without MetS were obtained from the cardiorespiratory fitness and health in eastern armed forces study (CHIEF) in Taiwan and followed for incident MetS from baseline (2014) through the end of 2020. Incident MetS event was defined by the International Diabetes Federation guideline and confirmed in the annual health examinations. A self-report was used to assess the alcohol, tobacco and betel nut use status (active vs. former/never). Multivariable Cox regression model was performed to determine the association with adjustments for sex, age, body mass index and physical activity at baseline.
Results
At baseline, there were 279 active betel nut chewers (9.7%), 991 active smokers (34.3%) and 1,159 active alcohol consumers (40.1%). During a mean follow-up of 6.0 years, 673 incident MetS (23.3%) were observed. As compared to no substance users, only one substance, and two and three substances users had a greater risk of incident MetS [hazard ratios (HRs) and 95% confidence intervals: 1.27 (1.06–1.54), 1.38 (1.12–1.69) and 1.78 (1.37–2.32), respectively]. In subgroup analyses, the risk of incident MetS in two and three substances users was significantly greater in those free of baseline low high-density lipoprotein [HRs: 1.54 (1.21–1.95) and 2.57 (1.92–3.46), respectively], as compared to their counterparts (both p for interactions <0.05).
Conclusion
A dose-response association of more substances use for new-onset MetS was noted in military personnel. This finding suggests that the combined alcohol, tobacco and betel nut use may play a role in the development of MetS. Further study is required to establish causation and to investigate the potential benefits of substance use cessation in reducing the risk of MetS.
... Secondly, women are more prone to accumulate fat in the abdomen and hips, leading to increased systemic inflammation [49]. Recent studies suggest that inflammatory markers produced by adipose tissue contribute to T2DM risk factors [50]. ...
Objective
This study aims to assess the relationship between NHHR (non-high-density lipoprotein cholesterol to high-density lipoprotein cholesterol ratio) and Type 2 diabetes mellitus (T2DM) in US adults, using National Health and Nutrition Examination Survey (NHANES) data from 2007 to 2018.
Methods
This study explored the connection between NHHR and T2DM by analyzing a sample reflecting the adult population of the United States (n = 10,420; NHANES 2007–2018). NHHR was characterized as the ratio of non-high-density lipoprotein cholesterol to high-density lipoprotein cholesterol. T2DM was defined based on clinical guidelines. This research used multivariable logistic models to examine the connection between NHHR and T2DM. Additionally, it included subgroup and interaction analyses to assess variations among different groups. Generalized additive models, smooth curve fitting, and threshold effect analysis were also employed to analyze the data further.
Results
The study included 10,420 subjects, with 2160 diagnosed with T2DM and 8260 without. The weighted multivariate logistic regression model indicated an 8% higher probability of T2DM for each unit increase in NHHR (OR: 1.08, 95% CI: 1.01–1.15) after accounting for all covariates. Subgroup analysis outcomes were uniform across various categories, demonstrating a significant positive relationship between NHHR and T2DM. Interaction tests showed that the positive link between NHHR and T2DM remained consistent regardless of age, body mass index, smoking status, moderate recreational activities, hypertension, or stroke history, with all interaction P-values exceeding 0.05. However, participants’ sex appeared to affect the magnitude of the connection between NHHR and T2DM (interaction P-value < 0.05). Also, a nonlinear association between NHHR and T2DM was discovered, featuring an inflection point at 1.50.
Conclusions
Our study suggests that an increase in NHHR may be correlated with a heightened likelihood of developing T2DM. Consequently, NHHR could potentially serve as a marker for estimating the probability of T2DM development.
... There is a physiological interrelationship between insulin sensitivity, muscle mass, and body fat. Adipose tissue affects the resistance to insulin through the activity of many mediators, such as adipokines, pro-and anti-inflammatory cytokines, and chemokines [59,60]. Because skeletal muscle uses glucose as an energy source and as a substrate for glycogen synthesis, it promotes insulin sensitivity [61]. ...
... En el presente estudio los niveles de TNF-α e IL-6 se correlacionaron con mayores perímetros de tríceps y de cintura en adultos mayores. Esta correlación se puede explicar debido a que un aumento de tejido adiposo está asociado a mayores niveles sanguíneos de marcadores inflamatorios 30 . La hipertrofia de adipocitos conduce a una mayor liberación de citoquinas inflamatorias para crear un medio proinflamatorio que promueve la resistencia a la insulina y la disfunción endotelial 30 , precursores importantes en el desarrollo de enfermedades metabólicas, un deterioro de la función física y la fuerza muscular en adultos mayores 31 , debido a la alteración de la diferenciación y la infiltración de macrófagos en el tejido adiposo 32 . ...
... Esta correlación se puede explicar debido a que un aumento de tejido adiposo está asociado a mayores niveles sanguíneos de marcadores inflamatorios 30 . La hipertrofia de adipocitos conduce a una mayor liberación de citoquinas inflamatorias para crear un medio proinflamatorio que promueve la resistencia a la insulina y la disfunción endotelial 30 , precursores importantes en el desarrollo de enfermedades metabólicas, un deterioro de la función física y la fuerza muscular en adultos mayores 31 , debido a la alteración de la diferenciación y la infiltración de macrófagos en el tejido adiposo 32 . La acción de TNF-α sobre el tejido adiposo puede alterar el metabolismo mediante la inhibición de la absorción de ácidos grasos libres, y liberación de los ácidos grasos libres a través de lipogénesis 33 . ...
RESUMEN Introducción: El envejecimiento está relacionado con diversas enfermedades crónicas que causan inflamación sistémica, caracterizada por un aumento en los niveles sanguíneos de interleucina 6 (IL-6) y factor de necrosis tumoral alfa (TNF-α). La función física y la composición corporal podrían estar relaciona-das con estos marcadores inflamatorios en adultos mayores. Objetivo: Analizar la correlación entre marcadores inflamatorios sanguíneos, función física y composición corporal en adultos mayores de la comunidad. Metodología: Estudio transversal con 242 adultos mayo-res (la media de edad fue de 68±6 años para varones y 70±6 años en mujeres; el porcentaje de varones fue de 36,6 % y de 69,4% en mujeres) de la ciudad de Londrina, Brasil. Se analizaron los niveles sanguíneos de IL-6 y TNF-α con citometría de flujo. Para la evaluación física fue considerado el equilibrio estático con la prueba de estación unipodal (PEU), la fuerza de prensión manual (FPM) utilizando un dinamómetro digital y la capacidad aeróbica con la prueba de caminata de seis minutos (PC6M). Para la evaluación de la composición corporal, fueron considerados los siguientes perímetros: cadera, pantorrilla, cuádriceps, bíceps braquial, tríceps braquial y cintura. Se analizó la correlación de las variables inflamatorias con las de función física y composición corporal, utilizando Pearson o Spearman con el software SPSS versión 22. Resultados: Los niveles de IL-6 se correlacionaron con la PEU (r:-0.22; p: 0.002), el perímetro de tríceps (r: 0.16; p: 0.023) y el de cintura (r: 0.34; p: 0.000). Los niveles de TNF-α se correlacionaron con FPM (r:-0.15; p: 0.035), el perímetro de tríceps (r: 1.79; p: 0.012) y el de cintura (r: 0.27; p< 0.001). Conclusión: Los marcadores inflamatorios están relacionados con menor fuerza, equilibrio estático y un aumento en el perímetro de tríceps y cintura en adultos mayores de la comunidad.
... Apelin as a biomarker of AT. apelin is a short peptide hormone, which belongs to adipokines and is produced by adipocytes in proportion to the present amount of fat; it plays an important role in energy metabolism and is considered to be linked with obesity and diabetes (39,101,102). apelin exerts its effects by binding with angiotensin II protein J (APJ) receptor (101,103). apelin promotes brown adipocyte development through the phosphatidylinositol 3-kinase (PI3K)/Akt and AMPK signaling pathways (102). ...
... apelin exerts its effects by binding with angiotensin II protein J (APJ) receptor (101,103). apelin promotes brown adipocyte development through the phosphatidylinositol 3-kinase (PI3K)/Akt and AMPK signaling pathways (102). Also, apelin is able to increase the browning in white adipocytes (102,104). ...
... apelin promotes brown adipocyte development through the phosphatidylinositol 3-kinase (PI3K)/Akt and AMPK signaling pathways (102). Also, apelin is able to increase the browning in white adipocytes (102,104). in addition, it has been found that apelin relieves the TNF-α suppression on brown adipogenesis (102). apelin stimulates glucose uptake, increases insulin sensitivity and regulates lipolysis and fatty acid oxidation (101). ...
Obesity reaches up to epidemic proportions globally and increases the risk for a wide spectrum of co-morbidities, including type-2 diabetes mellitus (T2DM), hypertension, dyslipidemia, cardiovascular diseases, non-alcoholic fatty liver disease, kidney diseases, respiratory disorders, sleep apnea, musculoskeletal disorders and osteoarthritis, subfertility, psychosocial problems and certain types of cancers. The underlying inflammatory mechanisms interconnecting obesity with metabolic dysfunction are not completely understood. Increased adiposity promotes pro-inflammatory polarization of macrophages toward the M1 phenotype, in adipose tissue (AT), with subsequent increased production of pro-inflammatory cytokines and adipokines, inducing therefore an overall, systemic, low-grade inflammation, which contributes to metabolic syndrome (MetS), insulin resistance (IR) and T2DM. Targeting inflammatory mediators could be alternative therapies to treat obesity, but their safety and efficacy remains to be studied further and confirmed in future clinical trials. The present review highlights the molecular and pathophysiological mechanisms by which the chronic low-grade inflammation in AT and the production of reactive oxygen species lead to MetS, IR and T2DM. In addition, focus is given on the role of anti-inflammatory agents, in the resolution of chronic inflammation, through the blockade of chemotactic factors, such as monocytes chemotractant protein-1, and/or the blockade of pro-inflammatory mediators, such as IL-1β, ΤΝF-α, visfatin, and plasminogen activator inhibitor-1, and/or the increased synthesis of adipokines, such as adiponectin and apelin, in obesity-associated metabolic dysfunction.
... The consumption of food marketing or larger food portions causes an inflammatory status and a higher production of oxidant products. The replacing of energy intake from saturated fatty acids with an equivalent energy intake from PUFAs or MUFAs could inhibit adipose inflammasome-mediated IL1-beta secretion [43]. ...
Metabolic dysfunction-associated hepatic steatosis (MAFLD) indicates the metabolic risk associated with hepatic steatosis, overweight and obesity, and clinical evidence of metabolic dysregulation. Since MAFLD is one of the diseases that show a high frequency of alterations in the lipid content of cell membranes, the aim of this study was to evaluate the indices of oxidative damage of erythrocyte membranes in overweight and obese MAFLD subjects. The study was conducted on serum samples and red blood cell membranes of overweight and obese MAFLD subjects. For each patient, biochemical measurements and lipidomic analyses of erythrocytes membranes were performed. Significant differences in fatty acid profiles of RBC membranes were found between overweight and obese patients. In particular, the Peroxidation Index (PI) was higher in the erythrocyte membranes of obese subjects than in overweight subjects. The same behavior was observed for Unsaturation Index (UI) and Free Radical Stress Index (Free RSI), supporting the fact that the systemic increase in oxidative stress was associated with obesity. The study shows that there is a different susceptibility to erythrocyte membrane peroxidation for overweight and obese subjects, and the increased values of oxidative stress indices observed in the erythrocyte membranes of obese patients with MAFLD may be a possible indicator of pro-oxidative events occurring in obesity-related diseases.
... Extracts of functional foods often contain components including polyphenols and flavonoids that have been shown to have the ability to reduce inflammation and cholesterol buildup associated with metabolic disorders including hypertension and obesity [9]. In situations of excessive fat accumulation, dysfunctional expanded adipocytes release different pro-inflammatory adipokines, including interleukin (IL) 6 and IL-1β and tumor necrosis factor (TNF) α [10]. The expansion of adipocytes also increases adipocyte death and recruitment of macrophages to adipose tissue [11]. ...
... Similar results were shown in this trial with PGA-K therapy. Additionally, the process of adipocyte differentiation is paralleled by an upregulation in the expression of inflammatory cytokines [10]. Thus, we tested the inflammatory cytokine expression in WATs, and the results showed that PGA-K treatment decreased the expression of TNF-α and IL-6 in serum. ...
The purpose of this work was to examine the effects of potassium poly-γ-glutamate (PGA-K) on mice fed a high-fat diet consisting of 60% of total calories for 12 weeks. PGA-K administration reduced the increase in body weight, epididymal fat, and liver weight caused by a high-fat diet compared to the obese group. The triglyceride, low-density lipoprotein cholesterol and high-density lipoprotein cholesterol levels, which are blood lipid indicators, were significantly increased in the obese group but were significantly decreased in the PGA-K-treated group. The administration of PGA-K resulted in a significant inhibition of pro-inflammatory cytokines, including tumor necrosis factor α and interleukin 6. Moreover, the levels of leptin and insulin, which are insulin resistance indicators, significantly increased in the obese group but were significantly decreased in the PGA-K-treated group. These results suggest that PGA-K exhibits a protective effect against obesity induced by a high-fat diet, underscoring its potential as a candidate for obesity treatment.
... Tis infammatory state is primarily attributed to chronic infammation within adipose tissue, which involves the infltration of macrophages and other infammatory cells, accompanied by the release of proinfammatory cytokines, all of which are closely associated with obesity [2]. Te presence of macrophages in adipose tissue promotes the secretion of proinfammatory cytokines such as tumor necrosis factor alpha (TNF-α), monocyte chemotactic protein-1 (MCP-1), and interleukin 6 (IL-6), leading to the initiation of an infammatory response and the development of insulin resistance within adipose tissue [3]. Consequently, reducing macrophage-induced infammation in adipose tissue could potentially mitigate the progression of obesity-related diseases. ...
Obesity, which is characterized by chronic low-grade inflammation, involves the infiltration of immune cells into adipose tissue, leading to the secretion of inflammatory cytokines and subsequent inflammation. Therefore, the aim of this study was to examine the potential of passion fruit seed extract (PSEE) in mitigating lipopolysaccharide (LPS)-induced inflammation in a coculture system comprising macrophages and adipocytes. PSEE demonstrated significant reductions in reactive oxygen species (ROS) and nitric oxide (NO) levels, primarily achieved through the downregulation of inducible nitric oxide synthase (iNOS) protein expression in LPS-induced adipocyte-macrophage cocultures. Furthermore, PSEE effectively suppressed the secretion of TNF-α and IL-1β by attenuating the gene expression of these cytokines, as well as other inflammation-related genes such as MMP-2, IL-6, and MCP-1. Notably, PSEE exhibited potent inhibitory effects on the p38 and NF-κB signaling pathways, thus alleviating inflammation in the LPS-induced adipocyte-macrophage cocultures. Additionally, PSEE led to a decrease in the expression of ACC, HSL, and FaSN, while aP2 and ATGL showed increased expression in LPS-induced cocultured macrophages and adipocytes. These findings suggest that passion fruit seed extract effectively combats inflammation by suppressing the p38 and NF-κB signaling pathways, resulting in reduced levels of proinflammatory cytokines, NO, and ROS production.
... Male infertility associated with obesity has dramatically risen worldwide [46] and has also received much significant attention from the medical community [47,48].The mechanisms through which obesity affects male reproductive function are complex. Research by Hotamisligil and colleagues suggests that obesity is a systemic state of chronic low-grade inflammation, with the resulting inflammatory response believed to be a key risk factor for obesity-related complications [9].This chronic low-grade inflammatory state associated with obesity is closely linked to the release and induction of numerous related inflammatory factors [4].TNF-α and IL-6 are inflammatory cytokines associated with obesity, particularly abdominal obesity [49]. For instance, elevated levels of IL-6 have been positively correlated with the expansion of adipose tissue [50].TNF-α, IL-6, and IL-1β can enhance the inflammatory cascade reaction and promote inflammatory responses [49], which are considered key triggering factors for obesity-related complications. ...
... Research by Hotamisligil and colleagues suggests that obesity is a systemic state of chronic low-grade inflammation, with the resulting inflammatory response believed to be a key risk factor for obesity-related complications [9].This chronic low-grade inflammatory state associated with obesity is closely linked to the release and induction of numerous related inflammatory factors [4].TNF-α and IL-6 are inflammatory cytokines associated with obesity, particularly abdominal obesity [49]. For instance, elevated levels of IL-6 have been positively correlated with the expansion of adipose tissue [50].TNF-α, IL-6, and IL-1β can enhance the inflammatory cascade reaction and promote inflammatory responses [49], which are considered key triggering factors for obesity-related complications. Reports have indicated the detection of high levels of IL-6, TNF-α, and NF-κB in the reproductive tissue of SD obese rats and C57BL/6 obese mice fed a high-fat diet, along with reduced testosterone levels, thereby affecting spermatogenesis [31,32].Therefore, we hypothesize that obesityinduced chronic inflammation is indeed related to damage in the male reproductive system. ...
Obesity is associated with chronic inflammation that affects various organs in the body, including the reproductive system, which is a key factor in male infertility. 1-Deoxynojirimycin (1-DNJ) is a natural alkaloid in mulberry leaves, which has anti-inflammatory capabilities, yet, it’s effects on obesity-induced inflammation-related male infertility remain unclear. Therefore, this research investigates the underlying mechanism by which 1-DNJ may mitigate fertility impairment in male mice caused by obesity-related inflammation. Male mice with high-fat diet (HFD)-induced obesity were treated with 1-DNJ or metformin for 8 weeks. Metabolic profiles were evaluated by enzyme method. Reproductive capacity was assessed by sperm viability, motility and counts, immunohistochemistry was performed to evaluate the testicular damage caused by obesity and inflammation. The inflammation was assessed by measuring the levels of tumor necrosis factor α (TNFα), interleukin 1β (IL-1β), and interleukin 6 (IL-6). The activation of IκB kinase β (IKKβ) and nuclear factor κB (NF-κB) was examined using western blot and immunohistochemistry. HFD induced obesity in mice with obvious lipid metabolism disorder. The obese male mice had a decreased testosterone level, impaired sperm motility, and increased inflammatory factors. 1-DNJ treatment improved the testosterone level in the obese mice, ameliorated the testicular structure damage and improve sperm viability. In addition, 1-DNJ treatment inhibited IKKβ/NF-kB signaling pathway and reduced inflammation in obese mice. 1-DNJ can improve the fertility of obese men by reducing obesity as well as obesity-induced inflammation. These findings provide new insights for 1-DNJ to alleviate inflammation caused by obesity and provide future possibilities for treating male infertility.
