Inflammatory Markers in Pediatric Obesity

2012 ◽  
Vol 4 (5) ◽  
pp. 297-302 ◽  
Author(s):  
Stacy Stolzman ◽  
Marie Hoeger Bement

The prevalence of childhood obesity has recently peaked in the USA with ~17% of children considered obese. With the increase in adiposity that occurs with weight gain, a persistent low-grade inflammatory state is created. The most commonly studied inflammatory markers associated with obesity are the cytokines, tumor necrosis factor α and interleukin-6, and the acute-phase reactant, C-reactive protein. Understanding the relation between adiposity and inflammation is an important concept because these inflammatory markers influence insulin sensitivity, glucose metabolism, and atherosclerosis, ultimately leading to impaired health. In addition to obesity, physical inactivity is associated with elevated inflammatory markers. The literature, however, is inconsistent as to whether the association between physical activity and inflammation is independent of adiposity. In some obese children, physical fitness appears to circumvent the increase in inflammatory markers that are associated with obesity. The purpose of this review is to examine the relation between adiposity and inflammatory markers, including potential health implications and the impact of physical activity. We exposed a dearth of literature in understanding the interaction between obesity and physical activity on inflammatory markers, especially in children because their anthropometrics change. This review highlights the necessity for further research to better understand the complexity of the chronic inflammatory state associated with obesity.

2018 ◽  
Vol 30 (2) ◽  
pp. 198-207
Author(s):  
Liina Remmel ◽  
Vallo Tillmann ◽  
Eva Mengel ◽  
Pille Kool ◽  
Priit Purge ◽  
...  

Purpose: To investigate the differences in the pattern of changes in serum inflammatory cytokines measured annually over a 24-month period, between less active and more active overweight boys. Participants/Methods: In total, 25 pubertal overweight boys were divided by their moderate to vigorous physical activity (MVPA) levels into 2 groups: less active group (LAG; n = 10; MVPA < 60 min/d) and more active group (MAG; n = 15; MVPA > 60 min/d). Physical activity was measured by 7-day accelerometry. Serum concentration of 13 inflammatory cytokines [interleukin (IL)-2, IL-4, IL-6, IL-8, IL-10, IL-1α, IL-1β, vascular endothelial growth factor, interferon-γ, tumor necrosis factor-α, monocyte chemotactic protein-1, epidermal growth factor, and C-reactive protein] was measured at baseline (T0), after 12 months (T1), and after 24 months (T2) from fasting blood samples. Results: Serum IL-6 level was significantly higher [LAG: 1.27 (0.86, 1.98) pg/mL; MAG: 0.80 (0.52, 0.84) pg/mL] at T0 and IL-8 level [LAG: 10.26 (8.80, 11.64) pg/mL; MAG: 7.42 (6.10, 9.54) pg/mL] at T2 in LAG compared with MAG. The changes over the study period varied between different inflammatory markers. None of the slopes of any measured markers were statistically different between the LAG and MAG, although the slopes of interferon-γ and IL-10 tended to be different between the groups. Conclusions: The pattern of changes over the study period varied between different inflammatory markers, but these changes were not different between the MVPA groups. More longitudinal studies are needed to investigate whether IL-6, IL-8, IL-10, and interferon-γ would be the choice of inflammatory markers to study the associations between obesity and physical activity in future.


Author(s):  
Kiran S. Panickar ◽  
Dennis E. Jewell

AbstractAging in humans is associated with chronic low-grade inflammation (systemic), and this condition is sometimes referred to as “inflammaging”. In general, canines also age similarly to humans, and such aging is associated with a decline in mobility, joint problems, weakened muscles and bones, reduced lean body mass, cancer, increased dermatological problems, decline in cognitive ability, reduced energy, decreased immune function, decreased renal function, and urinary incontinence. Each of these conditions is also associated with an increase in pro-inflammatory cytokines. An inflammatory state characterized by an increase in pro-inflammatory markers including but not restricted to tumor necrosis factor-α, interleukin-6, IL-1β, and C-reactive protein (CRP) is believed to contribute to or worsen a general decline in biological mechanisms responsible for physical function with aging. Nutritional management of inflammation in aging dogs is important in maintaining health. In particular, natural botanicals have bioactive components that appear to have robust anti-inflammatory effects and, when included in the diet, may contribute to a reduction in inflammation. While there are scientific data to support the anti-inflammatory effects and the efficacy of such bioactive molecules from botanicals, the clinical data are limited and more studies are needed to validate the efficacy of these ingredients. This review will summarize the role of dietary ingredients in reducing inflammatory molecules as well as review the evidence available to support the role of diet and nutrition in reducing chronic low-grade systemic inflammation in animal and human studies with a special reference to canines, where possible.


Author(s):  
Sisi Yan ◽  
Jinli Ding ◽  
Yi Zhang ◽  
Jiayu Wang ◽  
Sainan Zhang ◽  
...  

Abstract Polycystic ovary syndrome (PCOS) is a common reproductive endocrine disease. It has been reported that chronic low-grade inflammation might participate in its pathogenesis. C1q and TNF related 6 (C1QTNF6) is a newly identified adiponectin paralog associated with inflammation. The aim of the present study was to investigate the role of C1QTNF6 in the development of chronic inflammation in PCOS and the underlying molecular mechanism. After analyzing the expression of C1QTNF6 in the serum and granulosa cells (GCs) of PCOS patients and healthy controls, we verified the roles of C1QTNF6 in inflammation through dehydroepiandrosterone-induced PCOS mouse models and cell models of lipopolysaccharide (LPS)-induced inflammation. The results demonstrated that C1QTNF6 expression in the serum and GCs of patients with PCOS was significantly elevated compared with those of the controls, and similar results were observed in the serum and ovary of PCOS mouse models. In PCOS mice and C1QTNF6-overexpressing PCOS mice, serum levels of pro-inflammatory factors including C-reactive protein (CRP), interleukin 6 (IL6) and tumor necrosis factor-α (TNFα) were increased, while the opposite effects were observed when C1QTNF6 was downregulated in PCOS mice. Furthermore, C1QTNF6 overexpression upregulated the levels of TNFα, IL6, and CRP and activated the AKT/NF-κB pathway in LPS-treated KGN cells, whereas C1QTNF6 knockdown and BAY-117082 (an NF-κB inhibitor) treatment resulted in the opposite effects. Taken together, our results indicate that C1QTNF6 is involved in the pathogenesis of PCOS by affecting the inflammatory response via the AKT/NF-κB signaling pathway.


2016 ◽  
Vol 13 (7) ◽  
pp. 733-739 ◽  
Author(s):  
Mette S. Nielsen ◽  
Jonas S. Quist ◽  
Jean-Philippe Chaput ◽  
Stine-Mathilde Dalskov ◽  
Camilla T. Damsgaard ◽  
...  

Background:Inflammatory markers, adiponectin, and movement/nonmovement behaviors have all been linked to risk factors for cardiovascular disease; however, the association between childhood movement/nonmovement behaviors and inflammatory markers and adiponectin is unknown.Methods:We explored the association between accelerometer determined moderate-to-vigorous physical activity (MVPA), sedentary time, and sleep (7 days/8 nights) and fasting C-reactive protein (CRP), interleukin-6 (IL-6), and adiponectin in 806 school children. A sleep variability score was calculated.Results:MVPA was negatively associated with adiponectin in boys and girls (P < .001) and with CRP and IL-6 in girls (P < .05) independent of sleep duration, sedentary time, age, fat mass index (FMI), and pubertal status. Sedentary time was positively associated with adiponectin in boys and girls (both P < .001), and sleep duration with adiponectin in boys independent of age, FMI, and pubertal status (P < .001); however, these associations disappeared after mutual adjustments for movement behavior. Sleep duration variability was positively associated with CRP in girls independent of all covariates (P < .01).Conclusion:MVPA remained negatively associated with inflammatory markers and adiponectin, and sleep duration variability positively associated with CRP after adjustment for FMI, pubertal status, and other movement behavior. The inverse association between MVPA and adiponectin conflicts with the anti-inflammatory properties of adiponectin.


2009 ◽  
Vol 107 (1) ◽  
pp. 63-68 ◽  
Author(s):  
Natalie C. Dixon ◽  
Tina L. Hurst ◽  
Duncan C. S. Talbot ◽  
Rex M. Tyrrell ◽  
Dylan Thompson

Physical activity modifies some postprandial responses such as glycemic control, although it is unclear whether this translates into lower postprandial inflammation. Our objective in this study was to determine whether postprandial inflammatory markers are lower in active compared with sedentary middle-aged men. Thirteen active and twelve sedentary middle-aged men consumed a mixed meal on one occasion. Blood was taken via a cannula before and up to 8 h after the meal and with a single-use needle before and 8 h after the meal. Active men had lower fasted IL-6 (0.6 ± 0.2 vs. 1.2 ± 0.3 pg/ml; P = 0.004) and C-reactive protein (1.3 ± 0.3 vs. 2.9 ± 0.6 mg/l; P = 0.04) concentrations than sedentary men. Cannula blood IL-6 concentrations increased by 3.49 pg/ml in the 8 h following the meal ( P < 0.001); however, this increase was minimal (0.36 pg/ml) in blood taken via a single-use needle from the contralateral arm ( P = 0.013). The sedentary group had larger glucose ( P = 0.034), insulin ( P = 0.013), and triacylglycerol ( P = 0.057) responses to the meal. These results provide further evidence that physical activity is associated with lower inflammatory marker concentrations in a fasted state and a lower postprandial metabolic response to a meal. However, this does not translate into lower postprandial inflammatory markers since the only evidence of postprandial inflammation (a large increase in serum IL-6) was actually due to the cannula used for blood sampling.


PLoS ONE ◽  
2021 ◽  
Vol 16 (6) ◽  
pp. e0253793
Author(s):  
Thao H. P. Nguyen ◽  
Morten Wang Fagerland ◽  
Gia Deyab ◽  
Gunnbjørg Hjeltnes ◽  
Ivana Hollan ◽  
...  

Background Patients with autoimmune arthritis (AA) are at increased risk for impaired cardiac function and heart failure. This may be partly due to the effect of inflammation in heart function. The impact of antirheumatic drugs on cardiac dysfunction in AA remains controversial. Therefore, we aimed to examine effects of antirheumatic treatment on serum N-terminal pro-brain natriuretic peptide (NT-proBNP) in AA patients and its relationship to inflammatory markers. Methods We examined 115 patients with AA (64 rheumatoid arthritis (RA), 31 psoriatic arthritis and 20 ankylosis spondylitis) starting with methotrexate (MTX) monotherapy or tumor necrosis factor inhibitors (TNFi) with or without MTX co-medication. NT-proBNP (measured in serum by ECLIA from Roche Diagnostics), and other clinical and laboratory parameters were evaluated at baseline, after 6 weeks and 6 months of treatment. Results NT-proBNP levels did not change significantly after 6 weeks and 6 months of antirheumatic therapy (pbaseline-6weeks = 0.939; pbaseline-6months = 0.485), although there was a modest improvement from 6 weeks to 6 months in the MTX only treatment group (median difference = -18.2 [95% CI = -32.3 to -4.06], p = 0.013). There was no difference in the effects of MTX monotherapy and TNFi regimen on NT-proBNP levels. The changes in NT-proBNP after antirheumatic treatment positively correlated with changes in C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR). Baseline NT-proBNP levels were related to baseline CRP and ESR levels, and some other established markers of disease activities in crude analyses. Conclusion Circulating levels of NT-proBNP were related to established inflammatory markers at baseline, and the changes in NT-proBNP after antirheumatic treatment were positively related to these markers. Nevertheless, antirheumatic therapy did not seem to affect NT-proBNP levels compared to baseline, even though inflammatory markers significantly improved.


2011 ◽  
Vol 51 (1) ◽  
pp. 7
Author(s):  
Frecilia Regina ◽  
Kristellina Tirtamulia ◽  
Sarah Maria Warouw

Background Childhood obesity is a widespread and growing problem associated with health problems such as metabolic syndrome, diabetes mellitus and cardiovascular disease. A low􀁗grade chronic inflammatory state, reflected by decreased adiponectin and increased highly sensitive C􀁗reactive  protein (hsCRP) levels, may play a role in metabolic syndrome associated with obesity.Objective To assess and compare adiponectin and hsCRP levels in obese and nonnal weight children.Methods We conducted a cross-sectional, case􀁗controlled study in Manado from May to July 2010. Subjects were selected from obese, but otherwise healthy children aged 9-15 years. Control subjects were schoolmates 'With normal body mass index (BMI). We perfonned physical examinations, measured blood pressure, weight and height, and calculated BMI for all subjects. After an overnight fast, all subjects were tested for fasting blood glucose, adiponectin and hsCRP levels.Results The mean adiponectin level in the obese group was 3.6 μg/mL (SD 1.43), lower than that of the normoweight group, 4.8 μg/mL (SD 1.67) (P<0.0001). The mean hsCRP level in the obese group was 3.3 mg/L (SD 3.62) while that of the normoweight group was 0.8 mg/L (SD 1.39) (P<0.0001). There was no inverse correlation between adiponectin and hsCRP levels in obese group (r= 0.048; P= 0.362).Conclusions Lower adiponectin and higher hsCRP levels in the obese group is consistent 'With a low-grade chronic inflammatory state. Other factors that influence adiponecrin and hsCRP production or inflammatory pathways of other adipokines need further evaluation. Early intervention is needed to reduce body weight in obese children.


2008 ◽  
Vol 93 (8) ◽  
pp. 3226-3229 ◽  
Author(s):  
Alessandra Bosutti ◽  
Grazia Malaponte ◽  
Michela Zanetti ◽  
Pietro Castellino ◽  
Martina Heer ◽  
...  

Abstract Context: Energy balance and physical activity potentially influence systemic inflammation. Objective: Our objective was to test the hypothesis that moderate energy restriction may prevent activation of inactivity-induced inflammatory response. Design: Participants were studied four times at the end of 14-d periods of experimental bed rest or controlled ambulation, after receiving eucaloric or hypocaloric diets. Setting: The study was conducted at the clinical research center of the German Space Agency. Subjects: Nine healthy young volunteers participated. Interventions: Energy intake was calibrated to physical activity and decreased by about 20% in hypocaloric conditions. Main Outcome Measures: Changes in body fat by dual-energy x-ray absorptiometry as well as plasma inflammatory markers and cytokine mRNA levels in blood cells were measured. Results: Fat mass did not change significantly in eucaloric conditions and decreased in hypocaloric periods (−1.0 ± 0.3 and −1.0 ± 0.3 kg in ambulatory and bed rest, respectively). Bed rest in eucaloric conditions increased plasma C-reactive protein (CRP) (+143 ± 53%) and both the ratios between plasma IL-6 and IL-10 (4±1 times) and white blood cell IL-6 and IL-10 mRNAs (5 ± 1 times). Energy restriction prevented bed-rest-mediated increases in CRP and the IL-6 to IL-10 ratio. Bed rest increased (P = 0.03) long pentraxin-3 (PTX3) plasma concentration, without significant activity-by-diet interaction. In all conditions (n = 36), CRP and PTX3 were inversely correlated (r = −0.61; P &lt; 0.001). Changes in fat mass, leptin, and IL-6 directly correlated with CRP and inversely correlated with PTX3. IL-10 inversely correlated with CRP and directly correlated with PTX3 (r = 0.52; P &lt; 0.01). Conclusions: Calorie restriction prevents the inflammatory response induced by 14 d of bed rest. We suggest an inverse regulation of CRP and PTX3 in response to changes in energy balance.


2012 ◽  
Vol 46 (3) ◽  
pp. 223-228 ◽  
Author(s):  
Athanasios Saratzis ◽  
Nikolaos Melas ◽  
James P. Hunter ◽  
Hannah Dixon ◽  
Peter Nightingale ◽  
...  

Aim: The aim of this study was to compare midterm mortality between anemic and nonanemic patients undergoing endovascular repair of abdominal aortic aneurysm and to assess a correlation with markers of inflammation. Methods: Anemia was defined as hemoglobin <13 (men) and <12 g/dL (women). The impact of anemia and inflammatory markers on mortality was assessed using Kaplan-Meier curves and Cox regression. Results: A total of 224 patients (12 females [5.36%]; age: 69.73 ± 8.72 years) were included; 102 (45.53%) were anemic. Median follow-up was 17 months (interquartile range: 7-25 months). Nine patients died (1.79%; 8 anemic vs 1 nonanemic). Survival was lower for patients with anemia (log-rank, P = .01). White blood cell count and C-reactive protein (CRP) differed significantly ( P < .001 and P = .01). Anemia and CRP were associated with decreased survival (Cox regression, P = .01, hazard ratio [HR]: 0.35, 95% confidence interval: 0.14-0.84 and P = .002, HR: 1.18, 95% CI: 1.06-1.31). Conclusion: Patients with anemia had decreased survival over the midterm; inflammatory markers were higher among this group.


2007 ◽  
Vol 98 (S1) ◽  
pp. S116-S120 ◽  
Author(s):  
Julia Wärnberg ◽  
Esther Nova ◽  
Javier Romeo ◽  
Luís A. Moreno ◽  
Michael Sjöström ◽  
...  

Inflammatory processes are involved in the pathogenesis of the most common chronic non-communicable diseases and may also play an important initiating role in their development. Only recently have inflammatory markers been included in epidemiological studies focusing on nutritional status, body composition and physical activity. We are just starting to understand how different lifestyles can determine basal levels of inflammatory biomarkers in early ages. This review aims to summarise what is known about the relationships between lifestyle-related determinants (focusing on overweight, physical activity and dietary habits) and inflammatory markers in apparently healthy young populations. Obesity is the most widely studied determinant. Several large-scale studies have now demonstrated that healthy young subjects with more body fat or higher BMI have moderately higher concentrations of inflammatory markers than their leaner peers, supporting the idea that obesity should be considered as a state of chronic low-grade inflammation. Less data is available to allow us to elucidate how physical activity/fitness or dietary patterns may have a direct effect on inflammation in apparently healthy, disease-free young populations.


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