Inflammation In Obese Individuals Research Articles

AMPK Regulates M1 Macrophage Polarization through the JAK2/STAT3 Signaling Pathway to Attenuate Airway Inflammation in Obesity-Related Asthma.

Abstract-Obesity-related asthma is primarily characterized by nonallergic inflammation, with pathogenesis involving oxidative stress, metabolic imbalance, and immunoinflammatory mechanisms. M1 macrophages, which predominantly secrete pro-inflammatory factors, mediate insulin resistance and systemic metabolic inflammation in obese individuals. Concurrently, adenosine monophosphate-activated protein kinase (AMPK) serves as a critical regulator of intracellular energy metabolism and is closely associated with macrophage activation. However, their specific roles and associated mechanisms in obesity-related asthma remain to be explored. In this study, we investigated the macrophage polarization status and potential interventional mechanisms through obesity-related asthmatic models and lipopolysaccharide (LPS) -treated RAW264.7 cell with a comprehensive series of evaluations, including HE, PAS and Masson staining of lung histopathology, immunohistochemical staining, immunofluorescence technology, qRT-PCR, Western Blot, and ELISA inflammatory factor analysis. The results revealed M1 macrophage polarization in obesity-related asthmatic lung tissue alongside downregulation of AMPK expression. Under LPS stimulation, exogenous AMPK activation attenuated M1 macrophage polarization via the Janus kinase 2/ signal transducer and activator of transcription 3 (JAK2/STAT3) signaling pathway. Additionally, in obesity-related asthmatic mice, AMPK activation was found to alleviate airway inflammation by regulating M1 macrophage polarization, the mechanism closely associated with the JAK2/STAT3 pathway. These findings not only advance our understanding of macrophage polarization in obesity-related asthma, but also provide new therapeutic targets for its treatment.

The obesity-induced expression of T-bet in B cells promotes metabolic dysfunction and alters antibody responses

Abstract Obesity is a leading risk factor for premature mortality and poor medical outcomes due to its increasing global prevalence and its profound impact on the human body. Obesity also has a significant immune component as the establishment of a chronic inflammation in obese individuals is a significant driver of metabolic dysfunction. Additionally, obesity alters anti-tumor immunity, and it impairs protective antibody responses during infection or vaccination. The outcome can be extremely catastrophic, as highlighted in the COVID-19 pandemic with obese patients being particular susceptible to the disease. This relationship warrants more investigation into the obesity-associated changes occurring in B cells, central players in both the obesity-associated chronic inflammation and in the production of antibodies. Our lab has identified a subset of B cells which is expanded in both humans and mice during obesity and is characterized by the expression of the transcription factor T-bet. In vivostudies using obese mice fed a high fat diet revealed that these Tbet+ B cells promote inflammation and metabolic dysfunction through the production of proinflammatory antibodies. Additionally, blocking the expression of T-bet in the B cells of obese mice resulted in significant changes in antibody responses, with a greater expansion of germinal center B cells and an increased ability to generate antigen-specific B cells following immunization. Based on our findings, T-bet+ B cells represent an interesting link between obesity, inflammation, and antibody responses. Identifying the mechanisms regulating their function will provide new potential ways to reduce inflammation and enhance protection against infectious diseases in obese patients.

Obstructive Sleep Apnea Disrupts Glycemic Control in Obese Individuals

The link between obstructive sleep apnea (OSA) and obesity, and their common comorbidities such as diabetes mellitus (DM) or cardiovascular diseases, is not fully understood. The aim of this study was to investigate the possible association of OSA severity in obese individuals with polysomnography-based sleep parameters, as well as C-reactive protein (CRP) and glycated hemoglobin (HbA1c) serum levels. Polysomnographic recordings and blood samples were retrospectively compared between a group of 23 adult obese individuals with mild OSA (apnea-hypopnea index (AHI) = 7.5 (5.5-12.5)/h, age = 42.57 ± 11.44 years, 16 male, 7 female, body mass index (BMI) = 37.35 ± 3.88 kg/m²) and an age-, sex-, and BMI-matched group of individuals with moderate or severe OSA (AHI 41.5 (25.7-71.8)/h, age = 43.43 ± 11.96 years, 16 male, 7 female, BMI = 37.87 ± 4.74 kg/m²). All respiratory sleep-associated parameters were significantly higher in individuals with moderate and severe OSA compared to those with mild OSA. CRP levels did not differ between the two OSA severity groups. However, serum levels of HbA1c were significantly higher in the moderate/severe OSA group. Therefore, OSA severity may have a significant impact on glycemic control in obese individuals. Additionally, OSA severity did not appear to be further associated with systemic inflammation in obese individuals. Obese individuals may benefit not only from lifestyle modification, but also from OSA screening and treatment, particularly to prevent DM-associated disorders and conditions.

The soluble epoxide hydrolase inhibitor GSK2256294 decreases the proportion of adipose pro-inflammatory T cells

Adipose tissue contains a complex immune environment and is a central contributor to heightened systemic inflammation in obese persons. Epoxyeicosatrienoic acids (EETs) are lipid signaling molecules that decrease inflammation in obese animals, but their effect on inflammation in humans is unknown. The enzyme soluble epoxide hydrolase (sEH) hydrolyzes EETs to less active diols, and we hypothesized that pharmacologic sEH inhibition would decrease adipose inflammation in obese individuals. We treated obese prediabetic adults with the sEH inhibitor GSK2256294 versus placebo in a crossover design, collected subcutaneous abdominal adipose tissue via lipoaspiration and characterized the tissue T cell profile. Treatment with GSK2256294 decreased the percentage of pro-inflammatory T cells producing interferon-gamma (IFNγ), but not interleukin (IL)-17A, and decreased the amount of secreted tumor necrosis factor-alpha (TNFα). Understanding the contribution of the EET/sEH pathway to inflammation in obesity could lead to new strategies to modulate adipose and systemic inflammation.

Single-Cell Proteomics Reveals the Defined Heterogeneity of Resident Macrophages in White Adipose Tissue.

Adipose tissue macrophages (ATMs) regulate homeostasis and contribute to the metabolically harmful chronic inflammation in obese individuals. While evident heterogeneity of resident ATMs has been described previously, their phenotype, developmental origin, and functionality remain inconsistent. We analyzed white adipose tissue (WAT) during homeostasis and diet interventions using comprehensive and unbiased single-cell mass cytometry and genetic lineage tracking models. We now provide a uniform definition of individual subsets of resident ATMs. We show that in lean mice, WAT co-harbors eight kinetically evolving CD206+ macrophage subpopulations (defined by TIM4, CD163, and MHC II) and two CD206– macrophage subpopulations. TIM4–CD163+, TIM4–CD163– and CD206– macrophage populations are largely bone marrow-derived, while the proliferating TIM4+CD163+ subpopulation is of embryonic origin. All macrophage subtypes are active in phagocytosis, endocytosis, and antigen processing in vitro, whereas TIM4+CD163+ cells are superior in scavenging in vivo. A high-fat diet induces massive infiltration of CD206– macrophages and selective down-regulation of MHC II on TIM4+ macrophages. These changes are reversed by dietary intervention. Thus, the developmental origin and environment jointly regulate the functional malleability of resident ATMs.

Circulating inflammatory markers may mediate the relationship between low carbohydrate diet and circadian rhythm in overweight and obese women

BackgroundLow carbohydrate diet (LCD) can improve inflammation and obesity and also circadian rhythm disorders can lead to increased inflammation in obese individuals. The purpose of this study is to evaluate the association between adherence of LCD and circadian rhythm mediated by inflammatory markers including transforming growth factor-β (TGF-β), interleukin-1β (IL-1β) and Galectin-3 in overweight and obese women.Methods304 women affected by overweight and obesity were enrolled. We evaluated LCD scores by Semi-quantitative food frequency questionnaire (FFQ) of 147 items. The morning-evening questionnaire (MEQ) was applied to evaluate the circadian rhythm. Biochemical parameters such as inflammatory markers and anthropometric components were assessed.ResultsThere was a negative significant correlation between adherence of LCD and circadian rhythm status. In other words, as the LCD scores increased, the odds of circadian rhythm disturbance in intermediate group and morning type persons decreased compared to evening type. It was showed that, IL-1β and Galectin-3 in intermediate and morning type groups, destroyed the significance of this relationship and may be considered as mediating markers.ConclusionAdherence of LCD can improve the circadian rhythm by reducing levels of inflammatory markers and may be considered as a treatment for obesity.

Elevated adipose tissue associated IL-2 expression in obesity correlates with metabolic inflammation and insulin resistance

Adipose tissue (AT) associated cytokines are involved in the development of chronic low-grade inflammation in obese individuals. IL-2, a pleiotropic cytokine, contributes to immune alterations during inflammation. However, the interaction between AT-IL-2 and other inflammatory biomolecules in obesity remains elusive. We investigated whether AT-IL-2 expression was associated with markers of inflammation and insulin resistance in overweight/obese individuals. Subcutaneous fat tissues were collected from 56 individuals (lean/overweight/obese) for RNA extraction. IL-2 and inflammatory mediators were quantified by qRT-PCR and immunohistochemistry. CRP was measured by ELISA. AT-IL-2 expression was higher in obese compared with lean individuals (P < 0.021) and correlated with BMI. IL-2 correlated with interleukins IL-8 and IL-12A (r = 0.333–0.481; p = 0.0001–0.029); as well as with chemokines and their receptors including CCL5, CCL19, CCR2 and CCR5 (r = 0.538–0.677; p < 0.0001). Moreover, IL-2 correlated with toll-like receptors (TLR2, TLR8, TLR10), interferon regulatory factor 5 (IRF5) and cluster of differentiation CD11c (r = 0.282–0.357; p < 0.039). Notably, IL-2 was associated positively with fasting blood glucose (FBG), HbA1c, TGL and CRP (r ≥ 0.423;P ≤ 0.007). In multiple regression analysis, IL-2 is an independent predictor of IL-8, IL-12A, TLR10, TGL and HbA1c. Overall, our data demonstrate that increased expression of the AT-IL-2, in obesity, may represent a novel biomarker for progression of metabolic inflammation and insulin-resistance.

Effect Of Exercise Training On Calprotectin Levels In Adults With And Without Obstructive Sleep Apnea

Obstructive sleep apnea (OSA) causes systemic inflammation which may contribute to the progression of cardiovascular pathology. Exercise training reduces chronic inflammation in obese individuals and is recommended as a behavioral treatment of OSA. Calprotectin is a useful marker of inflammation that has been associated with OSA severity. Yet, the extent to which OSA predicts a change in systemic inflammation with exercise training is not clear. PURPOSE: Examine the effect of 6 weeks of exercise training on plasma calprotectin in obese adults with and without OSA. METHODS: At baseline, participants underwent overnight polysomnography to determine the presence and severity of OSA, as defined by apnea hypopnea index (AHI). Body fat was analyzed using dual energy X-ray absorptiometry. Blood specimens were collected and plasma calprotectin levels were determined using a commercial enzyme-linked immunosorbent assay (ELISA) kit. Body fat and blood collections were repeated upon completion of a 6 week (3 sessions/wk; 1 hr/session) moderate intensity aerobic exercise training program. RESULTS: Seventeen (age: 52+7years; BMI: 34.0+4.1 kg/m2; 9 men: 8 women) adults completed the study. By design, the AHI of adults with moderate to severe OSA (n=7) was higher compared to those without or with mild OSA (n=10) (37+13 events/hour vs. 8+4 events/hour; p<0.001), yet no differences in BMI, total body fat percentage or calprotectin levels were observed between the groups at baseline. While no significant change in calprotectin levels (Baseline: 74+16 ng/ml vs. 6 weeks: 76+19 ng/ml; p=0.540) were observed following the exercise intervention, total body fat percentage was significantly reduced (Baseline: 44+7%, vs. 6 weeks: 43+7%; p=0.003). Baseline AHI was not associated with the change in plasma calprotectin [beta coefficient = -0.11, (95% CI -0.61 - 0.39), p=0.646)] or total body fat percentage [beta coefficient = 0.00017, (95% CI -0.00005 - 0.00038), p=0.120)]. CONCLUSIONS: Contrary to previous findings, we found no association between OSA severity and levels of plasma calprotectin at baseline. Furthermore, a six week moderate intensity aerobic exercise intervention failed to alter calprotectin levels despite decreasing total body fat. Research funded by R15HL133884

Clinical Implications

Clinical Implications

Evaluation of Interleukin-6, Leukotriene B-4, and Nitric Oxide Levels in Exhaled Breath Condensate of Asymptomatic Obese Individuals: Are Obese Patients Under Risk of Developing Asthma?

If systemic inflammation in relation with obesity causes asthma, the detection of increased airway inflammation among obese individuals who do not have any respiratory symptoms can be also beneficial in indentifying obese patients who are at risk of developing asthma. The aim of this study was to evaluate the systemic and airway inflammation of asymptomatic obese and non-obese individuals. Obese and non-obese individuals with no respiratory symptoms were included. Inflammatory biomarkers such as C-reactive protein (CRP), exhaled breath condensate (EBC) interleukin-6 (IL-6), EBC leukotriene B-4 (LTB-4), and EBC nitric oxide (NO) levels of obese and non-obese individuals were determined. Forty-five obese individuals (body mass index [BMI]≥30) and 31 non-obese individuals (BMI≤25) as a control group were included in this study. The mean age of the obese group (38.7±11.4 years) was significantly higher than the one of the non-obese group (29.5±8.6 years; p<0.001). There was no significant relationship between gender and BMI (χ2 =1.471, p=0.225). CRP levels were significantly higher in the obese group (6.94±8.28) than the non-obese group (3.29±0.39; p<0.001). The levels of EBC IL-6 in obese and non-obese group were found as 22.61±12.53 and 21.08±14.39, respectively (p=0.624). There was no significant difference between EBC NO levels of the obese group and non-obese group (24.35±10.9 vs. 21.56±7.83; p=0.226). No significant difference was found between the EBC LTB-4 level in the obese group and the non-obese group (36.39±89.82 vs. 16.64±17.45; p=0.231). Increased systemic inflammation in obese individuals who had no respiratory symptoms might indicate the tendency of asthma. However, airway inflammation was not significantly different between groups. Therefore the relationship between obesity and asthma should be investigated in future large-scale studies determining the direct effects of adipokines on airways.

Adipose-on-a-chip: a dynamic microphysiological in vitro model of the human adipose for immune-metabolic analysis in type II diabetes.

Infiltration of immune cells into adipose tissue is associated with chronic low-grade inflammation in obese individuals. To better understand the crosstalk between immune cells and adipocytes, in vivo-like in vitro models are required. Conventionally transwell culture plates are used for studying the adipocyte-immune cell interaction; however, the static culture nature of this approach falls short of closely recapitulating the physiological environment. Here we present a compartmentalized microfluidic co-culture system which provides a constant-rate of nutrient supply as well as waste removal, resembling the microvascular networks of the in vivo environment. Human adipocytes and U937 cells were co-cultured in close proximity in an enclosed system. The porous barrier between the adjacent compartments comprises an array of microchannels, which enables paracrine interaction between cells in adjacent compartments and improved perfusion-based long term cell feeding. Human pre-adipocytes were fully differentiated into adipocytes on the chip and remained viable for several weeks. Upon co-culturing with immune cells, adipocytes showed a tendency to develop insulin resistance. The immune-metabolic correlation has been studied by monitoring adiponectin and IL-6 expression, as well as glucose uptake upon treatment with insulin. Our microfluidic system can be potentially used to develop physiologically relevant adipose tissue models to study obesity-associated diseases such as insulin resistance and type 2 diabetes and therefore, facilitate drug development to treat these diseases.

Garlic extract favorably modifies markers of endothelial function in obese patients –randomized double blind placebo-controlled nutritional intervention

ObjectiveGarlic exerts a range of effects relevant to human health. However, its influence on the endothelium in obese individuals remains unknown. We aimed to determine the effects of garlic extract (GE) on arterial stiffness and markers of endothelial function. MethodsNinety-two subjects were enrolled in this study. The participants were randomly assigned to receive 400 mg of GE or placebo daily for 3 months. The arterial stiffness index (SI) and markers of endothelial function such as high-sensitivity C-reactive protein (hsCRP), cholesterol (total, LDL, HDL), triglycerides, and plasminogen activator inhibitor 1 (PAI-1), as well as total antioxidant status (TAS) were quantified at baseline and the end of study. ResultsAt the end of study SI (p = 0.01), hsCRP (p < 0.001, PAI-1 (p < 0.001), LDL cholesterol (p < 0.001), and TAS (p < 0.01) were reduced in the GE-supplemented group, but not in the placebo group. ConclusionThis randomized, double-blind, placebo-controlled trial demonstrates that supplementation with GE favorably modifies endothelial biomarkers associated with cardiovascular risk and suggests that GE can be used to suppress chronic inflammation in obese individuals.

Association of gut microbial communities with plasma lipopolysaccharide-binding protein (LBP) in premenopausal women.

The mechanisms by which obesity increases cancer risk are unclear, but some lines of evidence suggest that gut microbial communities (GMC) may contribute to chronic inflammation in obese individuals through raised systemic levels of lipopolysaccharides (LPS). We evaluated associations of the GMC in stool with plasma LPS-binding protein (LBP, a measure of LPS) and C-reactive protein (CRP) concentrations in 110 premenopausal women in the United States. Diet was assessed using 3-day food records and GMCs were evaluated using pyrosequencing of the 16S rRNA gene. OTUs were identified at 97% sequence similarity. Taxonomic classification and functional genes were imputed from 16S rRNA genes, and alpha and beta diversity were assessed using the Shannon index and MRPP, respectively. Multivariable linear regression analysis was used to assess the relation between LBP, specific bacterial genera identified with indicator species analysis, and CRP. Dietary fat intake, particularly saturated fat, and CRP were positively associated with increased LBP. GMC beta diversity, but not alpha diversity, was statistically significantly different between groups using unweighted Unifrac. Several taxa, particularly those in the Clostridia class, were more prevalent in women with low LBP, while Bacteroides were more prevalent in those with high LBP. Genes associated with gram-negative cell wall material synthesis were also associated with LBP and CRP. In contrast, Phascolarctobacterium was associated with lower concentrations of LBP and CRP. We found distinct differences between tertiles of LBP regarding the diversity and composition of the microbiome, as well as differences in functional genes that potentially activate LBP.

Insulin growth factor-1 correlates with higher bone mineral density and lower inflammation status in obese adult subjects

Obesity is a severe public health problem worldwide, leading to an insulin-resistant state in liver, adipose, and muscle tissue, representing a risk factor for type 2 diabetes mellitus, cardiovascular diseases, and cancer. We have shown that abdominal obesity is associated with homeostasis derangement, linked to several hormonal and paracrine factors. Data regarding potential link between GH/IGF1 axis, bone mineral density, and inflammation in obesity are lacking. Thus, aim of this study was to evaluate correlation among IGF-1, BMD, and inflammation in obese individuals. The study included 426 obese subjects, mean age 44.8 ± 14 years; BMI 34.9 ± 6.1. Exclusion criteria were chronic medical conditions, use of medications affecting bone metabolism, hormonal and nutritional status, recent weight loss, and prior bariatric surgery. Patients underwent measurements of BMD and body composition by DEXA and were evaluated for hormonal, metabolic profile, and inflammatory markers. In this population, IGF-1 was inversely correlated with abdominal FM% (p < 0.001, r 2 = 0.12) and directly correlated with osteocalcin (OSCA) (p < 0.002, r 2 = 0.14). A negative correlation was demonstrated between IGF-1 levels and nonspecific inflammatory index, such as fibrinogen (p < 0.01, r 2 = 0.04) and erythrocyte sedimentation rate (p < 0.0001, r 2 = 0.03). IGF-1 was directly correlated with higher BMD, at both lumbar (p < 0.02, r 2 = 0.03) and femoral site (p < 0.04, r 2 = 0.03). In conclusion, our results show that higher levels of serum IGF-1 in obese patients correlate with lower inflammatory pattern and better skeletal health, as demonstrated by higher BMD and osteocalcin levels. These results lead to speculate the existence of a bone-adipose-muscle interplay modulating energy homeostasis, glucose, bone metabolism, and chronic inflammation in individuals affected by abdominal obesity.

Hypomagnesemia and its relation with chronic low-grade inflammation in obesity.

The accumulation of visceral fat in obesity is associated with excessive production of proinflammatory adipokines, which contributes to low-grade chronic inflammation state. Moreover, the literature has shown that mineral deficiency, in particular of magnesium, has important role in the pathogenesis of this metabolic disorder with relevant clinical repercussions. To bring updated information about the participation of hypomagnesemia in the manifestation of low-grade chronic inflammation in obese individuals. Articles published in PubMed, SciELO, LILACS and ScienceDirect, using the following keywords: "obesity," "magnesium" and "low grade inflammation." Scientific evidence suggests that magnesium deficiency favors the manifestation of low-grade chronic inflammation in obese subjects. From literature data, it is evident the participation of magnesium through biochemical and metabolic reactions in protecting against this metabolic disorder present in obesity.

Relationship between Common Dietary Polyphenols and Obesity-Induced Inflammation

The incidence of obesity and its related metabolic disorders has escalated dramatically in the past decades worldwide. Defined as abnormal or excessive fat accumulation caused by an imbalance between energy intake and expenditure, obesity is presently the major health challenge in developed countries and the causative factor of numerous diseases such as heart problems, hypertension, hyperlipidemia and type 2 diabetes. Presence of high level of cytokines and acute phase proteins associated with inflammation in obese individuals relates obesity to chronic low-grade inflammation. Obesity-induced inflammation has an impact on insulin resistance and cardiac health. Polyphenols including catechins, tocopherols, resveratrol, curcumin and anthocyanins have been shown to reduce adipose tissue inflammation. It has been broadly accepted that adipocyte dysfunction plays a major role in development of obesity and obesity related complications. This state is characterised by hypersecretion of pro-atherogenic, pro-inflammatory and pro-diabetic adipokines as well as decreased secretion of adiponectin. The dietary polyphenols described in this review have potential as nutritional strategies for the prevention of obesity and associated inflammation as well as increase in insulin sensitivity in diabetic people.

Role of obesity and adipose tissue-derived cytokine leptin during Clostridium difficile infection

Obesity is among the most pressing health concerns in the world since it is increasingly common even in the developing world, and is clearly associated with increased risk for chronic debilitating diseases and death. Furthermore, obesity can influence the pathogenesis of infectious diseases by affecting the balance of pathogen clearance and pathological inflammation. The mechanisms that result in enhanced inflammation in obese individuals are poorly understood. Clostridium difficile is a major cause of nosocomial infections worldwide. Recent studies have shown that obesity is associated with increased risk of C. difficile infections. In this review, we will discuss our current knowledge of the role of obesity in determining risk of C. difficile infections, and focus on the role of the adipose tissue-derived cytokine leptin in C. difficile infections.

Association between ferritin and hepcidin levels and inflammatory status in patients with type 2 diabetes mellitus and obesity

ObjectiveThe aim of this study was to determine the association between iron parameters and inflammation in obese individuals with and without type 2 diabetes mellitus (T2DM). MethodsWe studied 132 obese individuals (OB), 60 individuals with T2DM, 106 obese individuals with T2DM (T2DOB), and 146 controls (C). All of were men aged >30 y. Biochemical, iron nutrition, and oxidative stress parameters were determined. Peripheral mononuclear cells were isolated and total RNA was extracted to quantify tumor necrosis factor (TNF)-α, nuclear factor (NF)-κB, interleukin (IL)-6, toll-like receptor (TLR)-2/4 and hepcidin by quantitative reverse transcription polymerase chain reaction. ResultsOB, T2DM, and T2DOB individuals had higher ferritin, retinol-binding protein 4, and thiobarbituric acid reactive substance (TBAR) levels than controls. T2DOB and T2DM individuals showed high high-sensitivity C-reactive protein (hsCRP) levels and OB with and without T2DM had elevated levels of serum hepcidin. Heme oxygenase activity was high in OB and T2DM and there were no differences observed in superoxide dismutase and glutathione parameters. A correlation between TBARS and ferritin in T2DOB was observed (r = 0.31; P < 0.006). Multiple linear regression analysis showed an association between diabetes and obesity with ferritin, TBARS, and hsCRP levels. The upper quartiles of ferritin, TBARS and hepcidin showed an adjusted odd ratio for T2DM of 1.782, 2.250, and 4.370, respectively. TNF-α, IL-6, hepcidin, NF-κB, TLR-2/4 mRNA abundances were increased in T2DM and T2DOB. ConclusionElevated hsCRP and hepcidin levels, and increased gene expression of TNF-α, IL-6, NF-κB, and TLR-2/4 in patients with diabetes, obesity, or both exacerbate and perpetuate the insulin resistance and inflammatory state.

Health-related quality of life relates to obesity and low-grade inflammation in obese individuals

Searchable abstracts of presentations at key conferences in endocrinology ISSN 1470-3947 (print) | ISSN 1479-6848 (online)

Associations between obesity and asthma in a low-income, urban, minority population

BackgroundCommunity-based studies of obesity, asthma, biomarkers of oxidative stress, and adipokines among low-income, urban, minority populations are lacking. Oxidative stress, perhaps modulated by adipokines, may increase airway inflammation in obese individuals. ObjectivesTo characterize associations between obesity and asthma in a low-income, urban, minority community and evaluate adipokines, biomarkers of inflammation, and oxidant-antioxidant balance in association with asthma and obesity. MethodsA door-to-door evaluation of asthma and obesity prevalence was performed in a low-income housing development. Nonsmoking adults and children underwent additional evaluation, including allergy skin testing, and measures of serum adipokines, and indicators of oxidative stress in blood and exhaled breath. ResultsThe prevalences of current asthma and a body mass index in the 85th percentile or higher were 15.8% and 35.3%, respectively, among 350 nonsmokers older than 4 years. Asthma and obesity were not associated with one another (odds ratio, 1.0; 95% confidence interval, 0.55-1.84). Among 116 nonsmoking participants who underwent biomarker evaluation, obesity was not associated with exhaled nitric oxide. In multivariate logistic models that adjusted for age category, sex, and a body mass index in 85th percentile or higher, leptin concentrations in the highest quartile were associated with asthma (odds ratio, 8.34; 95% confidence interval, 1.29-50.2) but not with atopy. Adiponectin was associated with total antioxidant capacity in exhaled breath. ConclusionAsthma and obesity, although both common in a low-income, minority community, were not associated with one another. Nevertheless, adipokines were associated with asthma status and with markers of oxidative stress in the lungs, providing some support for an adipokine-inflammatory mechanistic link between the two conditions.