Body mass index is associated with reduced exhaled nitric oxide and higher exhaled 8-isoprostanes in asthmatics
Sushma KomakulaSumita KhatriJoel MermisSamira SavillShireen HaqueMauricio RojasL S BrownGerald TeagueFernando Holguín
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Abstract Background Recently, it has been shown that increasing body mass index (BMI) in asthma is associated with reduced exhaled NO. Our objective in this study was to determine if the BMI-related changes in exhaled NO differ across asthmatics and controls, and to determine if these changes are related to increased airway oxidative stress and systemic levels of leptin and adiponectin. Methods Observational study of the association of BMI, leptin, and adiponectin with exhaled nitric oxide (NO) and exhaled 8-isoprostanes in 67 non-smoking patients with moderate to severe persistent asthma during baseline conditions and 47 controls. Measurements included plasma levels of leptin, adiponectin, exhaled breath condensates for 8-isoprostanes, exhaled NO, pulmonary function tests, and questionnaires regarding asthma severity and control. Results In asthmatics, BMI and the ratio of leptin to adiponectin were respectively associated with reduced levels of exhaled NO (β = -0.04 [95% C.I. -0.07, -0.1], p < 0.003) and (β = -0.0018 [95% C.I. -0.003, -0.00034], p = 0.01) after adjusting for confounders. Also, BMI was associated with increased levels of exhaled 8-isoprostanes (β = 0.30 [95% C.I. 0.003, 0.6], p = 0.03) after adjusting for confounders. In contrast, we did not observe these associations in the control group of healthy non-asthmatics with a similar weight distribution. Conclusion In adults with stable moderate to severe persistent asthma, but not in controls, BMI and the plasma ratio of leptin/adiponectin is associated with reduced exhaled NO. Also, BMI is associated with increased exhaled 8-isoprostanes. These results suggest that BMI in asthmatics may increase airway oxidative stress and could explain the BMI-related reductions in exhaled NO.Keywords:
Exhaled breath condensate
The aim of this study was to investigate whether recurrent pregnancy loss (RPL) is associated with adipokine gene polymorphisms (namely the leptin -2548 (G/A), adiponectin 276 (G/T), and adiponectin 45 (T/G) polymorphisms) and/or adipokine serum levels.A total of 145 women participated in the study. For the analysis of serum adipokine levels, 19 healthy fertile women (control group) and 60 women suffering from RPL were included. For the polymorphism analysis, 126 women suffering from RPL were included. Serum adipokine levels were determined using a commercial radioimmunoassay kit. Adipokine polymorphisms were analyzed using an allele-specific polymerase chain reaction (PCR).Our immunoassays revealed that serum leptin levels were similar in control and RPL groups (17.34 and 20.16 ng/mL, respectively). In contrast, serum adiponectin levels were significantly higher in women with RPL than in controls (9.83 and 6.89 μg/mL, respectively; P < 0.05). Unfortunately, our allele-specific PCR experiments did not reveal any significant differences in allele frequency between women with RPL and NCBI allele frequencies.This study demonstrates that adiponectinemia is increased in patients suffering from RPL. However, association of adiponectin with adverse pregnancy outcomes remains to be elucidated.
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Adipose tissue has been identified as an endocrine organ secreting adipokines involved in metabolic and inflammatory pathways. Adiponectin, an anti-inflammatory adipokine, is reduced in sepsis. High Molecular Weight (HMW) adiponectin, the biologically most relevant molecule, has been investigated very little in human sepsis. Zinc-alpha2-glycoprotein (ZAG) is a novel adipokine and its expression in adipose tissue is positively correlated with adiponectin expression. It is not yet known whether ZAG has a role in sepsis. In this study we assessed levels of HMW adiponectin and ZAG during different stages of sepsis. A prospective observational pilot study was carried out on 21 septic patients. Serum samples were taken on day 1 and 2 post ICU admission and on day of discharge. Samples were analysed for total and HMW adiponectin, HMW/total adiponectin ratio, and ZAG. Results were correlated with clinical and metabolic data. There were no differences in total adiponectin, HMW adiponectin and ZAG plasma concentrations between day 1 (admission) and day 2 of the sepsis episode. Compared to admission, a significant increase in total and HMW adiponectin and ZAG was observed on the day of discharge when clinical improvement had been achieved. There was also an increase in the HMW/total adiponectin ratio at that time. Our data demonstrate an increase in both HMW adiponectin and total adiponectin in patients who had clinically recovered from sepsis. The increase in HMW/total adiponectin ratio with improvement of the clinical condition suggests that HMW adiponectin may have a greater role in the inflammatory process and insulin resistance seen in sepsis. In this pilot study, we have also demonstrated a significant increase in ZAG in critically ill patients temporally related to recovery from sepsis.
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Background: Adipose tissue dysfunction has been implicated in the pathophysiology of Alzheimer’s disease. However, the involvement of adipokines, particularly adiponectin, remains unclear. Objective: To compare serum and cerebrospinal fluid (CSF) levels of adiponectin, leptin and leptin-to-adiponectin ratio in patients within the spectrum of Alzheimer’s disease and evaluate their relationship with classical biomarkers and their value as markers of progression. Methods: Amnestic mild cognitive impairment (MCI, n = 71) and Alzheimer’s dementia (AD, n = 53) subjects were consecutively recruited for serum and CSF adiponectin and leptin determination using an analytically validated commercial enzyme-linked immunosorbent assay (ELISA). Correlations were explored using adjusted Spearman’s correlation coefficients. A logistic regression model and ROC analysis were performed to evaluate the staging predictive value of adipokines. Results: Serum adiponectin was 33% higher in AD when compared to MCI patients. Adiponectin CSF levels, similar in both groups, were positively correlated with A β 42 and cognitive function, though only in women. The area under the ROC curve was 0.673 (95% CI:0.57-0.78) for serum adiponectin as predictor of dementia stage and the cut-off 10.85 μg/ml maximized the sum of specificity (87%) and sensitivity (44%). Conclusion: Although longitudinal studies are required, we hypothesize that higher serum adiponectin in AD patients constitutes a strategy to compensate possible central signaling defects. In addition, adiponectin might be specifically assigned to neuroprotective functions in women and eventually involved in the female-biased incidence of Alzheimer’s disease.
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Adiponectin is a most abundant secretory protein produced by adipocytes of white adipose tissue. Adiponectin circulates in blood as three different (high-molecular, middle-molecular, and low-molecular weight) isoforms, gives its effects through AdipoR1 and AdipoR2 receptor. Primary data suggesting that adiponectin has insulin-sensitizing, anti-atherogenic, and anti-inflammatory effects. High serum level of adiponectin is positively associated with inflammation severity and pathological progression in chronic kidney disease, liver disease and inflammatory bowel disease. It has emerged as a valuable biomarker for insulin sensitivity, cardiovascular risk and inflammation. Adiponectin is gaining attention for its therapeutic role in Alzheimer’s disease. Adiponectin appears to play a crucial role not only in glucose and lipid metabolism but also the development and progression of different cancers. Adiponectin also produced locally in the retinas participate in defense of various eye diseases. This review summarizes the role of adiponectin as benevolent adipokine in different disorders.
Adiponectin receptor 1
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Adipose tissue is a major site for energy storage.Increasingly,however,it has been recognized as an important endocrine organ that secretes a number of biologically active adipokines.Of these adipokines,adiponectin has attracted much attention.Many studies have showed protective effects of adiponectin on metabolic syndrome and cardiovascular diseases.Promoting the secretion of adiponectin is expected to be a novel therapeutic tool for metabolic syndrome and cardiovascular disease.
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Adipocytokines, such as adiponectin, TNF-alpha, and leptin, are cytokines secreted by visceral adipocytes, and they are associated with metabolic syndrome. Adiponectin is one of the adipocytokines, and is a protein comprised of 244 amino acids. It is known as ACRP30, GBP28, and AdipoQ. Adiponectin is secreted by adipocytes, has three different isoforms, including trimers (low-molecular weight: LMW), hexamers (middle-molecular-weight: MMW), and higher-order oligomeric (high-molecular-weight: HMW) structures, and affects the biological activity. Adiponectin is a clinically relevant parameter measured routinely in subjects at risk of type 2 diabetes and metabolic syndrome. We investigated the adiponectin levels using a number of ELISA assay kits.
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Adiponectin (also known as APM1, Acrp 30, AdipoQ or GBP28) is a 30kD circulating plasma protein and is the most abundant adipokine secreted by adipose tissue. In humans, adiponectin accounts for approximately 0.01% of circulating plasma proteins.1 It is thought to have a unique spectrum of properties for an adipokine, many of which are anti-atherosclerotic, and is downregulated in the presence of increasing central adiposity.
Intravascular Ultrasound
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Adipose tissue is an active metabolic tissue that secretes multiple metabolically important proteins, known as adipokines. Adiponectin is an important adipokine because of its beneficial effects on glucose and lipid metabolism. Low levels of adiponectin are associated with disease states such as diabetes and cardiovascular disease. Direct administration of adiponectin has been shown to be beneficial in animal models of diabetes, obesity and atherosclerosis. Adiponectin levels in humans can be increased through indirect methods such as weight loss or treatment with thiazolidinediones. This article will review the epidemiology and therapeutic options with adiponectin.
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이 연구의 목적은 30-40대 남성 근로자에 있어서 대사증후군 구성인자와 adiponectin 및 leptin의 생리적 농도가 비만에 미치는 영향을 보고자 하였다. 방법: 체질량지수(BMI) 측정은 체성분분석기, 혈압과 혈청생화학 검사는 수은혈압계와 자동생화학분석기를 이용하여 측정하였다. Adiponectin과 leptin은 ELISA kit으로 분석하였고, 대사증후군은 NCEP-ATP III 진단기준에 의하여 진단하였다. 결과: 허리와 엉덩이둘레, 체지방, 수축기와 이완기 혈압은 BMI≤25 ㎏/㎡보다 BMI>25 ㎏/㎡군에서 유의하게 높았다. BMI>25 ㎏/㎡군에서 공복혈당, 인슐린, 인슐린저항성과 leptin의 농도가 BMI≤25 ㎏/㎡군보다 높은 반면, HDL-콜레스테롤과 adiponectin의 농도는 BMI≤25 ㎏/㎡군에서 높았다. 연령, 흡연 및 음주습관을 보정한 후, 다중 로지스틱 회귀분석 실시결과 규칙적인 운동, adiponectin과 leptin은 비만하지 않은(BMI≤25 ㎏/㎡) 남성 근로자에서 대사증후군 유발에 관여하는 독립적 인자로 나타났다. 결론: 이 연구결과 남성의 비만은 대사증후군의 되먹임 조절에 관여하는 adiponectin과 leptin의 생리적 농도와 관련이 있으며, adiponectin과 leptin과 같은 신경영양물질의 변화와 관련되어 되먹임 조절의 기능손상과 저하는 궁극적으로 대사증후군을 유발시킬 수 있다.
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Adipokines secreted by adipose tissue exert powerful regulatory effects on metabolism and energy balance. The contribution of various fat depots to circulating adipokine concentrations has not been clarified. Moreover, it is unknown whether these adipokines play a role in hepatic steatosis (ST) or progression to portal fibrosis and non-alcoholic steatohepatitis (PT/NASH). The purpose of this study was to explore the relationship between adipokines produced in omental (OM) and subcutaneous (SQ) fat with circulating concentrations, and to examine whether adipokines determine which patients with ST develop PT/NASH. We studied 20 females undergoing bariatric surgery (BMI 48 ± 7 kg/m2; age 40 ± 4 yr) categorized as ST or PF/NASH by liver biopsy. In serum and in OM and SQ fat samples, we quantified the adipokines leptin, resistin, MCP-1, and adiponectin by ELISA. In serum, we also measured high molecular weight (HMW) and low MW (LMW) adiponectin multimers by immunoblot, since we reported that HMW adiponectin was correlated with insulin sensitivity and reduced risk of Metabolic Syndrome. In comparing ST and PT/NASH, there were no differences in serum leptin, resistin, MCP-1, total adiponectin, and HMW and LMW adiponectin. In adipose tissues, OM adiponectin was higher in PF/NASH compared with ST (102.1 ± 8.7 vs. 82.5 ± 19.7 ng/mL; P < 0.05), while SQ adiponectin and tissue leptin levels did not differ between subgroups. OM adiponectin was also correlated with serum HMW adiponectin (r = 0.67, P < 0.05) but not LMW; in contrast, SQ adiponectin did not correlate with either serum HMW or LMW. In conclusion: 1) Serum levels of leptin, resistin, MCP-1, adiponectin, and adiponectin multimers were similar in ST and PT/NASH patients. 2) PT/NASH patients had higher OM adiponectin. 3) OM but not SQ adiponectin was highly correlated with serum HMW, the multimer associated with insulin sensitivity. The data suggest that factors intrinsic to liver, rather than secreted adipokines, determine which patients with hepatic steatosis progress to PT/NASH.
Resistin
Steatohepatitis
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