scholarly journals Severely Obese Adolescents and Adults Exhibit a Different Association of Circulating Levels of Adipokines and Leukocyte Expression of the Related Receptors with Insulin Resistance

2013 ◽  
Vol 2013 ◽  
pp. 1-12 ◽  
Author(s):  
Antonello E. Rigamonti ◽  
Fiorenza Agosti ◽  
Alessandra De Col ◽  
Giancarlo Silvestri ◽  
Nicoletta Marazzi ◽  
...  

Obese adults frequently exhibit a low-grade inflammation and insulin resistance, which have been hypothesized to be established early in childhood. Aim of this study was to evaluate the age-dependent relationships between inflammatory state and insulin resistance in obese adolescents and adults. Clinical and metabolic parameters, circulating adipokines (TNF-α, adiponectin, and leptin), ghrelin, their leukocyte receptors (TNFR1, ADIPOR2, OBRL and GHSR1a), and acute phase reactants (CRP and white blood cells) were assessed in lean and obese adolescents compared with the adult counterparts. Only obese adults had higher HOMA-IR, insulin, and triglycerides compared to the lean group. An inflammatory state was present in obese adolescents and adults, as demonstrated by the higher values of CRP and neutrophils. There were no group differences in circulating levels of TNF-αand leukocyte expression of TNFR1. Adiponectin concentrations and leukocyte expression of ADIPOR2 were higher in the lean groups than in the corresponding obese counterparts. For leptin and leukocyte expression of OBRL, the results were opposed. Circulating levels of ghrelin were higher in lean adolescents and adults than the related lean groups, while there was a higher leukocyte expression of GHSR1a in (only) lean adults than obese adults. When the analysis was performed in (lean or obese) adults, TNF-α, neutrophils, leptin, and GHSR1a were predictors of HOMA-IR. None of the considered independent variables accounted for the degree of insulin resistance in the adolescent group. In conclusion, a dissociation between the low-grade inflammation and insulin resistance is supposed to exist in the early phases of obesity.

2009 ◽  
Vol 53 (2) ◽  
pp. 145-150 ◽  
Author(s):  
Bernardo Léo Wajchenberg ◽  
Marcia Nery ◽  
Maria Rosaria Cunha ◽  
Maria Elizabeth Rossi da Silva

The authors analyze insulin resistance, the metabolic syndrome and endothelial dysfunction as consequence of a common antecedent, a low grade inflammation, indicating that in obesity there is a chronically activated inflammatory state of the adipose tissue. Furthermore, the inflammatory signaling is discussed according to the adipose tissue depot, visceral or subcutaneous.


2014 ◽  
Vol 112 (10) ◽  
pp. 1724-1734 ◽  
Author(s):  
Eirini C. Spyridaki ◽  
Panagiotis Simos ◽  
Pavlina D. Avgoustinaki ◽  
Eirini Dermitzaki ◽  
Maria Venihaki ◽  
...  

Published evidence suggests that obesity impairs cognition. Development of chronic low-grade inflammation (CLGI) represents the earliest consequence of obesity. The present study investigated the association between obesity and fluid intelligence impairment and assessed the potential mediating role of CLGI and psychological (depression/anxiety symptoms), lifestyle (exercise) and physiological (metabolic dysfunction indices) factors in this association. Clinically healthy participants (n 188), grouped as per BMI, underwent cognitive (General Ability Measure for Adults), psychological (Beck Depression Inventory-II and State-Trait Anxiety Inventory) and activity (Godin leisure-time physical activity) measurements. Biochemical parameters included the following: (a) indices of CLGI (high-sensitivity C-reactive protein, erythrocyte sedimentation rate and fibrinogen); (b) insulin resistance (Homeostasis Model Assessment of Insulin Resistance index); (c) adiposity (plasma adiponectin). An inverse association between elevated BMI and fluid intelligence was observed, with obese participants displaying significantly poorer performance compared with age-matched normal-weight peers. Structural equation modelling results were consistent with a negative impact of obesity on cognition that was mediated by CLGI. The results of the present study support the hypothesis that reduced general cognitive ability is associated with obesity, an adverse effect mainly mediated by obesity-associated activation of innate immunity.


Author(s):  
Charmaine S. Tam ◽  
Leanne M. Redman

AbstractObesity is characterized by a state of chronic low-grade inflammation due to increased immune cells, specifically infiltrated macrophages into adipose tissue, which in turn secrete a range of proinflammatory mediators. This nonselective low-grade inflammation of adipose tissue is systemic in nature and can impair insulin signaling pathways, thus, increasing the risk of developing insulin resistance and type 2 diabetes. The aim of this review is to provide an update on clinical studies examining the role of adipose tissue in the development of obesity-associated complications in humans. We will discuss adipose tissue inflammation during different scenarios of energy imbalance and metabolic dysfunction including obesity and overfeeding, weight loss by calorie restriction or bariatric surgery, and conditions of insulin resistance (diabetes, polycystic ovarian syndrome).


2022 ◽  
Author(s):  
Xin Yu ◽  
Ming-Hui Zhang ◽  
Yan-Hao Huang ◽  
Yu Deng ◽  
You-Zhen Feng ◽  
...  

Abstract Background: Obesity is associated with excessive airway collapse and reduced lung volume; it is unknown whether it affects airway-lung interactions. We sought to compare the airway tree to lung volume ratio, assessed by CT, in obese individuals with and without ventilation disorders.Methods: Participants underwent inspiratory chest CT and pulmonary function. The percentage ratio of the whole airway tree to lung volume, automatically segmented via deep learning, was defined as CT airway volume percent (AWV%). Total airway count (TAC), airway wall area percent (WA%), and other CT indexes were also measured. Results: We evaluated 88 participants including adolescents(age: 14-18, n= 12) and adults (age: 19-25, n= 17; age: 26-35, n= 39; age> 35, n= 20). Obese adolescents had higher forced vital capacity (FVC) (P = 0.001) and lower AWV% (P = 0.008) than obese adults (age >35). Among obese adults, participants with restrictive disorders had larger AWV% (P < 0.001) and those with obstructive disorders showed smaller AWV% (P < 0.001) compared to participants with normal ventilation. AWV% was positively correlated with age and forced expiratory volume in 1 second (FEV1)/FVC and adversely related to FVC (P< 0.05 for all), and in multivariate models, AWV% independently predicted FEV1/FVC (R2 = 0.49, P < 0.001) and FVC (R2 = 0.60, P < 0.001).Conclusion: Transitions in lung function patterns between obese adolescents and adults are associated with airway to lung ratios. The obesity-induced disproportion between the airway tree and lung volume may adversely affect and complicate lung ventilation.


Endocrinology ◽  
2007 ◽  
Vol 149 (3) ◽  
pp. 1350-1357 ◽  
Author(s):  
Florian W. Kiefer ◽  
Maximilian Zeyda ◽  
Jelena Todoric ◽  
Joakim Huber ◽  
René Geyeregger ◽  
...  

Obesity is associated with a chronic low-grade inflammation characterized by macrophage infiltration of adipose tissue (AT) that may underlie the development of insulin resistance and type 2 diabetes. Osteopontin (OPN) is a multifunctional protein involved in various inflammatory processes, cell migration, and tissue remodeling. Because these processes occur in the AT of obese patients, we studied in detail the regulation of OPN expression in human and murine obesity. The study included 20 morbidly obese patients and 20 age- and sex-matched control subjects, as well as two models (diet-induced and genetic) of murine obesity. In high-fat diet-induced and genetically obese mice, OPN expression was drastically up-regulated in AT (40 and 80-fold, respectively) but remained largely unaltered in liver (&lt;2-fold). Moreover, OPN plasma concentrations remained unchanged in both murine models of obesity, suggesting a particular local but not systemic importance for OPN. OPN expression was strongly elevated also in the AT of obese patients compared with lean subjects in both omental and sc AT. In addition, we detected three OPN isoforms to be expressed in human AT and, strikingly, an obesity induced alteration of the OPN isoform expression pattern. Analysis of AT cellular fractions revealed that OPN is exceptionally highly expressed in AT macrophages in humans and mice. Moreover, OPN expression in AT macrophages was strongly up-regulated by obesity. In conclusion, our data point toward a specific local role of OPN in obese AT. Therefore, OPN could be a critical regulator in obesity induced AT inflammation and insulin resistance.


2011 ◽  
Vol 165 (4) ◽  
pp. 639-645 ◽  
Author(s):  
Francisco J Ortega ◽  
José M Moreno-Navarrete ◽  
Mónica Sabater ◽  
Wifredo Ricart ◽  
Gema Frühbeck ◽  
...  

BackgroundAcute phase mediators promote metabolic changes by modifying circulating hormones. However, there is virtually no data about the link between glucagon and inflammatory parameters in obesity-related chronic low-grade inflammation.Study designWe performed both cross-sectional and longitudinal (diet-induced weight loss) studies.MethodsCirculating glucagon concentrations (ELISA), parameters of glucose and lipid metabolism, interleukin 6 (IL6), and complement factor B (CFB) were analyzed in 316 subjects (250 men and 66 women). The effects of weight loss were investigated in an independent cohort of 20 subjects.ResultsCirculating glucagon significantly correlated with glucose (r=0.407,P<0.0001), HbAlc (r=0.426,P<0.0001), fasting triglycerides (r=0.356,P=0.001), and parameters of innate immune response system such as IL6 (r=0.342,P=0.050) and CFB (r=0.404,P=0.002) in obese subjects with altered glucose tolerance, but not in individuals with normal glucose tolerance (NGT). In obese and NGT subjects, glucagon was associated with fasting triglycerides (r=0.475,P=0.003) and CFB (r=0.624,P=0.001). In obese subjects, glucagon (P=0.019) and CFB (P=0.002) independently contributed to 26% of fasting triglyceride variance (P<0.0001) after controlling for the effects of age and fasting serum glucose concentration in multiple lineal regression models. Moreover, concomitant with fat mass, fasting triglycerides, and CFB, weight loss led to significantly decreased circulating glucagon (−23.1%,P=0.004).ConclusionsAccording to the current results, acute phase reactants such as IL6 and CFB are associated with fasting glucagon in metabolically compromised subjects. This suggests that glucagon may be behind the association between inflammatory and metabolic parameters in obesity-associated chronic low-grade inflammation.


2021 ◽  
pp. 1-13

1. Abstract Insulin Resistance is the leading cause of Type 2 diabetes mellitus (T2D). It occurs as a result of lipid disorders and increased levels of circulating free fatty acids (FFAs). FFAs accumulate within the insulin sensitive tissues such as muscle, liver and adipose tissues exacerbating different molecular mechanisms. Increased levels fatty acid has been documented to be strongly associated with insulin resistant states and obesity causing inflammation that eventually causes type 2-diabetes. Among the biomarkers that are accompanying low grade inflammation include IL-1β, IL-6 and TNF-α. The current review point out the importance of measuring the inflammatory biomarkers especially focusing on the conductance and measurement for IL-6 as a screening laboratory test and its diagnostic value in clinical practice.


2019 ◽  
Vol 20 (4) ◽  
pp. 839 ◽  
Author(s):  
Erika Di Zazzo ◽  
Rita Polito ◽  
Silvia Bartollino ◽  
Ersilia Nigro ◽  
Carola Porcile ◽  
...  

Adipose tissue is a key regulator of energy balance playing an active role in lipid storage as well as in synthesizing several hormones directly involved in the pathogenesis of obesity. Obesity represents a peculiar risk factor for a growing list of cancers and is frequently associated to poor clinical outcome. The mechanism linking obesity and cancer is not completely understood, but, amongst the major players, there are both chronic low-grade inflammation and deregulation of adipokines secretion. In obesity, the adipose tissue is pervaded by an abnormal number of immune cells that create an inflammatory environment supporting tumor cell proliferation and invasion. Adiponectin (APN), the most abundant adipokine, shows anti-inflammatory, anti-proliferative and pro-apoptotic properties. Circulating levels of APN are drastically decreased in obesity, suggesting that APN may represent the link factor between obesity and cancer risk. The present review describes the recent advances on the involvement of APN and its receptors in the etiology of different types of cancer.


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