Link between leptin and interleukin-6 levels in the initial phase of obesity related inflammation

Stelzer, Ingeborg; Zelzer, Sieglinde; Raggam, Reinhard B.; Prüller, Florian; Truschnig-Wilders, M.; Meinitzer, Andreas; Schnedl, Wolfgang J.; Horejsi, Renate; Möller, Reinhard; Weghuber, Daniel; Reeves, Gloria; Postolache, Teodor T.; Mangge, Harald

doi:10.1016/j.trsl.2011.10.001

Cited by 57 publications

(52 citation statements)

References 25 publications

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“…Leptin is considered as a proinflammatory cytokine with proatherogenic features, as it increases monocyte chemoattractant protein-1 and endothelin-1 secretion by endothelial cells, enhances oxidative stress, promotes migration and proliferation of smooth muscle cells and increases platelet aggregation, thus facilitating thrombosis [178] . In the initial phase of obesity-related inflammation, leptin is predictively associated with interleukin 6 plasma levels in juveniles [179] . However, leptin resistance, which later develops during obesity, does also favor atherogenesis.…”

Section: Nutrition Antioxidants and Cvdmentioning

confidence: 97%

Antioxidants, inflammation and cardiovascular disease

Mangge¹

2014

WJC

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Multiple factors are involved in the etiology of cardiovascular disease (CVD). Pathological changes occur in a variety of cell types long before symptoms become apparent and diagnosis is made. Dysregulation of physiological functions are associated with the activation of immune cells, leading to local and finally systemic inflammation that is characterized by production of high levels of reactive oxygen species (ROS). Patients suffering from inflammatory diseases often present with diminished levels of antioxidants either due to insufficient dietary intake or, and even more likely, due to increased demand in situations of overwhelming ROS production by activated immune effector cells like macrophages. Antioxidants are suggested to beneficially interfere with diseases-related oxidative stress, however the interplay of endogenous and exogenous antioxidants with the overall redox system is complex. Moreover, molecular mechanisms underlying oxidative stress in CVD are not fully elucidated. Metabolic dybalances are suggested to play a major role in disease onset and progression. Several central signaling pathways involved in the regulation of immunological, metabolic and endothelial function are regulated in a redox-sensitive manner. During cellular immune response, interferon γ-dependent pathways are activated such as tryptophan breakdown by the enzyme indoleamine 2,3-dioxygenase (IDO) in monocyte-derived macrophages, fibroblasts, endothelial and epithelial cells. Neopterin, a marker of oxidative stress and immune activation is produced by GTP-cyclohydrolase Ⅰ in macrophages and dendritic cells. Nitric oxide synthase (NOS) is induced in several cell types to generate nitric oxide (NO). NO, despite its low reactivity, is a potent antioxidant involved in the regulation of the vasomotor tone and of immunomodulatory signaling pathways. NO inhibits the expression and function of IDO. Function of NOS requires the cofactor tetrahydrobiopterin (BH4), which is produced in humans primarily by fibroblasts and endothelial cells. Highly toxic peroxynitrite (ONOO -) is formed solely in the presence of superoxide anion (O2 -). Neopterin and kynurenine to tryptophan ratio (Kyn/Trp), as an estimate of IDO enzyme activity, are robust markers of immune activation in vitro and in vivo . Both these diagnostic parameters are able to predict cardiovascular and overall mortality in patients at risk. Likewise, a significant association exists between increase of neopterin concentrations and Kyn/Trp ratio values and the lowering of plasma levels of vitamin-C, -E and -B. Vitamin-B deficiency is usually accompanied by increased plasma homoycsteine. Additional determination of NO metabolites, BH4 and plasma antioxidants in patients with CVD and related clinical settings can be helpful to improve the understanding of redox-regulation in health and disease and might provide a rationale for potential antioxidant therapies in CVD. REVIEWSubmit a

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Section: Nutrition Antioxidants and Cvdmentioning

confidence: 97%

Antioxidants, inflammation and cardiovascular disease

Mangge¹

2014

WJC

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“…hepatocyte, lymphocyte, endothelial cells). Genetic polymorphisms and plasma levels of IL6 have complex [8] and contradictory [9] relations with obesity [10][11][12], BMI (Body Mass Index) [13][14][15] and inflammation [16].…”

Section: Introductionmentioning

confidence: 99%

Potential association of obesity with IL6 G-174C polymorphism and TTV infections

Cimponeriu

Serafinceanu²,

Apostol

et al. 2013

Open Life Sciences

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Polymorphisms in IL6, ACE and ATR genes are associated with obesity. Torque Teno virus (TTV) seems to be able to interfere with production of some proinflammatory cytokines associated with obesity and related phenotypes. The aim of this study was to test the potential association between obesity, TTV infection and the IL6 G-174C (rs1800795), ACE I/D (rs4646994), AT1R A1166C (rs5186) polymorphisms. The polymorphisms and the presence of TTV were detected in blood samples from 150 obese and 150 normal-weight, healthy subjects using PCR based methods. IL6-174 CC genotype was more frequent in all obese patients (P=0.02) and in patients without TTV infections (P=0.03) than in controls. Obese women had more frequent TTV infections compared with normal-weight women (P=0.046). Obese subjects, regardless of gender (women P=0.03, men P=0.04), and healthy normal-weight men (P<0.01) carriers of AT1R C allele had higher triglycerides levels compared with non-carriers. The frequency of TTV in the control group (70.67%) was similar to data reported in other populations. The present study indicated that IL6-174 CC genotype and TTV infections in women could be associated with the common form of obesity.

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“…Obesity is marked by a peripheral chronic low inflammation state partly mediated via production of inflammatory adipokines such as IL-6 and TNF-α (Das, 2001). This chronic low inflammation state is already observed in obese children, manifested especially by elevated concentrations of IL-6 (Stelzer et al, 2012; Tam et al, 2010; Visser, 2001), which persist during adolescence and into adulthood (Stelzer et al, 2012). Furthermore, another inflammatory state is found in obese individuals, as examination of their brains via magnetic resonance imaging (MRI) showed increased gliosis in the mediobasal hypothalamus (Thaler et al, 2012).…”

Section: Interleukin-6mentioning

confidence: 95%

Obesity and dementia: Adipokines interact with the brain

Arnoldussen

Kiliaan

Gustafson

2014

European Neuropsychopharmacology

187

161

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Obesity is a pandemic and a serious global health concern. Obesity is a risk factor for multiple conditions and contributes to multi-morbidities, resulting in increased health costs and millions of deaths each year. Obesity has been associated with changes in brain structure, cognitive deficits, and dementia and Alzheimer's disease. Adipokines, defined as hormones, cytokines and peptides secreted by adipose tissue, may have more widespread influence and functionality in the brain than previously thought. In this review, six adipokines, and their actions in the obese and non-obese condition will be discussed. Included are: plasminogen activator inhibitor-1 (PAI-1), interleukin-6 (IL-6), tumor necrosis factors alpha (TNF-α), angiotensinogen (AGT), adiponectin and leptin. Their functionality in the periphery, their ability to cross the blood brain barrier (BBB) and their influence on dementia processes within the brain will be discussed.

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Link between leptin and interleukin-6 levels in the initial phase of obesity related inflammation

Cited by 57 publications

References 25 publications

Antioxidants, inflammation and cardiovascular disease

Antioxidants, inflammation and cardiovascular disease

Potential association of obesity with IL6 G-174C polymorphism and TTV infections

Obesity and dementia: Adipokines interact with the brain

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