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Fernando Aprile-Garcia, María Antunica-Noguerol, Maia Ludmila Budziñski, Ana C Liberman and Eduardo Arzt

proinflammatory mediators in order to remove the damaging agent and restoring tissue function and structure (1) . Biologically, inflammation advances through several stages. At the cellular level there is a marked response to proinflammatory stimuli, and as a

Open access

Henrik H Thomsen, Holger J Møller, Christian Trolle, Kristian A Groth, Anne Skakkebæk, Anders Bojesen, Christian Høst and Claus H Gravholt

have been linked to states of low-grade inflammation such as diabetes, obesity, liver disease, and atherosclerosis (5, 6, 7, 8, 9, 10, 11) , underscoring the important role of macrophages in initiating and propagating these conditions. Previously, we

Open access

Karim Gariani, Geneviève Drifte, Irène Dunn-Siegrist, Jérôme Pugin and François R Jornayvaz

toxicity of lipopolysaccharide (LPS) and sepsis (28) . FGF21 can also reduce the severity of cerulein-induced pancreatitis in mice (29) , further indicating that FGF21 could modulate inflammation. These findings highlight the possible role of FGF21 as a

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Wenqi Yang, Ling Liu, Yuan Wei, Chunlu Fang, Fu Zhou, Jinbao Chen, Qinghua Han, Meifang Huang, Xuan Tan, Qiuyue Liu, Qiang Pan, Lu Zhang, Xiaojuan Lei and Liangming Li

the liver and adipose tissue ( 11 , 12 , 13 ). The beneficial effects of exercise on glucose homeostasis are well documented ( 14 ), and exercise has been shown to reduce adipogenesis, alleviate adipose tissue inflammation and improve the disturbed

Open access

Renea A Taylor, Jennifer Lo, Natasha Ascui and Matthew J Watt

associated metabolic and endocrine co-morbidities including increased visceral adipose tissue deposition, glucose intolerance, mild hyperinsulinemia, dyslipidemia and subclinical inflammation. Xenograft studies that involve subcutaneous injection of

Open access

Fahim Ebrahimi, Sandrine A Urwyler, Philipp Schuetz, Beat Mueller, Luca Bernasconi, Peter Neyer, Marc Y Donath and Mirjam Christ-Crain

pathway in the development of metabolic complications and atherosclerosis is the release of pro-inflammatory cytokines from adipose tissue promoting a state of chronic low-grade inflammation ( 3 , 4 , 5 ). It has been suggested that inflammation in turn

Open access

Nikolaj Rittig, Mads Svart, Niels Jessen, Niels Møller, Holger J Møller and Henning Grønbæk

(kcal/day) 0.001 0.0004; 0.002 0.007  Ra palmitate (μmol/min) 3.3 1.8; 4.8 <0.005  pHSL/HSL 0.6 0.2; 0.9 <0.005  BHB (mmol/L) 0.004 0.001; 0.008 0.006 Inflammation  IL-6 (ng/mL) 0.0008 0.0006; 0

Open access

M A Webb, H Mani, S J Robertson, H L Waller, D R Webb, C L Edwardson, D H Bodicoat, T Yates, K Khunti and M J Davies

systemic inflammation seen within this group ( 7 , 8 ). In particular, the inflammatory cytokine IL6 has been found to be higher in women with PCOS compared with those without and further studies have reported that the higher IL6 levels directly contribute

Open access

Lars Peter Sørensen, Tina Parkner, Esben Søndergaard, Bo Martin Bibby, Holger Jon Møller and Søren Nielsen

-associated insulin resistance remain unclear, but it is well established that not only the amount, but also the distribution of excess body fat is important, and that white adipose tissue (WAT) inflammation and insulin resistance are inter-related (2) . Studies have

Open access

Simon Schimmack, Yongchao Yang, Klaus Felix, Markus Herbst, Yixiong Li, Miriam Schenk, Frank Bergmann, Thilo Hackert and Oliver Strobel

of the link between inflammation and cancer ( 22 ). Tumor-associated inflammatory cues in the tumor microenvironment, such as macrophages or tumor-associated fibroblasts and pro-inflammatory cytokines (including TNF-alpha and IL-6), contribute to