TY - JOUR A1 - Haß, Ulrike A1 - Herpich, Catrin A1 - Norman, Kristina T1 - Anti-Inflammatory Diets and Fatigue JF - Nutrients N2 - Accumulating data indicates a link between a pro-inflammatory status and occurrence of chronic disease-related fatigue. The questions are whether the observed inflammatory profile can be (a) improved by anti-inflammatory diets, and (b) if this improvement can in turn be translated into a significant fatigue reduction. The aim of this narrative review was to investigate the effect of anti-inflammatory nutrients, foods, and diets on inflammatory markers and fatigue in various patient populations. Next to observational and epidemiological studies, a total of 21 human trials have been evaluated in this work. Current available research is indicative, rather than evident, regarding the effectiveness of individuals’ use of single nutrients with anti-inflammatory and fatigue-reducing effects. In contrast, clinical studies demonstrate that a balanced diet with whole grains high in fibers, polyphenol-rich vegetables, and omega-3 fatty acid-rich foods might be able to improve disease-related fatigue symptoms. Nonetheless, further research is needed to clarify conflicting results in the literature and substantiate the promising results from human trials on fatigue. KW - chronic fatigue KW - cancer KW - fatigue reduction diet KW - probiotics KW - polyphenols KW - omega-3 fatty acids KW - anti-inflammatory nutrition KW - cytokines KW - inflammation KW - myalgic encephalomyelitis Y1 - 2019 U6 - https://doi.org/10.3390/nu11102315 SN - 2072-6643 VL - 11 IS - 10 PB - MDPI CY - Basel ER - TY - JOUR A1 - Manowsky, Julia A1 - Camargo, Rodolfo Gonzalez A1 - Kipp, Anna Patricia A1 - Henkel, Janin A1 - Püschel, Gerhard Paul T1 - Insulin-induced cytokine production in macrophages causes insulin resistance in hepatocytes JF - American journal of physiology : Endocrinology and metabolism N2 - Overweight and obesity are associated with hyperinsulinemia, insulin resistance, and a low-grade inflammation. Although hyperinsulinemia is generally thought to result from an attempt of the beta-cell to compensate for insulin resistance, there is evidence that hyperinsulinaemia itself may contribute to the development of insulin resistance and possibly the low-grade inflammation. To test this hypothesis, U937 macrophages were exposed to insulin. In these cells, insulin induced expression of the proinflammatory cytokines IL-1 beta, IL-8, CCL2, and OSM. The insulin-elicited induction of IL-1 beta was independent of the presence of endotoxin and most likely mediated by an insulin-dependent activation of NF-kappa B. Supernatants of the insulin-treated U937 macrophages rendered primary cultures of rat hepatocytes insulin resistant; they attenuated the insulin-dependent induction of glucokinase by 50%. The cytokines contained in the supernatants of insulin-treated U937 macrophages activated ERK1/2 and IKK beta, resulting in an inhibitory serine phosphorylation of the insulin receptor substrate. In addition, STAT3 was activated and SOCS3 induced, further contributing to the interruption of the insulin receptor signal chain in hepatocytes. These results indicate that hyperinsulinemia per se might contribute to the low-grade inflammation prevailing in overweight and obese patients and thereby promote the development of insulin resistance particularly in the liver, because the insulin concentration in the portal circulation is much higher than in all other tissues. KW - metabolic syndrome KW - type 2 diabetes KW - inflammation KW - macrophage KW - insulin KW - cytokines Y1 - 2016 U6 - https://doi.org/10.1152/ajpendo.00427.2015 SN - 0193-1849 SN - 1522-1555 VL - 310 SP - E938 EP - E946 PB - American Chemical Society CY - Bethesda ER - TY - JOUR A1 - Zwaag, Jelle A1 - Horst, Rob ter A1 - Blaženović, Ivana A1 - Stößel, Daniel A1 - Ratter, Jacqueline A1 - Worseck, Josephine M. A1 - Schauer, Nicolas A1 - Stienstra, Rinke A1 - Netea, Mihai G. A1 - Jahn, Dieter A1 - Pickkers, Peter A1 - Kox, Matthijs T1 - Involvement of lactate and pyruvate in the anti-inflammatory effects exerted by voluntary activation of the sympathetic nervous system JF - Metabolites N2 - We recently demonstrated that the sympathetic nervous system can be voluntarily activated following a training program consisting of cold exposure, breathing exercises, and meditation. This resulted in profound attenuation of the systemic inflammatory response elicited by lipopolysaccharide (LPS) administration. Herein, we assessed whether this training program affects the plasma metabolome and if these changes are linked to the immunomodulatory effects observed. A total of 224 metabolites were identified in plasma obtained from 24 healthy male volunteers at six timepoints, of which 98 were significantly altered following LPS administration. Effects of the training program were most prominent shortly after initiation of the acquired breathing exercises but prior to LPS administration, and point towards increased activation of the Cori cycle. Elevated concentrations of lactate and pyruvate in trained individuals correlated with enhanced levels of anti-inflammatory interleukin (IL)-10. In vitro validation experiments revealed that co-incubation with lactate and pyruvate enhances IL-10 production and attenuates the release of pro-inflammatory IL-1 beta and IL-6 by LPS-stimulated leukocytes. Our results demonstrate that practicing the breathing exercises acquired during the training program results in increased activity of the Cori cycle. Furthermore, this work uncovers an important role of lactate and pyruvate in the anti-inflammatory phenotype observed in trained subjects. KW - metabolomics KW - LPS KW - endotoxin KW - pyruvate KW - lactate KW - cytokines KW - inflammation KW - human endotoxemia KW - cori cycle KW - warburg effect Y1 - 2020 U6 - https://doi.org/10.3390/metabo10040148 SN - 2218-1989 VL - 10 IS - 4 SP - 1 EP - 18 PB - MDPI CY - Basel ER - TY - JOUR A1 - Kessler, Katharina A1 - Hornemann, Silke A1 - Rudovich, Natalia A1 - Weber, Daniela A1 - Grune, Tilman A1 - Kramer, Achim A1 - Pfeiffer, Andreas F. H. A1 - Pivovarova-Ramich, Olga T1 - Saliva samples as a tool to study the effect of meal timing on metabolic and inflammatory biomarkers JF - Nutrients N2 - Meal timing affects metabolic regulation in humans. Most studies use blood samples fortheir investigations. Saliva, although easily available and non-invasive, seems to be rarely used forchrononutritional studies. In this pilot study, we tested if saliva samples could be used to studythe effect of timing of carbohydrate and fat intake on metabolic rhythms. In this cross-over trial, 29 nonobese men were randomized to two isocaloric 4-week diets: (1) carbohydrate-rich meals until13:30 and high-fat meals between 16:30 and 22:00 or (2) the inverse order of meals. Stimulated salivasamples were collected every 4 h for 24 h at the end of each intervention, and levels of hormones andinflammatory biomarkers were assessed in saliva and blood. Cortisol, melatonin, resistin, adiponectin, interleukin-6 and MCP-1 demonstrated distinct diurnal variations, mirroring daytime reports inblood and showing significant correlations with blood levels. The rhythm patterns were similar forboth diets, indicating that timing of carbohydrate and fat intake has a minimal effect on metabolicand inflammatory biomarkers in saliva. Our study revealed that saliva is a promising tool for thenon-invasive assessment of metabolic rhythms in chrononutritional studies, but standardisation of sample collection is needed in out-of-lab studies. KW - meal timing KW - saliva KW - circadian clock KW - adiponectin KW - resistin KW - visfatin KW - insulin KW - melatonin KW - cortisol KW - cytokines Y1 - 2020 U6 - https://doi.org/10.3390/nu12020340 SN - 2072-6643 IS - 2 SP - 1 EP - 12 PB - MDPI CY - Basel ER - TY - JOUR A1 - Szymanski, Kolja V. A1 - Tönnies, Mario A1 - Becher, Anne A1 - Fatykhova, Diana A1 - N'Guessan, Philippe D. A1 - Gutbier, Birgitt A1 - Klauschen, Frederick A1 - Neuschäfer-Rube, Frank A1 - Schneider, Paul A1 - Rückert, Jens A1 - Neudecker, Jens A1 - Bauer, Torsten T. A1 - Dalhoff, Klaus A1 - Droemann, Daniel A1 - Gruber, Achim D. A1 - Kershaw, Olivia A1 - Temmesfeld-Wollbrueck, Bettina A1 - Suttorp, Norbert A1 - Hippenstiel, Stefan A1 - Hocke, Andreas C. T1 - Streptococcus pneumoniae-induced regulation of cyclooxygenase-2 in human lung tissue JF - The European respiratory journal : official journal of the European Society for Clinical Respiratory Physiology N2 - The majority of cases of community-acquired pneumonia are caused by Streptococcus pneumoniae and most studies on pneumococcal host interaction are based on cell culture or animal experiments. Thus, little is known about infections in human lung tissue. Cyclooxygenase-2 and its metabolites play an important regulatory role in lung inflammation. Therefore, we established a pneumococcal infection model on human lung tissue demonstrating mitogen-activated protein kinase (MAPK)-dependent induction of cyclooxygenase-2 and its related metabolites. In addition to alveolar macrophages and the vascular endothelium, cyclooxygenase-2 was upregulated in alveolar type II but not type I epithelial cells, which was confirmed in lungs of patients suffering from acute pneumonia. Moreover, we demonstrated the expression profile of all four E prostanoid receptors at the mRNA level and showed functionality of the E prostanoid(4) receptor by cyclic adenosine monophosphate production. Additionally, in comparison to previous studies, cyclooxygenase-2/prostaglandin E-2 related pro- and anti-inflammatory mediator regulation was partly confirmed in human lung tissue after pneumococcal infection. Overall, cell type-specific and MAPK-dependent cyclooxygenase-2 expression and prostaglandin E-2 formation in human lung tissue may play an important role in the early phase of pneumococcal infections. KW - Alveolar epithelial cells KW - cytokines KW - inflammation KW - lung infection KW - pneumonia KW - prostaglandins Y1 - 2012 U6 - https://doi.org/10.1183/09031936.00186911 SN - 0903-1936 VL - 40 IS - 6 SP - 1458 EP - 1467 PB - European Respiratory Society CY - Sheffield ER -