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Plasma metabolomics profiles suggest beneficial effects of a low-glycemic load dietary pattern on inflammation and energy metabolism.
Navarro, SL, Tarkhan, A, Shojaie, A, Randolph, TW, Gu, H, Djukovic, D, Osterbauer, KJ, Hullar, MA, Kratz, M, Neuhouser, ML, et al
The American journal of clinical nutrition. 2019;(4):984-992
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Abstract
BACKGROUND Low-glycemic load dietary patterns, characterized by consumption of whole grains, legumes, fruits, and vegetables, are associated with reduced risk of several chronic diseases. METHODS Using samples from a randomized, controlled, crossover feeding trial, we evaluated the effects on metabolic profiles of a low-glycemic whole-grain dietary pattern (WG) compared with a dietary pattern high in refined grains and added sugars (RG) for 28 d. LC-MS-based targeted metabolomics analysis was performed on fasting plasma samples from 80 healthy participants (n = 40 men, n = 40 women) aged 18-45 y. Linear mixed models were used to evaluate differences in response between diets for individual metabolites. Kyoto Encyclopedia of Genes and Genomes (KEGG)-defined pathways and 2 novel data-driven analyses were conducted to consider differences at the pathway level. RESULTS There were 121 metabolites with detectable signal in >98% of all plasma samples. Eighteen metabolites were significantly different between diets at day 28 [false discovery rate (FDR) < 0.05]. Inositol, hydroxyphenylpyruvate, citrulline, ornithine, 13-hydroxyoctadecadienoic acid, glutamine, and oxaloacetate were higher after the WG diet than after the RG diet, whereas melatonin, betaine, creatine, acetylcholine, aspartate, hydroxyproline, methylhistidine, tryptophan, cystamine, carnitine, and trimethylamine were lower. Analyses using KEGG-defined pathways revealed statistically significant differences in tryptophan metabolism between diets, with kynurenine and melatonin positively associated with serum C-reactive protein concentrations. Novel data-driven methods at the metabolite and network levels found correlations among metabolites involved in branched-chain amino acid (BCAA) degradation, trimethylamine-N-oxide production, and β oxidation of fatty acids (FDR < 0.1) that differed between diets, with more favorable metabolic profiles detected after the WG diet. Higher BCAAs and trimethylamine were positively associated with homeostasis model assessment-insulin resistance. CONCLUSIONS These exploratory metabolomics results support beneficial effects of a low-glycemic load dietary pattern characterized by whole grains, legumes, fruits, and vegetables, compared with a diet high in refined grains and added sugars on inflammation and energy metabolism pathways. This trial was registered at clinicaltrials.gov as NCT00622661.
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Autologous fat transplantation alters gene expression patterns related to inflammation and hypoxia in the irradiated human breast.
Lindegren, A, Schultz, I, Sinha, I, Cheung, L, Khan, AA, Tekle, M, Wickman, M, Halle, M
The British journal of surgery. 2019;(5):563-573
Abstract
BACKGROUND Radiation-induced fibrosis, an adverse effect of breast cancer treatment, is associated with functional and cosmetic impairment as well as surgical complications. Clinical reports suggest improvement following autologous fat transplantation, but the mechanisms underlying this effect are unknown. A global gene expression analysis was undertaken to identify genetic pathways dysregulated by radiation and evaluate the impact of autologous fat transplantation on gene expression. METHODS Adipose tissue biopsies were taken synchronously from irradiated and contralateral non-irradiated breasts, before and 1 year after autologous fat transplantation. Whole-genome gene expression analyses were performed, and Hallmark gene set analysis used to explore the effect of radiotherapy and autologous fat transplantation on gene expression. RESULTS Forty microarrays were analysed, using bilateral biopsies taken from ten patients before and after autologous fat transplantation. Forty-five pathways were identified among the 3000 most dysregulated transcripts after radiotherapy in irradiated compared with non-irradiated breast (P ≤ 0·023; false discovery rate (FDR) no higher than 0·026). After autologous fat transplantation, 575 of the 3000 genes were again altered. Thirteen pathways (P ≤ 0·013; FDR 0·050 or less) were identified; the top two canonical pathways were interferon-γ response and hypoxia. Correlative immunohistochemistry showed increased macrophage recruitment in irradiated tissues. CONCLUSION The present findings contribute to understanding of how autologous fat transplantation can ameliorate radiation-induced fibrosis. This further supports the use of autologous fat transplantation in the treatment of radiation-induced fibrosis. Surgical relevance Clinical studies have indicated that autologous fat transplantation (AFT) stimulates regression of chronic inflammation and fibrosis caused by radiotherapy in skin and subcutaneous fat. However, there is a paucity of biological evidence and the underlying processes are poorly understood. Human data are scarce, whereas experimental studies have focused mainly either on the effect of irradiation or AFT alone. The present results indicate that radiotherapy causes dysregulated gene expression in fibrosis-related pathways in adipose tissues in humans. They also show that AFT can cause a reversal of this, with several dysregulated genes returning to nearly normal expression levels. The study provides biological evidence for the impact of AFT on radiation-induced dysregulated gene expression in humans. It supports the use of AFT in the treatment of radiation-induced fibrosis, associated with severe morbidity and surgical challenges.
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The effects of vitamin D supplementation on mental health, and biomarkers of inflammation and oxidative stress in patients with psychiatric disorders: A systematic review and meta-analysis of randomized controlled trials.
Jamilian, H, Amirani, E, Milajerdi, A, Kolahdooz, F, Mirzaei, H, Zaroudi, M, Ghaderi, A, Asemi, Z
Progress in neuro-psychopharmacology & biological psychiatry. 2019;:109651
Abstract
BACKGROUND In the current meta-analysis of randomized controlled trials (RCTs), the effects of vitamin D supplementation on mental health, and biomarkers of inflammation and oxidative stress in patients with psychiatric disorders are assessed. METHODS The following databases were search up to March 2019: MEDLINE, EMBASE, Web of Science, and Cochrane Central Register of Controlled Trials. The quality of the relevant extracted data was assessed according to the Cochrane risk of bias tool. Data were pooled by the use of the inverse variance method and expressed as mean difference with 95% Confidence Intervals (95% CI). RESULTS Eleven effect sizes from nine studies were included in the final analyses. A pooled analysis of 9 effect sizes showed a significant reduction in Beck Depression Inventory (BDI) score following supplementation with vitamin D [weighted mean difference (WMD): -3.91; 95% CI: -5.15 -2.66), I2= 85.9%]. Combining data from two available studies on the effects of vitamin D supplementation on Pittsburgh Sleep Quality Index (PSQI) also revealed a significant reduction in this score following the intervention (WMD: -1.78; 95% CI: -2.28, -1.28). In addition, there were significant increase in glutathione (GSH) through 3 studies (WMD: 180.70; 95% CI: 6.76, 354.64), and in total antioxidant capacity (TAC) through 3 studies (WMD: 90.09; 95% CI: 56.36, 123.82) after vitamin D supplementation. Combining data from five studies, we found a significant reduction in C-reactive protein (CRP) concentrations after vitamin D supplementation (WMD: -1.74; 95% CI: -2.82, -0.66). CONCLUSIONS Overall, the current meta-analysis demonstrated that taking vitamin D supplements among patients with psychiatric disorders had beneficial effects on BDI, PSQI, GSH, TAC and CRP levels, but did not affect other biomarkers of inflammation and oxidative stress.
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Neoplasia and intraocular inflammation: From masquerade syndromes to immunotherapy-induced uveitis.
Touhami, S, Audo, I, Terrada, C, Gaudric, A, LeHoang, P, Touitou, V, Bodaghi, B
Progress in retinal and eye research. 2019;:100761
Abstract
Masquerade syndromes represent a large set of ophthalmological entities that mimic inflammatory conditions. Any delay in their diagnosis may be correlated with systemic dissemination or worsening of the causal disease and, therefore, with poor prognosis. One of the disadvantages of the new potent treatments of uveitis is the delay that they can induce in the diagnosis of neoplastic intraocular infiltrations. Thorough and careful clinical examination of all patients referred for uveitis, especially when they are Caucasian, over 50 years of age, and with posterior segment involvement, is of paramount importance in this context. Ancillary investigations and often-invasive histo-pathologic evaluation of tissue specimens or ocular fluids are regularly required in these situations. The most common masquerade syndrome is primary vitreoretinal lymphoma (PVRL). New molecular diagnostic tools may be helpful in challenging cases lacking cytological confirmation. Therapeutic strategies targeting tumoral cells in the eye and also in the central nervous system can improve the life expectancy of affected patients. In this review, we discuss diagnostic strategies and current therapies in PVRL and provide an overview of other conditions that can mimic primary ocular inflammation, especially in the field of oncology and its new therapeutic armamentarium.
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Dietary Inflammatory Potential and the Risk of Neurodegenerative Diseases in Adults.
Kheirouri, S, Alizadeh, M
Epidemiologic reviews. 2019;(1):109-120
Abstract
Nutrition and diet have been suggested to enhance or inhibit cognitive performance and the risk of several neurodegenerative diseases. We conducted a systematic review to elucidate the relationship between the inflammatory capacity of a person's diet and the risk of incident neurodegenerative diseases. We searched major medical databases for articles published through June 30, 2018. Original, full-text, English-language articles on studies with human participants which investigated the link between dietary inflammatory potential and risk of developing neurodegenerative diseases were included. Duplicate and irrelevant studies were removed, and data were compiled through critical analysis. Initially, 457 articles were collected via the searching method, of which 196 studies remained after removal of duplicates. Fourteen articles were screened and found to be relevant to the scope of the review. After critical analysis, 10 were included in the final review. In all studies but one, a higher dietary inflammatory index (DII) was related to higher risk of developing neurodegenerative disease symptoms, including memory and cognition decline and multiple sclerosis. Of 3 studies that assessed the association of DII with levels of circulating inflammation markers, 2 indicated that DII was positively correlated with inflammatory marker levels. Low literacy, an unhealthy lifestyle, and individual nutritional status were the factors involved in a diet with inflammatory potential. These findings enhance confidence that DII is an appropriate tool for measurement of dietary inflammatory potential and validate the role of diets with inflammatory potential in the pathophysiology of neurodegenerative diseases. DII may be correlated with levels of circulating inflammatory markers.
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Effect of vitamin D supplementation along with weight loss diet on meta-inflammation and fat mass in obese subjects with vitamin D deficiency: A double-blind placebo-controlled randomized clinical trial.
Lotfi-Dizaji, L, Mahboob, S, Aliashrafi, S, Vaghef-Mehrabany, E, Ebrahimi-Mameghani, M, Morovati, A
Clinical endocrinology. 2019;(1):94-101
Abstract
BACKGROUND & AIMS Low serum 25-hydroxyvitamin D (25OHD) is common in obese people. Obesity is associated with a state of low-grade inflammation (meta-inflammation). There is an increasing evidence indicating that vitamin D has anti-adipogenic activity and immunoregulatory effect. This study aimed to assess the effect of vitamin D supplementation on meta-inflammation and fat mass in obese subjects with vitamin D deficiency. MATERIALS AND METHODS In this double-blind placebo-controlled randomized clinical trial, 44 obese subjects with vitamin D deficiency (25OHD < 50 nmol/L) were assigned into vitamin D (a weight reduction diet + bolus weekly dose of 50 000 IU vitamin D) or placebo group (weight reduction diet + edible paraffin weekly) for 12 weeks. Weight, fat mass and serum levels of 25OHD, calcium, parathyroid hormone (PTH), monocyte chemoattractant protein-1 (MCP-1), interleukin-1β (IL-1β) and Toll-like receptor 4 (TLR4) were assessed before and after the intervention. RESULTS Vitamin D supplementation resulted in significant increase of serum 25OHD level (P < 0.001), and significant decrease in PTH (P < 0.001), MCP-1 (P < 0.05), IL-1β (P < 0.05) and TLR-4 (P < 0.05); compared to the baseline values in vitamin D group. Weight, BMI and fat mass decreased in both groups (P < 0.05). Between the groups, there were significant decrease in weight, fat mass, serum MCP-1 and PTH concentrations and significant increase in serum 25OHD concentrations after intervention with vitamin D supplementation compared to placebo (P < 0.05). CONCLUSIONS Improvement in vitamin D status in obese subjects with vitamin D deficiency in combination with weight loss diet resulted in weight, fat mass and MCP-1 decrease. Weight loss and vitamin D supplementation may act synergistically to reduce levels of meta-inflammation.
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NOD-like receptor signaling in inflammation-associated cancers: From functions to targeted therapies.
Liu, P, Lu, Z, Liu, L, Li, R, Liang, Z, Shen, M, Xu, H, Ren, D, Ji, M, Yuan, S, et al
Phytomedicine : international journal of phytotherapy and phytopharmacology. 2019;:152925
Abstract
BACKGROUND Recently, many studies have reported that some botanicals and natural products were able to regulate NOD-like receptor signaling. NOD-like receptors (NLRs) have been established as crucial regulators in inflammation-associated tumorigenesis, angiogenesis, cancer cell stemness and chemoresistance. NLRs specifically sense pathogen-associated molecular patterns and respond by activating other signaling regulators, including Rip2 kinase, NF-κB, MAPK and ASC/caspase-1, leading to the secretion of various cytokines. PURPOSE The aim of this article is to review the molecular mechanisms of NOD-like receptor signaling in inflammation-associated cancers and the NLRs-targeted botanicals and synthetic small molecules in cancer intervention. RESULTS Aberrant activation of NLRs occurs in various cancers, orchestrating the tissue microenvironment and potentiating neoplastic risk. Blocking NLR inflammasome activation by botanicals or synthetic small molecules may be a valuable way to prevent cancer progression. Moreover, due to the roles of NLRs in regulating cytokine production, NLR signaling may be correlated with senescence-associated secretory phenotype. CONCLUSION In this review, we discuss how NLR signaling is involved in inflammation-associated cancers, and highlight the NLR-targeted botanicals and synthetic small molecules in cancer intervention.
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Cholesterol and inflammatory risk: Insights from secondary and primary prevention.
Stock, JK
Atherosclerosis. 2019;:192-193
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Enzymatic hydrolysates obtained from Trametes versicolor polysaccharopeptides protect human skin keratinocyte against AAPH-induced oxidative stress and inflammatory.
Chou, CH, Tsai, MS, Lu, HY, Chang, CK, Cheng, KC, Jhan, MH, Hsieh, CW
Journal of cosmetic dermatology. 2019;(6):2011-2018
Abstract
BACKGROUND Polysaccharopeptides (PSPs) extracted from Trametes versicolor show antitumor, anti-inflammatory, and immunomodulation effects. According to our previous report, the enzymatic hydrolysates obtained from T versicolor PSPs by 80 U/mL β-1,3-D-glucanase (PSPs-EH80) did not change the functional groups of PSPs but enhanced their antioxidative activities. However, the mechanism elevating the antioxidant and anti-inflammatory effect of PSPs-EH80 is not clear. AIMS This research focused on the protective mechanism(s) of PSPs-EH80 against free radical and 2,2'-azobis (2-amidinopropane) dihydrochloride (AAPH)-induced oxidative damage in human keratinocyte (HaCaT) cells. METHODS We evaluated the anti-inflammatory potential of PSPs-EH80 by assessing its free radical-induced oxidative damage. Using the HaCaT cell as the experimental system, we tested the protective effects of PSPs-EH80 on a model of AAPH-induced cellular oxidative damage through the assessment of cell survival rate. Heme oxygenase 1 (HO-1), nuclear factor erythroid 2-related factor 2 (Nrf2), cyclooxygenase-2 (COX-2), nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase were determined using MTT assays and Western blotting. RESULTS We demonstrated that PSPs-EH80 significantly enhanced keratinocyte viability, and augmented the antioxidant HO-1 expressions through upregulation of the Nrf2, compared with PSPs. Furthermore, PSPs-EH80 significantly reduced AAPH-induced COX-2 expressions through downregulation of the ERK, p38, and NF-κB signaling pathways. CONCLUSION The PSPs-EH80 exhibits a stronger antioxidant and anti-inflammatory capacity than PSPs. Therefore, PSPs-EH80 could be effective for attenuating free radical-induced oxidative damage in human skin and can be applied widely in the fields of cosmetics and medicine.
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Effects of propolis and melatonin on oxidative stress, inflammation, and clinical status in patients with primary sepsis: Study protocol and review on previous studies.
Pahlavani, N, Sedaghat, A, Bagheri Moghaddam, A, Mazloumi Kiapey, SS, Gholizadeh Navashenaq, J, Jarahi, L, Reazvani, R, Norouzy, A, Nematy, M, Safarian, M, et al
Clinical nutrition ESPEN. 2019;:125-131
Abstract
BACKGROUND Previous studies have explored the anti-inflammatory, anti-infection and oxidative stress reduction effects of propolis and melatonin in experimental studies. However, there are no studies at present exploring the effects of propolis and melatonin in patients with primary sepsis. The present study aims to evaluate the potential effects of propolis and melatonin as a pharmaceutical agent in patients with primary sepsis. METHODS/DESIGN The study will be conducted as a randomized controlled clinical trial at the Imamreza hospital. Patients with primary sepsis, in four equal groups, will be recruited for the study. The treatment drugs are propolis and melatonin and the placebo. The following primary and secondary outcome measures will be evaluated: APACHE II Score, SOFA score, NUTRIC score, inflammatory factors, and oxidative stress markers. DISCUSSION We describe the protocol for a clinical trial design evaluating the effects of simultaneous administration of propolis and melatonin in patients with primary sepsis. The result of the present study, positive or negative, should provide a step change in the evidence guiding current and future policies regarding the use of propolis and melatonin as an auxiliary treatment in patients with primary sepsis. TRIAL REGISTRATION Iranian Registry of Clinical Trials: IRCT20181025041460N1. Registered on 6 November 2018.