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Choline Intake as Supplement or as a Component of Eggs Increases Plasma Choline and Reduces Interleukin-6 without Modifying Plasma Cholesterol in Participants with Metabolic Syndrome.
DiBella, M, Thomas, MS, Alyousef, H, Millar, C, Blesso, C, Malysheva, O, Caudill, MA, Fernandez, ML
Nutrients. 2020;(10)
Abstract
Metabolic syndrome (MetS) is characterized by low-grade inflammation and insulin resistance, which increase the risk of heart disease. Eggs have numerous nutrients including choline, carotenoids, and fat-soluble vitamins that may protect against these conditions. Egg phosphatidylcholine (PC) is a major contributor of dietary choline in the American diet. However, uncertainty remains regarding eggs due to their high concentration of cholesterol. In this study, we evaluated the effect of two sources of choline, whole eggs (a source of PC) and a choline supplement (choline bitartrate, CB), on plasma lipids, glucose, insulin resistance, and inflammatory biomarkers. We recruited 23 subjects with MetS to participate in this randomized cross-over intervention. After a 2-week washout, with no choline intake, participants were randomly allocated to consume three eggs/day or CB (~400 mg choline/d for both) for 4 weeks. After a 3-week washout period, they were allocated to the alternate treatment. Dietary records indicated higher concentrations of vitamin E and selenium during the egg period (p < 0.01). Interestingly, there were no changes in plasma total, low density lipoprotein (LDL)- or high density lipoprotein (HDL)-cholesterol, triglycerides, or glucose, compared either to baseline or between treatments. In contrast, interleukin-6 was reduced, with both sources of choline compared to baseline, while eggs also had an effect on lowering C-reactive protein, insulin, and insulin resistance compared to baseline. This study demonstrates that in a MetS population, intake of three eggs per day does not increase plasma LDL cholesterol, and has additional benefits on biomarkers of disease compared to a choline supplement, possibly due to the presence of other antioxidants in eggs.
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Iron overload in congenital haemolytic anaemias: role of hepcidin and cytokines and predictive value of ferritin and transferrin saturation.
Barcellini, W, Zaninoni, A, Gregorini, AI, Soverini, G, Duca, L, Fattizzo, B, Giannotta, JA, Pedrotti, P, Vercellati, C, Marcello, AP, et al
British journal of haematology. 2019;(3):523-531
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Abstract
Iron overload (IO) is poorly investigated in the congenital haemolytic anaemias (CHAs), a heterogeneous group of rare inherited diseases encompassing abnormalities of the erythrocyte membrane and metabolism, and defects of the erythropoiesis. In this study we systematically evaluated routine iron parameters and cardiac and hepatic magnetic resonance imaging, together with erythropoietin, hepcidin, non-transferrin bound iron (NTBI), and cytokine serum levels in patients with different CHAs. We found that 40% of patients had a liver iron concentration (LIC) >4 mg Fe/g dry weight. Hepatic IO was associated with ferritin levels (P = 0·0025), transferrin saturation (TfSat, P = 0·002) and NTBI (P = 0·003). Moreover, ferritin >500 μg/l plus TfSat >60% was demonstrated as the best combination able to identify increased LIC, and TfSat alteration as more important in cases with discordant values. Possible confounding factors, such as transfusions, hepatic disease, metabolic syndrome and hereditary haemochromatosis-associated mutations, had negligible effects on IO. Erythropoietin and hepcidin levels were increased in CHAs compared with controls, correlating with LIC and ferritin, respectively. Regarding cytokines, γ-interferon (IFN-γ) was increased, and both interleukin 6 and IFN-γ levels positively correlated with ferritin and hepcidin levels. Overall, these findings suggest the existence of a vicious cycle between chronic haemolysis, inflammatory response and IO in CHAs.
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[Anemic syndrome in rheumatoid arthritis: Diagnostic approaches and treatment opportunities].
Grinshtein, YI, Shabalin, VV, Kusaev, VV
Terapevticheskii arkhiv. 2016;(5):107-112
Abstract
Anemia of chronic disease (ACD) is a leading cause of anemic syndrome in patients with rheumatoid arthritis (RA). Enhanced hepcidin production mainly stimulated by excess interleukin-6 levels is a key pathodgentic component of ACD (frequently known as anemia of inflammation) by causing the degradation of the transmembrane protein ferroportin, hepcidin impairs iron metabolism. On the basis of the material of recent publications the review gives present-day views on the pathodgenesis of ACD in RA, approaches to the diagnosis and differential diagnosis of ACD, especially in its concomitance with iron-deficiency anemia, as well as approaches to therapy for the type of anemic syndrome with the complex mechanism for its development.
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Effect of nutritional status and dietary patterns on human serum C-reactive protein and interleukin-6 concentrations.
Smidowicz, A, Regula, J
Advances in nutrition (Bethesda, Md.). 2015;(6):738-47
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Abstract
The inflammatory process plays an important role in the pathogenesis of many chronic diseases, such as cardiovascular diseases, diabetes mellitus type 2, and metabolic syndrome. Serum C-reactive protein (CRP) and interleukin-6 (IL-6) are widely tested inflammatory markers involved in the development of these diseases. Several studies indicate a relation between nutritional status and the concentrations of human high-sensitivity CRP and IL-6. Similarly, the role of diet in reducing inflammation and thereby modulating the risk of non-communicable diseases is supported by numerous studies. This review focuses on the effects of the selected nutrition models in humans on the concentrations of CRP and IL-6. It seems that the Mediterranean diet model is most effective in inhibiting inflammation. The Dietary Approaches to Stop Hypertension model and the plant nutrition model also have proven to be beneficial. The data on low-fat and low-carbohydrate diets are inconclusive. Comprehensive studies are necessary, taking into account the cumulative effect of dietary and other factors on the inflammatory process.
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Effects of endurance exercise training on risk components for metabolic syndrome, interleukin-6, and the exercise capacity of postmenopausal women.
Wang, CH, Chung, MH, Chan, P, Tsai, JC, Chen, FC
Geriatric nursing (New York, N.Y.). 2014;(3):212-8
Abstract
We conducted this study to investigate how an exercise program affects the risk components of metabolic syndrome (MS), serum interleukin (IL)-6 levels, and exercise capacity in postmenopausal women. A randomized clinical trial design was used. Women in an exercise group participated in a treadmill-exercise program for 12 weeks, whereas women in a control group maintained their customary lifestyle. Data on variables were collected at baseline and after 12 weeks of the study, which was completed by 46 women (mean age, 56.0 ± 7.0 y). Our results indicate endurance exercise exerted significant beneficial effects on waist circumference, serum high-density lipoprotein cholesterol (HDL-C) and IL-6 levels, and exercise capacity (all P < 0.05). The beneficial effects on IL-6 and exercise capacity were correlated with improvements in HDL-C levels (r = -0.33, P = 0.03 and r = 0.31, P = 0.04, respectively). Our results suggest that health-care providers can incorporate an exercise program in treatments to improve the health of postmenopausal women.
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The effect of vitamin-mineral supplementation on CRP and IL-6: a systemic review and meta-analysis of randomised controlled trials.
Sun, CH, Li, Y, Zhang, YB, Wang, F, Zhou, XL, Wang, F
Nutrition, metabolism, and cardiovascular diseases : NMCD. 2011;(8):576-83
Abstract
BACKGROUND AND AIMS Inflammation is regarded as a risk predictor for metabolic syndrome and atherogenesis. The objective of this study was to conduct a systematic review and a meta-analysis to confirm the effect of vitamin-mineral supplementation on cytokine levels. METHODS AND RESULTS We searched the PubMed, EMBASE and Cochrane databases up to May 2009 for randomised controlled trials regarding the effect of vitamin-mineral supplementation on C-reactive protein (CRP) and interleukin-6 (IL-6). Eighteen trials with 1747 participants for CRP and nine trials with 1037 participants for IL-6 were included, respectively. Pooled estimates and 95% confidence intervals (CIs) were calculated by fixed- or random-effects model. No significant differences were observed for CRP and IL-6 reduction between the subjects with vitamin-mineral supplementation and placebo control. A dose-dependent manner for different body mass index (BMI) subgroups in CRP analysis was observed (weighted mean difference (WMD), -0.057; 95%CI: -0.753 to 0.639 for BMI<25; WMD, -0.426; 95%CI: -0.930 to 0.079 for 25 ≤ BMI < 30; WMD, -0.491; 95%CI: -1.407 to 0.424 for BMI ≥ 30). However, no significance was detected in meta-regression (-0.046, 95%CI: -0.135 to 0.044). Moreover, the best effect for reduction in CRP levels in a supplementation duration of 4 weeks-6 months (WMD, -0.449; 95%CI: -1.004 to 0.106) was observed compared with supplementation duration less than 4 weeks (WMD, -0.137; 95%CI, -0.816 to 0.541) and more than 6 months (WMD, -0.389; 95%CI, -1.034 to 0.257) without statistical significance (P = 0.059). CONCLUSION No statistically significant evidences for the potential dose-dependent manner of BMI and best supplement duration were detected in this study. Large and well-designed studies are recommended to confirm this conclusion.
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Fenofibrate reduces systemic inflammation markers independent of its effects on lipid and glucose metabolism in patients with the metabolic syndrome.
Belfort, R, Berria, R, Cornell, J, Cusi, K
The Journal of clinical endocrinology and metabolism. 2010;(2):829-36
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Abstract
CONTEXT Fenofibrate is a peroxisome proliferator-activated receptor alpha agonist widely used in clinical practice, but its mechanism of action is incompletely understood. OBJECTIVE The aim of the study was to assess whether improvement in subclinical inflammation or glucose metabolism contributes to its antiatherogenic effects in insulin-resistant subjects with the metabolic syndrome (MetS). DESIGN AND SETTING We conducted a randomized, double-blind, placebo-controlled study in the research unit at an academic center. PATIENTS We studied 25 nondiabetic insulin-resistant MetS subjects. INTERVENTION(S): We administered fenofibrate (200 mg/d) and placebo for 12 wk. MAIN OUTCOME MEASURES Before and after treatment, we measured plasma lipids/apolipoproteins, inflammatory markers (high-sensitivity C-reactive protein, IL-6, intercellular adhesion molecule/vascular cell adhesion molecule), adipocytokines (adiponectin, TNFalpha, leptin), and insulin secretion (oral glucose tolerance test). We also assessed adipose tissue, hepatic and peripheral (muscle) insulin resistance fasting and during a euglycemic insulin clamp with (3)H glucose and (14)C palmitate infusion combined with indirect calorimetry. RESULTS Subjects displayed severe insulin resistance and systemic inflammation. Fenofibrate significantly reduced plasma triglyceride, apolipoprotein (apo) CII, apo CIII, and apo E (all P < 0.01), with a modest increase in high-density lipoprotein-cholesterol (+12%; P = 0.06). Fenofibrate markedly decreased plasma high-sensitivity C-reactive protein by 49.5 +/- 8% (P = 0.005) and IL-6 by 29.8 +/- 7% (P = 0.03) vs. placebo. However, neither insulin secretion nor adipose tissue, hepatic or muscle insulin sensitivity or glucose/lipid oxidation improved with treatment. Adiponectin and TNF-alpha levels were also unchanged. Improvement in plasma markers of vascular/systemic inflammation was dissociated from changes in triglyceride/high-density lipoprotein-cholesterol, apo CII/CIII, or free fatty acid concentrations or insulin secretion/insulin sensitivity. CONCLUSIONS In subjects with the MetS, fenofibrate reduces systemic inflammation independent of improvements in lipoprotein metabolism and without changing insulin sensitivity. This suggests a direct peroxisome proliferator-activated receptor alpha-mediated effect of fenofibrate on inflammatory pathways, which may be important for the prevention of CVD in high-risk patients.