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      Dietary Intake of Free Sugars is Associated with Disease Activity and Dyslipidemia in Systemic Lupus Erythematosus Patients

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          Abstract

          Diet has been closely associated with inflammatory autoimmune diseases, including systemic lupus erythematosus (SLE). Importantly, the consumption of dietary sugars has been positively linked to elevated levels of some inflammation markers, but the potential role of their consumption on the prognosis of autoimmune diseases has not yet been examined. The aim of this study was to evaluate the association between the dietary intake of free sugars and clinical parameters and cardiovascular (CVD) risk markers in patients with SLE. A cross-sectional study including a total of 193 patients with SLE (aged 48.25 ± 12.54 years) was conducted. The SLE Disease Activity Index (SLEDAI-2K) and the SDI Damage Index were used to asses disease activity and disease-related damage, respectively. Levels of C-reactive protein (CRP; mg/dL), homocysteine (Hcy; µmol/L), anti-double stranded DNA antibodies (anti-dsDNA) (IU/mL), complement C3 (mg/dL), and complement C4 (mg/dL), among other biochemical markers, were measured. The main factors we considered as risk factors for CVD were obesity, diabetes mellitus, hypertension, and blood lipids. The dietary-intrinsic sugar and added-sugar content participants consumed were obtained via a 24-h patient diary. Significant differences were observed in dietary sugar intake between patients with active and inactive SLE (in grams: 28.31 ± 24.43 vs. 38.71 ± 28.87; p = 0.035) and free sugar intake (as a percentage: 6.36 ± 4.82 vs. 8.60 ± 5.51; p = 0.020). Linear regression analysis revealed a significant association between free sugars intake (by gram or percentage) and the number of complications (β (95% CI) = 0.009 (0.001, 0.0018), p = 0.033)); (β (95% CI) = 0.046 (0.008, 0.084), p = 0.018)), and SLEDAI (β (95% CI) = 0.017 (0.001, 0.034), p = 0.043)); (β (95% CI) = 0.086 (0.011, 0.161), p = 0.024)) after adjusting for covariates. Free sugars (g and %) were also associated with the presence of dyslipidaemia (β (95% CI) = −0.003 (−0.005, 0.000), p = 0.024)) and (β (95% CI) = −0.015 (−0.028, −0.002), p = 0.021)). Our findings suggest that a higher consumption of free sugars might negatively impact the activity and complications of SLE. However, future longitudinal research on SLE patients, including dietary intervention trials, are necessary to corroborate these preliminary data.

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          Sweetened beverage consumption, incident coronary heart disease, and biomarkers of risk in men.

          Sugar-sweetened beverage consumption is associated with weight gain and risk of type 2 diabetes mellitus. Few studies have tested for a relationship with coronary heart disease (CHD) or intermediate biomarkers. The role of artificially sweetened beverages is also unclear. We performed an analysis of the Health Professionals Follow-Up Study, a prospective cohort study including 42 883 men. Associations of cumulatively averaged sugar-sweetened (eg, sodas) and artificially sweetened (eg, diet sodas) beverage intake with incident fatal and nonfatal CHD (myocardial infarction) were examined with proportional hazard models. There were 3683 CHD cases over 22 years of follow-up. Participants in the top quartile of sugar-sweetened beverage intake had a 20% higher relative risk of CHD than those in the bottom quartile (relative risk=1.20; 95% confidence interval, 1.09-1.33; P for trend <0.01) after adjustment for age, smoking, physical activity, alcohol, multivitamins, family history, diet quality, energy intake, body mass index, pre-enrollment weight change, and dieting. Artificially sweetened beverage consumption was not significantly associated with CHD (multivariate relative risk=1.02; 95% confidence interval, 0.93-1.12; P for trend=0.28). Adjustment for self-reported high cholesterol, high triglycerides, high blood pressure, and diagnosed type 2 diabetes mellitus slightly attenuated these associations. Intake of sugar-sweetened but not artificially sweetened beverages was significantly associated with increased plasma triglycerides, C-reactive protein, interleukin-6, and tumor necrosis factor receptors 1 and 2 and decreased high-density lipoprotein, lipoprotein(a), and leptin (P<0.02). Consumption of sugar-sweetened beverages was associated with increased risk of CHD and some adverse changes in lipids, inflammatory factors, and leptin. Artificially sweetened beverage intake was not associated with CHD risk or biomarkers.
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            High-Glucose or -Fructose Diet Cause Changes of the Gut Microbiota and Metabolic Disorders in Mice without Body Weight Change

            High fat diet-induced changes in gut microbiota have been linked to intestinal permeability and metabolic endotoxemia, which is related to metabolic disorders. However, the influence of a high-glucose (HGD) or high-fructose (HFrD) diet on gut microbiota is largely unknown. We performed changes of gut microbiota in HGD- or HFrD-fed C57BL/6J mice by 16S rRNA analysis. Gut microbiota-derived endotoxin-induced metabolic disorders were evaluated by glucose and insulin tolerance test, gut permeability, Western blot and histological analysis. We found that the HGD and HFrD groups had comparatively higher blood glucose and endotoxin levels, fat mass, dyslipidemia, and glucose intolerance without changes in bodyweight. The HGD- and HFrD-fed mice lost gut microbial diversity, characterized by a lower proportion of Bacteroidetes and a markedly increased proportion of Proteobacteria. Moreover, the HGD and HFrD groups had increased gut permeability due to alterations to the tight junction proteins caused by gut inflammation. Hepatic inflammation and lipid accumulation were also markedly increased in the HGD and HFrD groups. High levels of glucose or fructose in the diet regulate the gut microbiota and increase intestinal permeability, which precedes the development of metabolic endotoxemia, inflammation, and lipid accumulation, ultimately leading to hepatic steatosis and normal-weight obesity.
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              Lipotoxicity in nonalcoholic fatty liver disease: not all lipids are created equal.

              Nonalcoholic fatty liver disease (NAFLD) is currently the most common form of chronic liver disease affecting both adults and children in the USA and many other parts of the world. NAFLD encompasses a wide spectrum of conditions associated with the overaccumulation of lipids in the liver, ranging from steatosis to nonalcoholic steatohepatitis, to cirrhosis and its feared complications of portal hypertension, liver failure and hepatocellular carcinoma. In this article, we will focus on the growing evidence linking changes in hepatic lipid metabolism and accumulation of specific lipid types in the liver with hepatocellular damage, inflammation and apoptosis, resulting in disease progression to the more serious forms of this condition.
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                Author and article information

                Journal
                Nutrients
                Nutrients
                nutrients
                Nutrients
                MDPI
                2072-6643
                15 April 2020
                April 2020
                : 12
                : 4
                : 1094
                Affiliations
                [1 ]Department of Nursing, Health Sciences Faculty, University of Granada (UGR), Avenida de la Ilustración s/n, 18100 Granada, Spain; macoro@ 123456ugr.es (M.C.-R.); irenemedina@ 123456correo.ugr.es (I.M.-M.).; blarume@ 123456ugr.es (B.R.-M.)
                [2 ]Instituto de Investigación Biosanitaria, IBS, Avda, de Madrid, 15, Pabellón de consultas externas 2, 2ª planta, 18012 Granada, Spain; nortego@ 123456gmail.com
                [3 ]Unidad de Enfermedades Autoinmunes Sistémicas, Servicio de Medicina Interna, Hospital Universitario San Cecilio, Av, de la Investigación, s/n, 18016 Granada, Spain; jlcalleja@ 123456telefonica.net (J.-L.C.-R.); rriosfer@ 123456hotmail.com (R.R.F.)
                [4 ]Unidad de Enfermedades Autoinmunes Sistémicas, Servicio de Medicina Interna, Complejo Hospitalario de Jaén, Av. del Ejército Español, 10, 23007 Jaén, Spain; madfmar@ 123456gmail.com
                [5 ]Unidad de Enfermedades Autoinmunes Sistémicas, Servicio de Medicina Interna, Hospital de Poniente, Carretera de Almerimar, 31, 04700 El Ejido, Almería, Spain; grcrca@ 123456hotmail.com
                Author notes
                [* ]Correspondence: gpocovi@ 123456correo.ugr.es ; Tel.: +34-664-09-5541
                [†]

                These authors have contributed equally to this work.

                Author information
                https://orcid.org/0000-0001-9165-4349
                https://orcid.org/0000-0002-2720-7461
                https://orcid.org/0000-0003-1088-0032
                https://orcid.org/0000-0002-0263-7000
                Article
                nutrients-12-01094
                10.3390/nu12041094
                7231002
                32326626
                71eee5b2-b2bc-4540-8b48-3c362dbe77c9
                © 2020 by the authors.

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                : 28 February 2020
                : 13 April 2020
                Categories
                Article

                Nutrition & Dietetics
                autoimmune disease,lupus,sugar intake,free sugars intake,inflammation,cardiovascular factors

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