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      Does fetuin-A mediate the association between pro-inflammatory diet and type-2 diabetes mellitus risk? Translated title: ¿Fetuína-A media en la asociación entre la dieta proinflamatoria y el riesgo de diabetes mellitus tipo 2?

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          Abstract

          Abstract Introduction: recent studies indicate that diet increases T2DM risk via inflammation. Fetuin-A, identified as an acute-phase protein, plays a role in insulin resistance and is an independent predictor of type-2 diabetes. Objectives: the present study aimed to examine the association between diet and T2DM risk, and whether said association is mediated by fetuin-A, and to determine the effect of fetuin-A on T2DM risk. Methods: the case group included 40 individuals with T2DM, whereas 40 individuals without T2DM comprised the control group. The Dietary Inflammatory Index (DII), was used to determine the inflammatory potential of diet. A simple mediation analysis was used to investigate whether diet was associated with T2DM risk and whether the association was mediated by fetuin-A. Results: subjects who consumed a high pro-inflammatory diet had 2.0 times higher risk of developing T2DM (OR = 2.043; 95 % CI: 0.955 to 4.371, p = 0.066). In addition, subjects who had higher levels of fetuin-A had a 1,2 times higher risk of developing T2DM (OR = 1.155; 95 % CI: 1.030 to 1.296, p = 0.014). Both fetuin-A and hs-CRP had a significant full mediator role on the association between DII and HOMA-IR [respectively; β = 0.371 (95 % CI: -0.029-0.770), β = 0.424 (95 % CI: -0.007-0.856)]. Conclusion: these findings suggest that a pro-inflammatory diet, by creating an environment of increased inflammatory markers, affects in particular insulin resistance through these markers and ultimately causes T2DM. In addition, fetuin-A also acts as an important novel mediator between diet and T2DM by inducing insulin resistance.

          Translated abstract

          Resumen Introducción: estudios recientes indican que la dieta aumenta el riesgo de T2DM mediante la inflamación. La fetuína-A,identificada como proteína de fase aguda, desempeña un papel en la resistencia a la insulina y es un predictor independiente de la diabetes de tipo 2. Objetivos: el presente estudio pretende examinar la asociación entre la dieta y el riesgo de DMT2 y si la asociación está mediada por la fetuína-A y determinar el efecto de la fetuína-A sobre el riesgo de DMT2. Métodos: en el grupo de casos se incluyeron 40 individuos con DMT2, mientras que 40 individuos sin DMT2 se incluyeron en el grupo de control. El índice de inflamación de la dieta (DII) se usó para determinar el potencial inflamatorio de la dieta. El análisis de mediación simple se usó para investigar si la dieta estaba asociada con el riesgo de DMT2 y si la asociación estaba mediada por la fetuína-A. Resultados: los sujetos que consumieron una dieta más proinflamatoria tuvieron 2 veces más riesgo de desarrollar DMT2. Además, los sujetos que tenían niveles más altos de fetuína-A tuvieron 1,2 veces más riesgo de desarrollar DMT2. Tanto la fetuína-Acomo la hs-CRP tuvieron un papel significativo como mediadores completos sobre la asociación entre DII y HOMA-IR. Conclusión: estos hallazgos sugieren que la dieta proinflamatoria, al crear un ambiente con marcadores inflamatorios aumentados, afecta en particular a la resistencia a la insulina a través de estos marcadores y, finalmente, causa DMT2. Además, la fetuína-A también actúa como mediador novedoso importante entre la dieta y la DMT2 al inducir la resistencia a la insulina.

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          Most cited references34

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          Asymptotic and resampling strategies for assessing and comparing indirect effects in multiple mediator models

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            Designing and developing a literature-derived, population-based dietary inflammatory index.

            To design and develop a literature-derived, population-based dietary inflammatory index (DII) to compare diverse populations on the inflammatory potential of their diets.
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              Inflammation as a link between obesity, metabolic syndrome and type 2 diabetes.

              It is recognized that a chronic low-grade inflammation and an activation of the immune system are involved in the pathogenesis of obesity-related insulin resistance and type 2 diabetes. Systemic inflammatory markers are risk factors for the development of type 2 diabetes and its macrovascular complications. Adipose tissue, liver, muscle and pancreas are themselves sites of inflammation in presence of obesity. An infiltration of macrophages and other immune cells is observed in these tissues associated with a cell population shift from an anti-inflammatory to a pro-inflammatory profile. These cells are crucial for the production of pro-inflammatory cytokines, which act in an autocrine and paracrine manner to interfere with insulin signaling in peripheral tissues or induce β-cell dysfunction and subsequent insulin deficiency. Particularly, the pro-inflammatory interleukin-1β is implicated in the pathogenesis of type 2 diabetes through the activation of the NLRP3 inflammasome. The objectives of this review are to expose recent data supporting the role of the immune system in the pathogenesis of insulin resistance and type 2 diabetes and to examine various mechanisms underlying this relationship. If type 2 diabetes is an inflammatory disease, anti-inflammatory therapies could have a place in prevention and treatment of type 2 diabetes. Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.
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                Author and article information

                Journal
                nh
                Nutrición Hospitalaria
                Nutr. Hosp.
                Grupo Arán (Madrid, Madrid, Spain )
                0212-1611
                1699-5198
                April 2022
                : 39
                : 2
                : 383-392
                Affiliations
                [2] Ankara orgnameFamily Medicine and Dışkapı Yıldırım Beyazıt Training and Research Hospital orgdiv1University of Health Science Turkey
                [4] Ankara orgnameHacettepe University orgdiv1Faculty of Health Science orgdiv2Department of Nutrition and Dietetics Turkey
                [3] Ankara orgnameDışkapı Yıldırım Beyazıt Training and Research Hospital orgdiv1University of Health Sciences Turkey
                [1] Ankara orgnameDışkapı Yıldırım Beyazıt Training and Research Hospital orgdiv1University of Health Science Turkey
                Article
                S0212-16112022000200018 S0212-1611(22)03900200018
                10.20960/nh.03848
                34841880
                9989ab81-7acb-409f-af03-865717117295

                This work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License.

                History
                : 27 August 2021
                : 06 November 2021
                Page count
                Figures: 0, Tables: 0, Equations: 0, References: 35, Pages: 10
                Product

                SciELO Spain

                Categories
                Original Papers

                Fetuin A,Dietary inflammatory index (DII),Type 2 diabetes,Inflammation,Mediator,Fetuína-A,Índice de inflamación de la dieta (DII),Diabetes de tipo 2,Inflamación,Mediador

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