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      Exceso de peso y depresión asociados al Polimorfismo del Gen Transportador de la Serotonina (5-HTTLPR): Una revisión sistemática Translated title: Excess weight and depression associated with serotonin transporter gene polymorphism (5-HTTLPR): a systematic review

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          Abstract

          RESUMEN: Introducción: El exceso de peso y la depresión han sido objeto de estudio por su elevada prevalencia en la población, la evidencia refiere que existe una bidireccionalidad de origen y desarrollo entre éstas enfermedades. Además, la carga genética se ha asociado significativamente en estas enfermedades, un ejemplo es el polimorfismo de la región promotora del gen transportador de la serotonina (5-HTTLPR), estudios reportan que este factor genético puede condicionar y agravar los síntomas presentes de ambas condiciones. Objetivo: Recopilar, revisar y analizar estudios publicados de la relación que existe entre polimorfismo 5-HTTLPR para el desarrollo de la depresión en personas con sobrepeso-obesidad. Métodos: Por medio de los lineamientos del checklist de PRISMA se realizó una búsqueda sistemática en las bases de datos: PubMed, Scopus, Web of Science (Science Citation Index Expanded y Social Sciences Citation Index) y EBSCO (Academic Search Complete, Fuente Académica y MedicLatina). La plataforma Web 3.0: Ficheros de Lectura Crítica se utilizó para analizar la calidad de los estudios. Resultados: Se incluyeron siete estudios, los cuales aportaron evidencia de la relación entre el polimorfismo 5-HTTLPR, la depresión y el aumento de IMC/sobrepeso-obesidad. Conclusión: La evidencia analizada demuestra que el polimorfismo 5-HTTLPR está ligado al desarrollo y síntomas de la depresión y obesidad. Información que debe considerar el personal de salud para poder realizar tratamientos y planes de cuidado acorde a las necesidades de los individuos con estas condiciones.

          Translated abstract

          ABSTRACT: Background: Excess weight and depression have been studied due to the high prevalence in the population, the evidence indicates that there is a bidirectionality of origin and development of these diseases. Additionally, genetic load has been significantly associated in these diseases, an example is the polymorphism of the promoter region of the serotonin transporter gene (5-HTTLPR), studies report that this genetic factor can condition and aggravate the symptoms present in both conditions. Objective Collect, review, and analyze published studies of the relationship between 5-HTTLPR polymorphism for the development of depression in overweight-obese people. Methods: Using the PRISMA checklist guidelines, a systematic search was performed in the databases: PubMed, Scopus, Web of Science (Science Citation Index Expanded and Social Sciences Citation Index) and EBSCO (Academic Search Complete, Fuente Académica and MedicLatina). The Web 3.0 platform: Critical Reading Files was used to analyze the quality of the studies Results: Seven studies were included, which provided evidence of the relationship between 5-HTTLPR polymorphism, depression and increased BMI / overweight-obesity. Conclusion: The evidence analyzed shows that the 5-HTTLPR polymorphism is linked to the development and symptoms of depression and obesity. Information that health personnel must consider in order to carry out treatments and care plans according to the needs of individuals with these conditions.

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          Most cited references26

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          Overweight, obesity, and depression: a systematic review and meta-analysis of longitudinal studies.

          Association between obesity and depression has repeatedly been established. For treatment and prevention purposes, it is important to acquire more insight into their longitudinal interaction. To conduct a systematic review and meta-analysis on the longitudinal relationship between depression, overweight, and obesity and to identify possible influencing factors. Studies were found using PubMed, PsycINFO, and EMBASE databases and selected on several criteria. Studies examining the longitudinal bidirectional relation between depression and overweight (body mass index 25-29.99) or obesity (body mass index > or =30) were selected. Unadjusted and adjusted odds ratios (ORs) were extracted or provided by the authors. Overall, unadjusted ORs were calculated and subgroup analyses were performed for the 15 included studies (N = 58 745) to estimate the effect of possible moderators (sex, age, depression severity). Obesity at baseline increased the risk of onset of depression at follow-up (unadjusted OR, 1.55; 95% confidence interval [CI], 1.22-1.98; P or =60 years) but not among younger persons (aged <20 years). Baseline depression (symptoms and disorder) was not predictive of overweight over time. However, depression increased the odds for developing obesity (OR, 1.58; 95% CI, 1.33-1.87; P < .001). Subgroup analyses did not reveal specific moderators of the association. This meta-analysis confirms a reciprocal link between depression and obesity. Obesity was found to increase the risk of depression, most pronounced among Americans and for clinically diagnosed depression. In addition, depression was found to be predictive of developing obesity.
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            Brain structure and obesity.

            Obesity is associated with increased risk for cardiovascular health problems including diabetes, hypertension, and stroke. These cardiovascular afflictions increase risk for cognitive decline and dementia, but it is unknown whether these factors, specifically obesity and Type II diabetes, are associated with specific patterns of brain atrophy. We used tensor-based morphometry (TBM) to examine gray matter (GM) and white matter (WM) volume differences in 94 elderly subjects who remained cognitively normal for at least 5 years after their scan. Bivariate analyses with corrections for multiple comparisons strongly linked body mass index (BMI), fasting plasma insulin (FPI) levels, and Type II Diabetes Mellitus (DM2) with atrophy in frontal, temporal, and subcortical brain regions. A multiple regression model, also correcting for multiple comparisons, revealed that BMI was still negatively correlated with brain atrophy (FDR 30) showed atrophy in the frontal lobes, anterior cingulate gyrus, hippocampus, and thalamus compared with individuals with a normal BMI (18.5-25). Overweight subjects (BMI: 25-30) had atrophy in the basal ganglia and corona radiata of the WM. Overall brain volume did not differ between overweight and obese persons. Higher BMI was associated with lower brain volumes in overweight and obese elderly subjects. Obesity is therefore associated with detectable brain volume deficits in cognitively normal elderly subjects. 2009 Wiley-Liss, Inc.
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              Allelic variation of human serotonin transporter gene expression.

              Mood, emotion, cognition, and motor functions as well as circadian and neuroendocrine rhythms, including food intake, sleep, and reproductive activity, are modulated by the midbrain raphe serotonin (5-HT) system. By directing the magnitude and duration of postsynaptic responses, carrier-facilitated 5-HT transport into and release from the presynaptic neuron are essential for the fine tuning of serotonergic neurotransmission. Interest in the mechanism of environmental factor-, disease-, and therapy-induced modification of 5-HT transporter (5-HTT) function and its impact on early brain development, event-related synaptic plasticity, and neurodegeneration is widespread and intensifying. We have recently characterized the human and murine 5-HTT genes and performed functional analyses of their 5'-flanking regulatory regions. A tandemly repeated sequence associated with the transcriptional apparatus of the human 5-HTT gene displays a complex secondary structure, represses promoter activity in nonserotonergic neuronal cells, and contains positive regulatory components. We now report a novel polymorphism of this repetitive element and provide evidence for allele-dependent differential 5-HTT promoter activity. Allelic variation in 5-HTT-related functions may play a role in the expression and modulation of complex traits and behavior.
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                Author and article information

                Journal
                eg
                Enfermería Global
                Enferm. glob.
                Universidad de Murcia (Murcia, Murcia, Spain )
                1695-6141
                2021
                : 20
                : 62
                : 653-677
                Affiliations
                [2] orgnameUniversidad Autónoma de Nuevo León orgdiv1Facultad de Enfermería Mexico yolanda.florespe@ 123456uanl.edu.mx
                [1] orgnameUniversidad Autónoma de Coahuila orgdiv1Facultad de Enfermería “Dr. Santiago Valdés Galindo” Mexico
                Article
                S1695-61412021000200020 S1695-6141(21)02006200020
                10.6018/eglobal.432711
                74bbb1bd-2649-45de-ac89-a1bdccbc580d

                This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 3.0 International License.

                History
                : 16 June 2020
                : 30 December 2020
                Page count
                Figures: 0, Tables: 0, Equations: 0, References: 26, Pages: 25
                Product

                SciELO Spain

                Categories
                Revisiones

                Factor Genético,Obesity,Overweight,Depression,5-HTTLPR Polymorphism,Genetic Factor,Obesidad,Sobrepeso,Depresión,Polimorfismo 5-HTTLPR

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