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      Acanthosis nigricans as a composite marker of cardiometabolic risk and its complex association with obesity and insulin resistance in Mexican American children

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          Abstract

          Aim

          Acanthosis nigricans (AN) is a strong correlate of obesity and is considered a marker of insulin resistance (IR). AN is associated with various other cardiometabolic risk factors (CMRFs). However, the direct causal relationship of IR with AN in obesity has been debated. Therefore, we aimed to examine the complex causal relationships among the troika of AN, obesity, and IR in Mexican Americans (MAs).

          Methods

          We used data from 670 non-diabetic MA children, aged 6–17 years (49% girls). AN (prevalence 33%) severity scores (range 0–5) were used as a quasi-quantitative trait (AN-q) for analysis. We used the program SOLAR for determining phenotypic, genetic, and environmental correlations between AN-q and CMRFs (e.g., BMI, HOMA-IR, lipids, blood pressure, hs-C-reactive protein (CRP), and Harvard physical fitness score (PFS)). The genetic and environmental correlations were subsequently used in mediation analysis (AMOS program). Model comparisons were made using goodness-of-fit indexes.

          Results

          Heritability of AN-q was 0.75 (p<0.0001). It was positively/significantly (p<0.05) correlated with traits such as BMI, HOMA-IR, and CRP, and negatively with HDL-C and PFS. Of the models tested, indirect mediation analysis of BMI→HOMA-IR→AN-q yielded lower goodness-of-fit than a partial mediation model where BMI explained the relationship with both HOMA-IR and AN-q simultaneously. Using complex models, BMI was associated with AN-q and IR mediating most of the CMRFs; but no relationship between IR and AN-q.

          Conclusion

          Our study suggests that obesity explains the association of IR with AN, but no causal relationship between IR and AN in Mexican American children.

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          Most cited references 35

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          Type 2 diabetes in children and adolescents. American Diabetes Association.

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            The syndromes of insulin resistance and acanthosis nigricans. Insulin-receptor disorders in man.

            In six patients with acanthosis nigricans variable degrees of glucose intolerance, hyperinsulinemia and marked resistance to exogenous insulin were found. Studies of insulin receptors on circulating monocytes suggest that the insulin resistance in these patients was due to a marked decrease in insulin binding to its membrane receptors. When these patients were fasted, there was a fall in plasma insulin but no increase in insulin binding, suggesting that the receptor defect was not secondary to the hyperinsulinemia. The clinical features shared by these cases and several similar ones previously reported may be divided into two unique clinical syndromes: Type A, a syndrome in younger females with signs of virilization or accelerated growth, in whom the receptor defect may be primary, and Type B, a syndrome in older females with signs of an immunologic disease, in whom circulating antibodies to the insulin receptor are found.
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              2. Classification and Diagnosis of Diabetes: Standards of Medical Care in Diabetes—2020

              (2019)
              The American Diabetes Association (ADA) "Standards of Medical Care in Diabetes" includes the ADA's current clinical practice recommendations and is intended to provide the components of diabetes care, general treatment goals and guidelines, and tools to evaluate quality of care. Members of the ADA Professional Practice Committee (https://doi.org/10.2337/dc20-SPPC), a multidisciplinary expert committee, are responsible for updating the Standards of Care annually, or more frequently as warranted. For a detailed description of ADA standards, statements, and reports, as well as the evidence-grading system for ADA's clinical practice recommendations, please refer to the Standards of Care Introduction (https://doi.org/10.2337/dc20-SINT). Readers who wish to comment on the Standards of Care are invited to do so at professional.diabetes.org/SOC.
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                Author and article information

                Contributors
                Role: ConceptualizationRole: Formal analysisRole: ValidationRole: VisualizationRole: Writing – original draft
                Role: ConceptualizationRole: Formal analysisRole: Writing – original draft
                Role: ConceptualizationRole: MethodologyRole: Writing – original draft
                Role: Formal analysisRole: Writing – review & editing
                Role: Formal analysisRole: Writing – review & editing
                Role: Formal analysisRole: ValidationRole: Writing – review & editing
                Role: Data curationRole: InvestigationRole: Project administration
                Role: Data curationRole: InvestigationRole: Methodology
                Role: Data curationRole: MethodologyRole: Validation
                Role: MethodologyRole: ValidationRole: Writing – review & editing
                Role: MethodologyRole: ValidationRole: Writing – review & editing
                Role: MethodologyRole: Writing – review & editing
                Role: MethodologyRole: Writing – original draft
                Role: Formal analysisRole: MethodologyRole: Writing – review & editing
                Role: MethodologyRole: Writing – review & editing
                Role: ResourcesRole: Writing – review & editing
                Role: ConceptualizationRole: SupervisionRole: Writing – review & editing
                Role: ConceptualizationRole: SupervisionRole: Writing – review & editing
                Role: ConceptualizationRole: SupervisionRole: Writing – review & editing
                Role: ConceptualizationRole: Formal analysisRole: Funding acquisitionRole: MethodologyRole: Project administrationRole: ResourcesRole: SupervisionRole: ValidationRole: Writing – original draft
                Role: Editor
                Journal
                PLoS One
                PLoS One
                plos
                plosone
                PLoS ONE
                Public Library of Science (San Francisco, CA USA )
                1932-6203
                15 October 2020
                2020
                : 15
                : 10
                Affiliations
                [1 ] Department of Human Genetics and South Texas Diabetes and Obesity Institute, University of Texas Rio Grande Valley, Edinburg and Brownsville, TX, United States of America
                [2 ] Biomedical and Translational Informatics, Geisinger Health System, Danville, PA, United States of America
                [3 ] Department of Human Genetics, Sri Ramachandra Institute of Higher Education and Research, Porur, Chennai, Tamil Nadu, India
                [4 ] Department of Internal Medicine, Wake Forest University, Winston-Salem, NC, United States of America
                [5 ] Department of Medicine, University of Texas Health San Antonio, San Antonio, TX, United States of America
                [6 ] Department of Pharmacology, Hospital General de Mexico “Dr. Eduardo Liceaga”, Mexico City, Mexico
                [7 ] Border Health Office, College of Health Professions, University of Texas Rio Grande Valley, Edinburg, TX, United States of America
                [8 ] Department of Pediatrics, University of Texas Health San Antonio, San Antonio, TX, United States of America
                [9 ] Pediatric Endocrinology and Diabetes, Penn State University, Hershey, PA, United States of America
                Mexican Social Security Institute, MEXICO
                Author notes

                Competing Interests: The authors have declared that no competing interests exist.

                Article
                PONE-D-20-02036
                10.1371/journal.pone.0240467
                7561152
                33057385
                © 2020 Lopez-Alvarenga et al

                This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

                Page count
                Figures: 2, Tables: 2, Pages: 14
                Product
                Funding
                Funded by: funder-id http://dx.doi.org/10.13039/100000009, Foundation for the National Institutes of Health;
                Award ID: R01 HD049051/HD049051-5S1, HD041111, DK053889, DK042273, DK047482, MH059490, P01 HL045522, K01 DK064867, M01-RR- 01346
                Award Recipient :
                This study was supported RD received grants: R01 HD049051/HD049051-5S1 [ARRA], HD041111, DK053889, DK042273, DK047482, MH059490, P01 HL045522, K01 DK064867, M01-RR- 01346, and Veterans Administration Epidemiologic Grant. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. Some of the investigators received salaries from some of the grants as follows: R01 HD049051/HD049051-5S1 [ARRA] (RD, DEH, JB, RAD, CPJ, RA, SP, VSF, SPF, RGR), HD041111 (RD, JB, RAD, CPJ, RA, RGR), DK053889 (RD, JB, CPJ, SP, VSF, SPF, RGR), DK042273 (DML, RD, JB), DK047482 (DML), MH059490 (JB), P01 HL045522 (JB, RD), and Veterans Administration Epidemiologic Grant (RAD, CPJ). The AT&T Genomics Computing Center supercomputing facilities used for this work were supported in part by a gift from the AT&T Foundation and with support from the National Center for Research Resources Grant Number S10 RR029392. This investigation was conducted in facilities constructed with support from Research Facilities Improvement Program grants C06 RR013556 and C06 RR017515 from the National Center for Research Resources of the National Institutes of Health.
                Categories
                Research Article
                Biology and Life Sciences
                Physiology
                Physiological Parameters
                Body Weight
                Obesity
                Biology and Life Sciences
                Physiology
                Physiological Parameters
                Body Weight
                Obesity
                Childhood Obesity
                Biology and Life Sciences
                Genetics
                Biology and Life Sciences
                Physiology
                Physiological Parameters
                Body Weight
                Body Mass Index
                Medicine and Health Sciences
                Endocrinology
                Endocrine Physiology
                Insulin Resistance
                Biology and Life Sciences
                Physiology
                Endocrine Physiology
                Insulin Resistance
                Biology and Life Sciences
                Genetics
                Human Genetics
                Medicine and Health Sciences
                Vascular Medicine
                Blood Pressure
                Medicine and Health Sciences
                Endocrinology
                Endocrine Disorders
                Diabetes Mellitus
                Type 2 Diabetes
                Type 2 Diabetes Risk
                Medicine and Health Sciences
                Medical Conditions
                Metabolic Disorders
                Diabetes Mellitus
                Type 2 Diabetes
                Type 2 Diabetes Risk
                Custom metadata
                We provided supplementary files relating to the minimal data sets corresponding to the results including the matrices of genetic and environmental correlations and the data of residuals (i.e., residuals obtained for a given phenotype after adjusting for covariate effects) that we used for the analyses. None of them have any identification codes.

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