Maribel Cedillo1, Ingrid M Libman, Vincent C Arena, Lei Zhou, Massimo Trucco, Diego Ize-Ludlow, Massimo Pietropaolo, Dorothy J Becker. 1. Division of Pediatric Endocrinology and Diabetes (M.C., I.M.L., D.J.B.), Children's Hospital of Pittsburgh of University of Pittsburgh Medical Center and University of Pittsburgh, Pittsburgh, Pennsylvania 15224; Department of Biostatistics (V.C.A., L.Z.), Graduate School of Public Health, University of Pittsburgh, Pittsburgh, Pennsylvania 15261; Division of Pediatric Endocrinology (D.I.-L.), University of Illinois at Chicago, Chicago, Illinois 60612; Division of Immunogenetics (M.T.), Children's Hospital of Pittsburgh of University of Pittsburgh Medical Center and University of Pittsburgh, Pittsburgh, Pennsylvania 15213; and Department of Immunology (M.P.), University of Michigan, Ann Arbor, Michigan 48109.
Abstract
CONTEXT: The current increase in childhood type 1 diabetes (T1D) and obesity has led to two conflicting hypotheses and conflicting reports regarding the effects of overweight on initiation and spreading of islet cell autoimmunity vs earlier clinical manifestation of preexisting autoimmune β-cell damage driven by excess weight. OBJECTIVE: The objective of the study was to address the question of whether the degree of β-cell autoimmunity and age are related to overweight at diabetes onset in a large cohort of T1D youth. DESIGN: This was a prospective cross-sectional study of youth with autoimmune T1D consecutively recruited at diabetes onset. SETTING: The study was conducted at a regional academic pediatric diabetes center. PATIENTS: Two hundred sixty-three consecutive children younger than 19 years at onset of T1D participated in the study. MAIN OUTCOME MEASURES: Relationships between body mass index and central obesity (waist circumference and waist to height ratio) and antigen spreading (islet cell autoantibody number), age, and cardiovascular (CVD) risk factors examined at onset and/or 3 months after the diagnosis were measured. RESULTS: There were no significant associations between number of autoantibodies with measures of adiposity. Age relationships revealed that a greater proportion of those with central obesity (21%) were in the youngest age group (0-4 y) compared with those without central obesity (6%) (P = .001). PATIENTS with central obesity had increased CVD risk factors and higher onset C-peptide levels (P < .05). CONCLUSIONS: No evidence was found to support the concept that obesity accelerates progression of autoantibody spreading once autoimmunity, marked by standard islet cell autoantibody assays, is present. Central obesity was present in almost one-third of the subjects and was associated with early CVD risk markers already at onset.
CONTEXT: The current increase in childhood type 1 diabetes (T1D) and obesity has led to two conflicting hypotheses and conflicting reports regarding the effects of overweight on initiation and spreading of islet cell autoimmunity vs earlier clinical manifestation of preexisting autoimmune β-cell damage driven by excess weight. OBJECTIVE: The objective of the study was to address the question of whether the degree of β-cell autoimmunity and age are related to overweight at diabetes onset in a large cohort of T1D youth. DESIGN: This was a prospective cross-sectional study of youth with autoimmune T1D consecutively recruited at diabetes onset. SETTING: The study was conducted at a regional academic pediatric diabetes center. PATIENTS: Two hundred sixty-three consecutive children younger than 19 years at onset of T1D participated in the study. MAIN OUTCOME MEASURES: Relationships between body mass index and central obesity (waist circumference and waist to height ratio) and antigen spreading (islet cell autoantibody number), age, and cardiovascular (CVD) risk factors examined at onset and/or 3 months after the diagnosis were measured. RESULTS: There were no significant associations between number of autoantibodies with measures of adiposity. Age relationships revealed that a greater proportion of those with central obesity (21%) were in the youngest age group (0-4 y) compared with those without central obesity (6%) (P = .001). PATIENTS with central obesity had increased CVD risk factors and higher onset C-peptide levels (P < .05). CONCLUSIONS: No evidence was found to support the concept that obesity accelerates progression of autoantibody spreading once autoimmunity, marked by standard islet cell autoantibody assays, is present. Central obesity was present in almost one-third of the subjects and was associated with early CVD risk markers already at onset.
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