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1.
Pediatr Diabetes ; 13(8): 638-46, 2012 Dec.
Article in English | MEDLINE | ID: mdl-23173877

ABSTRACT

AIM: It is recommended to assess health-related quality of life (HRQoL) in teenagers with diabetes as part of their ongoing medical care. Here, we describe the development and psychometric evaluation of the Monitoring Individual Needs in Diabetes Youth Questionnaire (MY-Q), a multi-dimensional self-report HRQoL questionnaire designed for use in pediatric diabetes care. DESIGN AND METHODS: In expert meetings, characteristics and domains of interest were defined. Existing questionnaires were reviewed, topics selected, and new items added, resulting in the 36-item MY-Q. To test face validity, we interviewed 22 teenagers. In addition, 84 teenagers with type 1 diabetes (age 10-18 yr) completed the MY-Q and Pediatric Quality of Life Inventory (PedsQL) generic and diabetes-modules to examine psychometric properties. Hemoglobin A1c (HbA1c) values were obtained by chart audit. RESULTS: The MY-Q consists of seven subscales (social impact, parents, diabetes control perceptions, responsibility, worries, treatment satisfaction, and body image and eating behavior) as well as general HRQoL and emotional well-being. Cronbach's alpha for the total scale was 0.80. Strong correlations between MY-Q total and PedsQL generic and diabetes-module scores (r = 0.58 and r = 0.71, p < 0.001) confirmed concurrent validity. Higher HbA1c was associated with lower diabetes control perceptions (r = -0.35, p = 0.001), worries (r = -0.24, p = 0.029), and body image and eating behavior (r = -0.26, p = 0.019) scores. Younger age was associated with higher diabetes control perceptions (r = -0.26, p = 0.020) and body image and eating behavior (r = -0.23, p = .038), and lower responsibility (r = 0.25, p = 0.027) scores. CONCLUSION: The MY-Q is the first HRQoL questionnaire designed for use in clinical care. It has acceptable measurement properties and seems suitable for implementation in routine care of teenagers with diabetes.


Subject(s)
Diabetes Mellitus, Type 1/psychology , Quality of Life , Surveys and Questionnaires , Adolescent , Body Image , Child , Diabetes Mellitus, Type 1/blood , Diabetes Mellitus, Type 1/therapy , Feeding Behavior , Female , Glycated Hemoglobin/analysis , Humans , Male , Parents , Patient Satisfaction , Reproducibility of Results , Social Behavior
2.
Cell Metab ; 16(4): 449-61, 2012 Oct 03.
Article in English | MEDLINE | ID: mdl-23000401

ABSTRACT

Reactive oxygen species (ROS) contribute to target-cell damage in inflammatory and iron-overload diseases. Little is known about iron transport regulation during inflammatory attack. Through a combination of in vitro and in vivo studies, we show that the proinflammatory cytokine IL-1ß induces divalent metal transporter 1 (DMT1) expression correlating with increased ß cell iron content and ROS production. Iron chelation and siRNA and genetic knockdown of DMT1 expression reduce cytokine-induced ROS formation and cell death. Glucose-stimulated insulin secretion in the absence of cytokines in Dmt1 knockout islets is defective, highlighting a physiological role of iron and ROS in the regulation of insulin secretion. Dmt1 knockout mice are protected against multiple low-dose streptozotocin and high-fat diet-induced glucose intolerance, models of type 1 and type 2 diabetes, respectively. Thus, ß cells become prone to ROS-mediated inflammatory damage via aberrant cellular iron metabolism, a finding with potential general cellular implications.


Subject(s)
Apoptosis/drug effects , Cation Transport Proteins/metabolism , Insulin-Secreting Cells/metabolism , Interleukin-1beta/pharmacology , Iron/metabolism , Reactive Oxygen Species/metabolism , Animals , Cation Transport Proteins/antagonists & inhibitors , Cation Transport Proteins/genetics , Diabetes Mellitus, Experimental , Diet, High-Fat , Glucose Intolerance , Homeodomain Proteins/genetics , Homeodomain Proteins/metabolism , Insulin-Secreting Cells/cytology , Mice , Mice, Knockout , Models, Biological , RNA Interference , RNA, Small Interfering/metabolism , Trans-Activators/genetics , Trans-Activators/metabolism
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