Abstract
The aim of this study was to determine the response to an oral glucose tolerance test (OGTT) in adult males with Becker muscular dystrophy (BMD) and Duchenne muscular dystrophy (DMD), and to investigate whether body composition contributes to any variance in the glucose response. Twenty-eight adult males with dystrophinopathy (BMD, n = 13; DMD, n = 15) and 12 non-dystrophic controls, ingested 75 g oral anhydrous glucose solution. Fingertip capillary samples were assessed for glucose at 30-min intervals over 2-h post glucose ingestion. Fat free mass relative to body mass (FFM/BM) and body fat (BF%) was assessed using bioelectrical impedance. Vastus lateralis muscle anatomical cross sectional area (VL ACSA) was measured using B-mode ultrasonography. Blood glucose was higher in MD groups than control at 60, 90 and 120 min post ingestion of glucose. Compared to controls, FFM/BM and VL ACSA were lower in MD groups compared to controls (p < 0.001). Glucose tolerance values at 120 min were correlated with FFM/BM and BF% in the BMD group only. Our results suggest that glucose tolerance is impaired following OGTT in adult males with BMD and DMD. It is recommended that adults with BMD and DMD undertake routine glucose tolerance assessments to allow early detection of impaired glucose tolerance.
Highlights
Muscular dystrophy (MD) represents an umbrella term encompassing a group of myogenic disorders of varying degrees of severity
Body mass and Body mass index (BMI) were higher in the Becker muscular dystrophy (BMD) group than the Duchenne muscular dystrophy (DMD) (p < 0.001, p = 0.001 and p = 0.035, respectively) and control groups (p < 0.001, p = 0.03 and p = 0.014, respectively); there was no difference in age, body mass or BMI between the DMD and control group
Fat mass was higher in the BMD group than the DMD (p = 0.04) and control groups (p = 0.001), and fat mass was higher in the DMD group compared to control (p = 0.005)
Summary
Muscular dystrophy (MD) represents an umbrella term encompassing a group of myogenic disorders of varying degrees of severity These conditions each present with specific genetic origins resulting in defects or absences within proteins of the dystrophin-sarcoglycan complex [1]. Both Duchenne (DMD) and Becker (BMD) muscular dystrophy share an identical genetic locus of impairment (Xp21) and subsequently a similar anatomical distribution of musculoskeletal weakness [2]. Each of these dystrophinopathies are characterised by either absent or reduced expression of the cytoskeletal protein dystrophin, resulting in progressive muscle degeneration with similar anatomical distribution but varied severity [2,3,4]. BMD involves partially functioning dystrophin, and is a milder yet more variable form of dystrophinopathy, Nutrients 2018, 10, 1947; doi:10.3390/nu10121947 www.mdpi.com/journal/nutrients
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