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Associations of total, bioavailable, and free 25(OH)D concentrations with insulin resistance and beta cell function in an Aboriginal Canadian community (628.5)
Author(s) -
Mansuri Sudaba,
Badawi Alaa,
Kayaniyil Sheena,
Cole David,
Harris Stewart,
Mamakeesick Mary,
Maguire Jonathon,
Zinman Bernard,
Hanley Anthony
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.628.5
Subject(s) - insulin resistance , medicine , insulin , endocrinology , population , odds ratio , vitamin d and neurology , diabetes mellitus , type 2 diabetes , bioavailability , anthropometry , pharmacology , environmental health
This study explores the associations of total, bioavailable, and free 25(OH)D concentrations with dysglycemia, insulin resistance (IR) and β‐cell function in an Aboriginal population in Ontario, Canada. We conducted a cross‐sectional analysis within the Sandy Lake Health and Diabetes Project (2003‐2005). A total of 387 participants (> 12 y) without treated type 2 diabetes mellitus (DM) were assessed for serum total 25(OH)D, fasting plasma glucose and insulin, and anthropometric and lifestyle variables. A 75‐g oral glucose tolerance test (OGTT) was administered, with additional blood samples collected at 30‐min and 2‐hr. Higher serum total 25(OH)D was associated with a decreased prevalence of dysglycemia (odds ratio (OR) 0.68, 95% CI 0.48‐0.96 per SD increase). In addition, there were significant associations of total and bioavailable 25(OH)D with measures of insulin action (total 25(OH)D: ISOGTT; β= 0.305; p= 0.001; HOMA IR; β= ‐0.322; p= 0.001; bioavailable 25(OH)D: ISOGTT; β= 0.183; p= 0.041; HOMA‐IR; β= ‐0.202; p= 0.037) and a significant inverse association of total 25(OH)D with β‐cell function as measured by ISSI‐2 (β= 0.152; p= 0.021) after adjustment for demographic and metabolic variables. These findings highlight a potential role for vitamin D in the etiology of type 2 DM in this population.