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Differences in extramyocellular lipid and physical function in older adults with sufficient and insufficient vitamin D status (260.2)
Author(s) -
Redzic Maja,
Powell David,
Lutz Charles,
Thomas D.
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.260.2
Subject(s) - vitamin d and neurology , medicine , endocrinology , vitamin , body mass index , vitamin d deficiency , skeletal muscle , gastrocnemius muscle
The metabolic role of extramyocellular lipid (EMCL) has yet to be elucidated. An inverse relationship between EMCL and physical function, and EMCL and vitamin D status has been described in vitamin D‐deficiency (25(OH)D < 20 ng/mL). The purpose of this study was to assess differences in muscle lipid and physical function in community dwelling elderly with vitamin D insufficiency (25(OH)D 蠄 30 ng/mL) compared to vitamin D levels that may promote extra‐skeletal health (25(OH)D 蠅 40 ng/mL). 25(OH)D and four square step test (FSST) were assessed in 21 adults aged 65 to 83 years. Gastrocnemius IMCL and EMCL were measured with magnetic resonance spectroscopy and fat ratio segmentation, respectively. Mean body mass index (BMI) was 26.9±0.9 kg/m2. Mean EMCL was 20.2±0.9% with a range of 11.8 to 25.9% and intramyocellular lipid (IMCL) to water ratio was 0.5±0.06. Participants who were vitamin D insufficient (23.9±1.1 ng/mL) had significant higher levels of lateral gastrocnemius EMCL and slower FSST times compared to vitamin D replete (54.7±3 ng/mL) (p<0.05). IMCL, BMI, age, and activity levels were not significantly different between vitamin D groups. These data suggest that vitamin D status 蠄 30 ng/mL may contribute to EMCL accumulation and impaired physical function independent of activity and body mass. A vitamin D status higher than what is normally deemed as sufficient may be needed to measure muscle function. Grant Funding Source : Partially sponsored by NIH CTSA UL1TR000117.