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Dietary vitamin D 3 restriction differentially alters quadriceps contractile proteins in both sexes in the transgenic G93A mouse model of amyotrophic lateral sclerosis: a pilot study
Author(s) -
Milionis Angelica,
Parkhomenko Egor,
Solomon Jesse Adam,
Gianforcaro Alexandro,
Hamadeh Mazen Jamal
Publication year - 2012
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.26.1_supplement.255.8
Subject(s) - amyotrophic lateral sclerosis , medicine , endocrinology , motor neuron , ucp3 , biology , actin , disease , biochemistry , uncoupling protein , adipose tissue , brown adipose tissue
Background We previously demonstrated that dietary vitamin D 3 (D 3 ) restriction hastened the decline in functional outcomes following disease onset in the G93A mouse model of amyotrophic lateral sclerosis (ALS). ALS is a fatal neuromuscular disease characterized by motor neuron death, muscle weakness and progressive paralysis. Objective In this pilot study, we investigated the effects of dietary D 3 at 2.5% the adequate intake (AI) in G93A mice on quadriceps contractile proteins (α‐actin; troponin C, trop C), inflammation (IL‐6), cell stress response (Hsp70), mitochondrial efficiency (UCP3) and apoptosis (CASP3 cleaved/pro ratio), mechanisms contributing to ALS pathology. Methods Starting at age 25 d, 42 G93A mice were provided food ad libitum with either adequate (AI; 1 IU D 3 /g feed; 12 M, 11 F) or deficient (DEF; 0.025 IU D 3 /g feed; 10 M, 9 F) D 3 . Differences in quadriceps protein content were considered significant at P ≤ 0.10. Results In males, DEF had 34% lower α‐actin (P = 0.096) and 38% higher trop C (P = 0.031) vs AI. In females, DEF had 32% lower trop C vs AI (P = 0.020). DEF males had 16% higher UCP3 (P = 0.093) and 57% higher trop C vs DEF females (P = 0.021). Conclusion Dietary D 3 restriction differentially alters markers of muscle contractile proteins in both sexes in G39A mice, which may explain the associated decline in functional capacity. (Supported by NSERC and Faculty of Health‐York U). Grant Funding Source : Supported by NSERC and Faculty of Health‐York U