Childhood obesity is an established risk factor for metabolic disease. The influence of obesity on bone development, however, remains controversial and may depend on the pattern of regional fat deposition. Therefore, we examined the associations of regional fat compartments of the calf and thigh with weight-bearing bone parameters in girls. Data from 444 girls aged 9 to 12 years from the Jump-In: Building Better Bones study were analyzed. Peripheral quantitative computed tomography (pQCT) was used to assess bone parameters at metaphyseal and diaphyseal sites of the femur and tibia along with subcutaneous adipose tissue (SAT, mm(2) ) and muscle density (mg/cm(3) ), an index of skeletal muscle fat content. As expected, SAT was positively correlated with total-body fat mass (r = 0.87-0.89, p < .001), and muscle density was inversely correlated with total-body fat mass (r = -0.24 to -0.28, p < .001). Multiple linear regression analyses with SAT, muscle density, muscle cross-sectional area, bone length, maturity, and ethnicity as independent variables showed significant associations between muscle density and indices of bone strength at metaphyseal (β = 0.13-0.19, p < .001) and diaphyseal (β = 0.06-0.09, p < .01) regions of the femur and tibia. Associations between SAT and indices of bone strength were nonsignificant at all skeletal sites (β = 0.03-0.05, p > .05), except the distal tibia (β = 0.09, p = .03). In conclusion, skeletal muscle fat content of the calf and thigh is inversely associated with weight-bearing bone strength in young girls.
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http://dx.doi.org/10.1002/jbmr.414 | DOI Listing |
J Clin Invest
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Department of Biochemistry, Molecular Biology & Biophysics, University of Minnesota, Minneapolis, United States of America.
Eccentric contraction- (ECC) induced force loss is a hallmark of murine dystrophin-deficient (mdx) skeletal muscle that is used to assess efficacy of potential therapies for Duchenne muscular dystrophy. While virtually all key proteins involved in muscle contraction have been implicated in ECC force loss, a unifying mechanism that orchestrates force loss across such diverse molecular targets has not been identified. We showed that correcting defective hydrogen sulfide (H2S) signaling in mdx muscle prevented ECC force loss.
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January 2025
Laboratory of Anatomy and Cell Biology, Department of Health Sciences, Kyorin University, 5-4-1 Shimorenjaku, Mitaka, Tokyo, 181-8612, Japan.
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Division of Pediatric Rheumatology, Department of Pediatrics, University of Health Sciences, Ankara Bilkent City Hospital, Ankara, Türkiye.
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Hum Mol Genet
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Division of Neurology, Cincinnati Children's Hospital, 3333 Burnet Ave, Cincinnati, OH 45229, United States.
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