Soft Tissue and Bone Development in Young Girls (STAR)
|The safety and scientific validity of this study is the responsibility of the study sponsor and investigators. Listing a study does not mean it has been evaluated by the U.S. Federal Government. Read our disclaimer for details.|
|ClinicalTrials.gov Identifier: NCT02654262|
Recruitment Status : Unknown
Verified September 2016 by Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD).
Recruitment status was: Recruiting
First Posted : January 13, 2016
Last Update Posted : September 26, 2016
|Condition or disease|
The pediatric obesity epidemic continues unabated. Its cardio-metabolic complications are undisputed, including inflammation, insulin resistance (IR), glucose intolerance and greater prevalence of type 2 diabetes (T2D) in youth. We contend an equally serious consequence of these obesity co-morbidities is their detrimental effects on bone development during adolescence, a critical time for mineral accrual and architectural modeling that underlies bone strength and fracture risk. This proposition has received little attention and the sparse results are mixed, with reports of augmented and impaired mineralization. In contrast, animal data demonstrates reduced mineral accrual and compromised architecture with insulin resistance and chronic inflammation. The conflicting results in youth are likely due to mixed samples and analyses that commingle obese youth with metabolic complications with so called metabolically healthy obese youth and the use of technology (i.e., dual energy x-ray absorptiometry, DXA) to measure bone outcomes that is confounded by the very changes that investigators seek to detect. We posit that the positive mechanical effect of excess adiposity on bone is countered by chronic low-grade inflammation and IR so that obese youth with these metabolic complications suffer impaired bone development whereas obesity in otherwise metabolically healthy youth augments development. A thorough understanding of the effects of adiposity and its co-morbidities on bone development is crucial to the development of efficacious interventions aimed at maximal mineral accrual and bone modeling. Thus, we propose primary aims designed to clarify the effects of obesity, insulin resistance and inflammation on bone around the time of peak height velocity. Adipose tissue (AT) distribution undoubtedly matters, especially abdominal visceral AT and skeletal muscle fat content, both strongly related to insulin resistance. Failure to characterize fat distribution is another important limitation of past studies. Consequently we will assess the effect of visceral AT and skeletal muscle fat along with whole body fatness and propose secondary aims designed to develop safe, cost effective methods that we and others can use for estimating AT distribution, a critical component of risk that has rarely been studied in youth relative to bone development.
- Assess the associations of total and regional adiposity (visceral AT and leg muscle fat content), insulin resistance, and inflammation with bone mass, density, structure and strength in normal weight, overweight, and obese pre-menarcheal girls
- Assess the effects of total and regional adiposity, insulin resistance, and inflammation on bone development (i.e., 2 year changes in bone parameters) in normal weight and obese pre-menarcheal girls.
|Study Type :||Observational|
|Estimated Enrollment :||450 participants|
|Official Title:||Obesity and Bone Development in Young Girls|
|Study Start Date :||January 2013|
|Estimated Primary Completion Date :||December 2017|
|Estimated Study Completion Date :||December 2017|
- Bone development [ Time Frame: 2 years ]Baseline cross-sectional (N=450) and longitudinal changes over 2 years (N=150) in bone mass, density, structure and strength, measured by peripheral quantitative computed tomography (pQCT) and dual-energy X-ray absorptiometry (DXA), as they relate to body composition by DXA and blood biomarkers of insulin resistance and inflammation.
Biospecimen Retention: Samples With DNA
To learn more about this study, you or your doctor may contact the study research staff using the contact information provided by the sponsor.
Please refer to this study by its ClinicalTrials.gov identifier (NCT number): NCT02654262
|Contact: Robert Blew, MSemail@example.com|
|Contact: Vinson Lee, MS||(520) firstname.lastname@example.org|
|United States, Arizona|
|University of Arizona, Nutritional Sciences Department||Recruiting|
|Tucson, Arizona, United States, 85714|
|Contact: Robert Blew, MS 520-626-3067 email@example.com|
|Contact: Vinson Lee, MS 520-626-9534 firstname.lastname@example.org|
|Principal Investigator:||Scott B Going, PhD||University of Arizona|