INSULIN RESISTANCE, CYTOKINES AND BONE MINERAL DENSITY IN CHILDREN WITH CYSTI

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This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Children with Cystic Fibrosis (CF) often develop recurrent pulmonary infections, exposing them to chronic inflammation. This inflammation may lead to peripheral insulin resistance, worsening glucose metabolism, leading to frank diabetes in some. Past studies have confirmed insulinopenia, but have shown conflicting results concerning insulin resistance as a factor in Cystic Fibrosis Related Diabetes (CFRD). Inflammatory markers have also been associated with increased bone breakdown, which may play a role in osteoporosis in this population. The purpose of this study is to investigate children with CF, looking specifically at serum inflammatory mediators, insulin resistance and bone density, and the possible interplay between them. Most of the CF studies in this area have been in patients in young adulthood. Few have studied the young CF population, especially those less than 6 years of age. The recognition of insulin resistance and decreased bone density at such a young age may lead to therapies targeting earlier intervention in these areas. By improving glucose metabolism, these children will have better nutritional states which make them stronger to fight off infections, or reduce the amount of infections they acquire, inhibiting the vicious cycle of infection leading to inflammation leading to worsened nutrition and increased bone breakdown. Studies have shown improved lung function in the adult CF population when glucose metabolism has been normalized. We are hopeful that these improvements will lead to improved quality of life and increased life expectancy in this population.