METABOLIC ABNORMALITIES IN HISPANIC CHILDREN WITH CYSTIC FIBROSIS

该子项目是利用NIH/NCRR资助的中心赠款提供的资源的许多研究子项目之一。子项目和研究者（PI）可能从另一个NIH来源获得了主要资金，因此可以在其他CRISP条目中表示。所列机构为中心，不一定是研究者所在机构。一般来说，西班牙裔囊性纤维化（CF）患者的发病率和死亡率低于白人CF患者。然而，这种恶化状态的潜在机制尚未阐明。该研究/资助的目的是探索西班牙裔CF儿童临床状况恶化的潜在代谢解释。 中心假设是，高血糖发生在年轻的西班牙裔CF，它主要是由潜在的胰岛素抵抗继发于西班牙裔遗传。进一步假设胰岛素抵抗包括肝胰岛素抵抗和对胰岛素的抗分解代谢作用的抵抗，其导致过量的氨基酸底物可用于胰岛素生成。

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. In general, cystic fibrosis (CF) patients who are Hispanic have worse morbidity and mortality than Caucasian CF patients. However, the underlying mechanism(s) for this worsened status has not been elucidated. The purpose of the study/grant is to explore potential metabolic explanations for the worsened clinical status of Hispanic children with CF. The central hypothesis is that hyperglycemia occurs at a younger age in Hispanics with CF and that it is principally caused by underlying insulin resistance secondary to the Hispanic heredity. It is further hypothesized that insulin resistance includes hepatic insulin resistance and resistance to insulin's anti-catabolic effect which results in excessive amino acid substrate availability for gluconeogenesis.