[et_pb_section fullwidth=”on” specialty=”off”][et_pb_fullwidth_slider admin_label=”Fullwidth Slider” show_arrows=”on” show_pagination=”on” auto=”off” parallax=”off” parallax_method=”off” module_id=”interior”][et_pb_slide background_image=”https:\/\/depts.washington.edu\/cfrtc\/wp-content\/uploads\/2014\/12\/microscope11.jpg” background_color=”#ffffff” alignment=”center” background_layout=”dark” \/][\/et_pb_fullwidth_slider][\/et_pb_section][et_pb_section][et_pb_row][et_pb_column type=”1_4″][et_pb_sidebar admin_label=”Pilots Sidebar” orientation=”left” area=”et_pb_widget_area_7″ background_layout=”light” \/][\/et_pb_column][et_pb_column type=”3_4″][et_pb_text admin_label=”Text” background_layout=”light” text_orientation=”left”]<\/p>\n
P.I.: Lynn Hajjar, DVM, PhD<\/a><\/strong> Piper Treuting, DVM, MS<\/a><\/strong> Cystic fibrosis (CF) results in inflammatory changes not just in the lungs but also in the gastrointestinal (GI) tract. It is not known, however, whether it is mutated CFTR or altered microbiota that plays a larger role in inflammation in CF. Two non-mutually exclusive pathways include a direct pathway, where CFTR mutation induces inflammation directly independent of microbiota, and an indirect pathway, where dysbiosis of the microbiota due to CFTR mutation results in inflammation. Using our newly derived CFTR-deficient mice that are germ-free (GF, i.e. devoid of all microbial life) we propose to differentiate these two pathways. We will identify any pathological consequences of lack of CFTR in the lungs and GI tract of GF CF mice as a measure of direct inflammation, without the confounding effects of innate and adaptive immune responses to commensal microbiota. In addition, colonization of GF CF or WT mice with CF or control microbiota will reveal the indirect pathway. Together, these experiments will demonstrate whether one pathway is dominant or whether both are active.<\/p>\n [\/et_pb_text][\/et_pb_column][\/et_pb_row][\/et_pb_section]<\/p>\n","protected":false},"excerpt":{"rendered":" P.I.: Steven Kahn, MB, ChB Kristina Utzschneider, MD With the increased life expectancy of patients with cystic fibrosis (CF), other co-morbidities have become apparent in these patients. One of these is abnormal glucose metabolism, where CF-related diabetes (CFRD) is common. More recently, another abnormality of glucose metabolism has been recognized; namely late hypoglycemia following oral glucose loading. In this study, we propose to test the hypothesis that the post-glucose load hypoglycemia observed in patients with CF results from a deficient counterregulatory hormone response and\/or an insulin response that is exaggerated and delayed.<\/p>\n","protected":false},"author":1,"featured_media":0,"comment_status":"closed","ping_status":"open","sticky":false,"template":"","format":"standard","meta":{"_et_pb_use_builder":"on","_et_pb_old_content":" P.I.: Steven Kahn, MB, ChB<\/a>
\nResearch Associate Professor
\nComparative Medicine<\/p>\n
\nAssociate Professor
\nComparative Medicine<\/p>\n
\nProfessor of Medicine
\nMetabolism, Endocrinology and Nutrition<\/p>\n
\nAssociate Professor of Medicine
\nMetabolism, Endocrinology and Nutrition<\/p>\n
Professor of Medicine
Metabolism, Endocrinology and Nutrition<\/p>