인문학
사회과학
자연과학
공학
의약학
농수해양학
예술체육학
복합학
DBpia AI
AI 에이전트
AI 아이디어
AI 리더
AI 뷰어
Citeasy
크롬 서지관리 다운로드
지원사업
학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
커뮤니티
연구자들이 자신의 연구와 전문성을 널리 알리고, 새로운 협력의 기회를 만들 수 있는 네트워킹 공간이에요.
초록·키워드
Real world problems are a valuable hook to engage undergraduate researchers in the lab. The Love-Rutledge lab is interested in Pathological Obesity, and the comorbid conditions that form when excess energy is store in inappropriate places like the liver. The underlying pathophysiological changes that lead to the transition from metabolically normal obesity to pathological obesity is an important research gap that has been studied in a multitude of ways. We are interested in understanding the underlying causes of hyperinsulinemia, nonalcoholic fatty liver disease and insulin resistance when diubiquitin (ubd/fat10) is upregulated. We hypothesized that increased expression of this inflammation sensitive gene leads to steatosis due to impaired mitochondrial function and decreased beta oxidation leading to increased lipid droplets. To test this we characterized the liver of a rat model known to have increased diubiquitin expression as well as followed the mitochondrial morphology changes and lipid content in hepatocytes in response to increased expression using a lentivirus. We validated that diubiquitin expression was upregulated in the livers of the rats. Utilizing undergraduate students in an upper-level biochemistry lab course we also measured insulin levels. Our ambition with these students was to encourage the development of resilience, critical thinking, and problem solving in the lab environment. Several undergraduate researchers evaluated the pathological state of the liver using a published series of scoring metrics. The rats showed a malignant form of non alcoholic fatty liver disease that was transitioning to steatohepatitis with indicators of fibrosis. To better understand the underlying mechanism of action a summer undergraduate student worked to assess lipid droplet size and content in response to increased fat10 expression in vitro. We observed increased lipid content and potential distortions in mitochondrial networks. This work suggests that diubiquitin may trigger to some of the poor liver metabolic outcomes in response-increased inflammation in obesity. Future work will provide mechanistic insight into how diubiquitin impacts mitochondrial turnover reducing metabolic efficiency. We hope to leave the audience with strategies for encouraging students to take ownership of projects, use course based experiences to increase access to meritorious research, and critically think about the successes and shortcoming of experimental design. We would like to thank ASIP SROPP, AAUW, NIH, NSF, UAH Department of Chemistry, UAH Office of the Provost, Alabama Space Grant Consortium, Adrian D Johnson Sr. Fellowship, UAH College of Science for their support of this research.
인공지능 문자 인식 모델을 통해 추출된 텍스트로, 일부 오타나 오류가 포함될 수 있으나 지속적으로 개선 중입니다.
오류를 발견하셨다면 해당 부분을 드래그한 후 ' 를 통해 신고해주세요.
오류를 발견하셨다면 해당 부분을 드래그한 후 ' 를 통해 신고해주세요.
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