Jose Cordoba-Chacon Lab:
Samuel M. Lee, PhD.
Lee received his PhD from University of Adelaide in 2017, and he spent a year as a postdoctoral fellow in Northwestern University before joining the Division of Endocrinology at UIC as a postdoctoral research associate in 2019. Dr. Lee is assessing the role of hepatocyte PPARgamma-regulated mechanisms in the development of non-alcoholic fatty liver disease. He recently published a manuscript in Cellular and Molecular Gastroenterology and Hepatology (PMID: 33444819) related with this project. He plans to use mouse models and mouse primary hepatocytes to investigate the specific contribution of PPARgamma to the development of fatty liver disease.
Rhonda Kineman Lab:
Maria del Carmen Vazquez Borrego, PhD
Maria del Carmen Vazquez-Borrego is a Postdoctoral Research Associate working in the laboratory of Dr. Rhonda Kineman, at the University of Illinois at Chicago. She earned her PhD in Biomedicine at the University of Cordoba (Spain) in 2019. Her main research focus is to understand the role growth hormone (GH) signaling (GHR/JAK2/STAT5b signaling pathway) and IGF1 plays in protecting the liver against excess fat accumulation. She specifically explores how GH controls directly controls hepatocyte de novo lipogenesis, using a unique adult-onset hepatocyte-specific growth hormone receptor knockdown mouse model (aHepGHRkd) under different nutritional states (fast-refeeding conditions).
Mercedes del Rio-Moreno, PhD
Mercedes del Rio-Moreno is currently a Postdoctoral Research Associate in the laboratory of Dr. Rhonda Kineman, at the University of Illinois at Chicago. She graduated with first class honors in Biochemistry from the University of Cordoba, Spain, and received her MS in Biotechnology and PhD in Biomedicine from the same university before moving to Chicago. Her research focus is to understand how growth hormone (GH) controls non-alcoholic steatohepatitis (NASH) development and progression. She is specifically exploring if GH acts directly on hepatocytes, through Stat5b-dependent or Stat5b-indpendent signals, to inhibit steatosis and prevent liver injury, with the ultimate goal of revealing novel drug targets to treat NASH.