SELECTED PUBLICATIONS (below)
When not running the Metabolic Core for the CASE MMPC, Colleen teaches metabolism to first-year medical students and graduate students in the Department of Nutrition.
In January 2008, Dr. Croniger was awarded one of two 2007 School of Medicine Scholarship-in-Teaching Awards, an award she proudly shared with Dr. Martin Snider from the Department of Biochemistry.
The main causes of liver disease in industrialized countries include alcoholic steatohepatitis (ASH), chronic hepatitis C virus (HCV) infection, and nonalcoholic steatohepatitis (NASH). In patients who chronically consume alcohol or are morbidly obese, the progression of liver disease is similar, originating with development of a fatty liver (hepatic steatosis) and then progresses to hepatitis, fibrosis and finally cirrhosis. However, of those patients that develop hepatitis, only a small subset will progress further to cirrhosis. Approximately 20-50% of patients with ASH and ~20% of patients with NASH will progress to cirrhosis suggesting a gene-environment interaction contributes to disease progression.
ONGOING RESEARCH in Dr. CRONIGER's LABORATORY:
Dr. Croniger’s research is focused on the underlying genetic-environment interactions that make one vulnerable to developing liver disease. Using an unbiased approach to find genes that modulate the development of fibrosis, Dr. Croniger’s lab surveyed chromosome substitution strains (CSSs) containing one chromosome from the A/J inbred strain that was substituted for the corresponding chromosome on the C57BL/6J (B6) genetic background. For example, CSS-17 contains only A/J chromosome 17 while the rest of the genome was derived from the B6 strain. Dr. Croniger’s lab have identified quantitative trait loci (QTLs) associated with resistance to diet-induced obesity and hepatic steatosis on high fat high sucrose diet, obesity resistant QTL 13 and 15 (Obrq13 and Obrq15) (Millward et al., 2009). The primary difference between these QTLs derived from A/J alleles is that Obrq15, develops insulin resistance on the high fat high sucrose diet, whereas Obrq13 remains insulin sensitive. Dr. Croniger’s lab is expanding these genetic studies to determine genetic susceptibility to liver fibrosis. These studies have produced several candidate genes for future study. The goal of the lab’s research is to identify novel genes and metabolic pathways and investigate the mechanism by which small changes in genome sequence from single nucleotide polymorphisms (SNPs) improve or reduce the possibility of developing liver disease. Understanding the mechanism for the progression of liver disease will enable us to generate novel therapies for the prevention and cure of liver disease.
INVITED BOOK CHAPTERS:
DeSantis D, Pisano S, McMullen MR, Pritchard MT, Nadeau JH, Nagy LE and Croniger CM. “Genetic differences in development of diet-induced steatosis compared to ethanol-induced steatosis in mice with a single substituted chromosome.” (2012) (in press) Recent Advances in Alcoholic Liver Disease, 2012: ISBN: 978-81-7895-571-1.
Hsieh CW, Huang C, Hatzoglou M, Puchowicz M, Croniger CM. “ Role of Triglyceride/Fatty Acid Cycle in Development of Diabetes” Type 2 Diabetes / Book 4, Intech publishers, (2011) (2011)ISBN 978-953-307-1090.
Croniger, CM. Role of the Adipocyte in Development of Type 2 Diabetes. InTech publishers, Croatia (2011). ISBN: 978-953-307-1090
Croniger, CM. Medical Complication of Type 2 Diabetes. InTech publishers, Croatia (2011). ISBN: 978-953-307-363-7
Case Western Reserve University
CASE School of Medicine
Department of Nutrition
Mouse Metabolic Phenotyping Ctr. BRB 925 Office | BRB 909 Lab
10900 Euclid Avenue
Cleveland, OH 44106-2624
Tel.: (216) 368-4967 ( 368-4512 Lab )
Fax: (216) 368-6560
MAILING ADDRESS /
10900 Euclid Avenue
School of Medicine
Cleveland, OH 44106-4954