Willenbring Lab »  Alumni »  Postdoctoral Fellows »  Andrew A. Grimm, M.D., Ph.D.
Andrew A. Grimm, M.D., Ph.D.

Andrew A. Grimm, M.D., Ph.D.

Medical Director, Shire

Contact Information

Andrew Grimm, MD PhD
Fellow, Pediatric Gastroenterology
UCSF Benioff Children's Hospital
MU-408E, Box 0136
500 Parnassus Ave
San Francisco, CA 94143-0136
Tel: 415-476-5892
Fax: 415-476-1343
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  • Washington University School of Medicine, St Louis, MO, M.D., 2008
  • Washington University School of Medicine, St Louis, MO, Ph.D., Molecular Genetics, 2008
  • Massachusetts Institute of Technology, Cambridge, MA, S.B., Biology, 2000
  • American Board of Pediatrics, General Pediatrics
  • Department of Pediatrics
  • Hepatology
  • Nutrition
  • Pediatric Gastroenterology
  • Developing stem cell therapies for metabolic liver disease
  • Liver development
  • Liver regeneration

Andrew A. Grimm M.D., Ph.D. is a clinical fellow in pediatric gastroenterology at the UCSF Benioff and a post-doctoral fellow in the Willenbring Lab. Dr. Grimm is certified by the American Board of Pediatrics in General Pediatrics and is a Pediatric Advanced Life Support (PALS) Provider. Dr. Grimm grew up in Minnesota, where he learned to appreciate cold, modesty, and extreme politeness.

At MIT, Dr. Grimm studied cell cycle regulation in ES cells in the laboratory of Robert Weinberg. Instead of becoming a productive member of society, he then decided instead to spend 8 more years in school, obtaining an MD and PhD at Washington University in St. Louis, where he studied the regulation of aging in the laboratory of Shin-ichiro Imai. He then trained in pediatrics at Children's Hospital Boston and St. Louis Children's Hospital. His hobbies include hiking, triathlons, rock climbing, and learning Russian.

Metabolic liver diseases, are a group of genetic disorders that lead to progressive liver injury and/or damage to other organs due to impaired functions in metabolism. Examples include alpha-1-antitrypsin deficiency, Wilson's disease, liver disease in cystic fibrosis, galactosemia, glycogen storage diseases, Crigler-Najjar, and hereditary hypercholesterolemia. Therapies for most of these diseases are limited, and together they account for about 10% of pediatric liver transplants. An alternative to liver transplant would be transplantation of genetically modified hepatocytes that could be created from a patient's stem cells. Hepatocyte transplantation has encountered significant technical obstacles, including poor engraftment and poor proliferation after transplant. Through genetic and bioinformatic screens, I seek to identify factors that promote hepatocyte engraftment, differentiation, and proliferation. The ultimate goal of my research is to make hepatocyte transplantation a viable therapy for metabolic liver disease.

Grimm AA*, Brace CS*, Wang T, Stormo GD, Imai S. A nutrient-sensitive interaction between Sirt1 and Hnf-1α regulates Crp expression. Aging Cell. 2011 10(2):305-17 (*equally contributing authors).

Revollo JR, Grimm AA, Imai S. The regulation of NAD biosynthesis by Nampt/PBEF/visfatin in mammals. Curr. Opin. Gastroenterol. 2007 23(2):164-70

Moynihan KA, Grimm AA, Plueger MM, Bernal-Mizrachi E, Ford E, Cras-Meneur C, Permutt MA, and Imai S. Increased dosage of mammalian Sir2 in pancreatic beta cells enhances glucose-stimulated insulin secretion in mice. Cell Metab. 2005 2(2):105-17

Revollo JR*, Grimm AA*, Imai S. The NAD biosynthesis pathway mediated by nicotinamidephosphoribosyltransferase regulates Sir2 activity in mammalian cells. J Biol Chem. 2004279(49):50754-63 (*equally contributing authors).