Geoffrey A. Preidis
|Baylor College of Medicine, Houston, TX|
Area:Liver and gastrointestinal physiology; gut microbiome
Geoffrey A. Preidis, M.D., Ph.D. is a board-certified Pediatric Gastroenterologist with basic research expertise in nutrition-sensitive mechanisms that regulate physiology, growth, and development. These include liver and intestinal gene regulation, enteric nervous system biology and gastrointestinal motility, bile acid homeostasis, and interactions between diet and the gut microbiome. He is actively involved in clinical and translational investigations of neonates and children with intestinal, liver, and nutritional disorders. His biomedical research career began during his undergraduate studies at Harvard University. He developed an interest in Pediatric Gastroenterology during his years in the Medical Scientist Training Program (M.D./Ph.D.) at Baylor College of Medicine. He completed internship and residency training in Pediatrics, as well as fellowship training in Pediatric Gastroenterology, Hepatology & Nutrition, at Baylor College of Medicine.
The goal of Dr. Preidis’s laboratory is to define mechanisms through which early life undernutrition alters metabolism and to determine how undernutrition impairs intestinal and liver function. Undernutrition causes acute medical problems, but also long term health problems that may result from permanent epigenetic changes that alter transcription or via changes in the gut microbiome. Current studies focus on how malnutrition alters hepatic secretion, transcriptional programming, gastrointestinal motility, and host-microbiome interactions to impact growth. This work is pertinent to those suffering from nutritional deficiencies caused by a wide range of medical and psychosocial factors, including preterm and underweight newborns in the neonatal intensive care unit, adolescents with anorexia nervosa, and children with severe acute malnutrition in the developing world.
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|Preidis GA, Soni KG, Suh JH, et al. (2020) Coagulopathy in Malnourished Mice Is Sexually Dimorphic and Regulated by Nutrient-Sensing Nuclear Receptors. Hepatology Communications. 4: 1835-1850|
|Soni KG, Dike PN, Suh JH, et al. (2020) Early-life malnutrition causes gastrointestinal dysmotility that is sexually dimorphic. Neurogastroenterology and Motility : the Official Journal of the European Gastrointestinal Motility Society. e13936|
|Su GL, Ko CW, Bercik P, et al. (2020) Spotlight: Probiotics Guidelines. Gastroenterology|
|Soni KG, Halder T, Conner ME, et al. (2019) Sexual dimorphism in upper gastrointestinal motility is dependent on duration of fast, time of day, age, and strain of mice. Neurogastroenterology and Motility : the Official Journal of the European Gastrointestinal Motility Society. e13654|
|Ford SL, Lohmann P, Preidis GA, et al. (2019) Improved feeding tolerance and growth are linked to increased gut microbial community diversity in very-low-birth-weight infants fed mother's own milk compared with donor breast milk. The American Journal of Clinical Nutrition. 109: 1088-1097|
|Alves da Silva AV, de Castro Oliveira SB, Di Rienzi SC, et al. (2019) Murine Methyl Donor Deficiency Impairs Early Growth in Association with Dysmorphic Small Intestinal Crypts and Reduced Gut Microbial Community Diversity. Current Developments in Nutrition. 3: nzy070|
|Alves da Silva AV, de Castro Olveira SB, Di Rienzi SC, et al. (2019) Murine methyl donor deficiency impairs early growth in association with dysmorphic small intestinal crypts and reduced gut microbial diversity Current Developments in Nutrition. 3: nzy070|
|Thaxton GE, Melby PC, Manary MJ, et al. (2018) New Insights into the Pathogenesis and Treatment of Malnutrition. Gastroenterology Clinics of North America. 47: 813-827|
|Shin A, Preidis GA, Shulman R, et al. (2018) The Gut Microbiome in Adult and Pediatric Functional Gastrointestinal Disorders. Clinical Gastroenterology and Hepatology : the Official Clinical Practice Journal of the American Gastroenterological Association|
|Preidis GA, Kim KH, Moore DD. (2017) Nutrient-sensing nuclear receptors PPARα and FXR control liver energy balance. The Journal of Clinical Investigation|