Email

gregory.guthrie@bcm.edu

Positions

Assistant Professor

Pediatrics
Nutrition
Baylor College of Medicine

Addresses

Children's Nutrition Research Center (Lab)

Room: CNRC-10062
Houston, TX 77030
United States

Children's Nutrition Research Center (Office)

Room: CNRC-10062
Houston, TX 77030
United States

Education

BS from Louisiana State University

05/2005 - Baton Rouge, Louisiana United States

MS from University of Louisiana at Lafayette

05/2007 - Lafayette, Louisiana United States

PhD from University of Florida

12/2013 - Gainesville, Florida United States

Professional Statement

My research centers on understanding the mechanisms that drive the development of parenteral nutrition associated liver disease in neonates on long-term parenteral nutrition. My current focus is the role of lipid emulsion constituents on causing the disease progression. This research is performed on a neonatal piglet model in order to assess both physiologic and molecular alterations that are similar to those seen in neonates.

Selected Publications

• Guthrie, G. Stoll, B. Chacko, S. Mohammad, M. Style, C. Verla, M. Olutoye, O. Schady, D. Lauridsen, C. Tataryn, N. Burrin, D. "Depletion and enrichment of phytosterols in soybean oil lipid emulsions directly associate with serum markers of cholestasis in preterm PN-fed pigs." JPEN. 2021 Feb 14;
• Guthrie, G. Burrin, D. "Impact of Parenteral Lipid Emulsion Components on Cholestatic Liver Disease in Neonates." Nutrients. 2021 Feb 10;13(2)
• Molina, T. L. Stoll, B. Mohammad, M. Mohila, C. A. Call, L. Cui, L. Guthrie, G. et al "New generation lipid emulsions increase brain DHA and improve body composition, but not short-term neurodevelopment in parenterally-fed preterm piglets." Brain Behav Immun. 2020 Apr 27;85
• Call, L. Molina, T. Stoll, B. Guthrie, G. et al. "Parenteral lipids shape gut bile acid pools and microbiota profiles in the prevention of cholestasis in preterm pigs." J Lipid Res. 2020 May 1;61(7):1038-1051.

Projects

A comparison of Vitamin E supplementation and Rifampicin treatment on the prevention of parenteral nutrition associated liver disease in the piglet model

(03/2014 - 05/2015)

Synergy between phytosterols and inflammation to antagonize nuclear hormone recepto function in PNALD

(05/2015 - present)

Memberships

American Society of Nutrition

Member (03/2008)

American Society of Parenteral and Enteral Nutrition

(03/2014)

Sigma Xi

(01/2011)

Funding

SYNERGY BETWEEN PHYTOSTEROLS AND INFLAMMATION TO ANTAGONIZE NUCLEAR HORMONE RECEPTOR FUNCTION IN PNALD

$75,000.00 (01/01/2016 - 12/31/2017)

Grant funding from ASPEN Rhoads Research Foundation

Modeling liver injury and treatment of biliary atresia using neonatal pigs

$50,000.00 (10/01/2021 - 03/31/2022)

Grant funding from Department of Pediatrics BCM

Biliary atresia (BA) is a disease that occurs in infants shortly after birth that results in the loss of bile ducts that move bile from the liver to the intestine. As the bile accumulates in the liver it causes inflammation and injury. The effects of this disease are so severe that BA is the leading cause of liver disease and liver transplant in children. The only effective treatment of BA is surgical connection of the liver to the intestine to clear bile to reduce bile accumulation in the liver. Even after a successful surgery, most patients with BA will eventually require a liver transplant. Given that the disease is rare, researchers are limited in finding ways to prevent the progression of liver disease in BA patients after surgery. The purpose of this grant application is to develop a model of BA using infant piglets that will have a similar bile duct injury to human patients with BA. To create this model, we will use multiple treatment approaches of a chemical that damages bile ducts of developing piglets while they are in the sow, to establish bile duct injury that is most similar to human patients. The long-term goal of this research will be to examine the post-surgical progression of the disease to minimize the injury that occurs to the liver. From the data we collect on the disease progression post-surgery, we will test targeted interventional approaches to decrease liver injury to delay or remove the need for liver transplant.

Parenteral lipid effect in an obstructive cholestasis model

$45,000.00 (01/01/2020 - 12/31/2021)

Grant funding from Digestive Diseases Center TMC

Neonatal cholestasis, as defined by elevated serum bilirubin concentrations, is a serious condition that can lead to liver transplant in the most severe of cases. Infants with long-term cholestasis have impaired fat absorption and increased energy needs. In some instances, they are placed on parenteral nutrition for support; however, there is limited data on whether this improves or worsens cholestasis. We have developed a neonatal piglet model of obstructive cholestasis utilizing ligation of the cystic and common bile duct to study liver disease development during enteral and parenteral nutrition administration. Our preliminary results suggest that soy-based lipid emulsions increase the severity of liver disease compared to enteral feeding in piglets with obstructive cholestasis. However, whether the cause of this increased liver injury is dependent upon the lipid composition, or the route of parenteral administration is not clear. New generation mixed-composition lipid emulsions have caused fewer liver-related complications in neonates when administered parenterally. Therefore, this lipid emulsion may give insight into whether lipid emulsion composition is the cause of increased liver disease in our obstructive cholestasis model and may normalize or potentially reduce liver disease. The aim of our study is to determine if parenteral lipid composition is the cause of increased liver injury during obstructive cholestasis by comparing soy-based and mixed oil-based lipid emulsions to enterally fed piglets. The results of this study will provide preliminary insight into the role lipid source can have on promoting or preventing liver injury during cases of cholestatic liver disease in neonates.