Abu-El-Haija M, Wilhelm R, Heinzman C, Siqueira BN, Zou Y, Fei L, Cole CR. Early enteral nutrition in children with acute pancreatitis. J Pediatr Gastroenterol Nutr. 2016 Mar;62(3):453-6.
Nutrition is an essential part in the management of acute pancreatitis and is not well studied in the pediatric population. Dr. Abu-El-Haija, MD, and coworkers performed a retrospective chart review of the prospectively collected nutrition database on acute pancreatitis admissions to Cincinnati Children’s. They found that there is no difference in the level of pain between the groups allowed to feed and those who were not allowed any food by mouth. This study shows that starting oral feeding upon admission of acute pancreatitis without increasing the pain severity and length of hospital stay.
Mezoff EA, Hawkins JA, Ollberding NJ, Karns R, Morrow AL, Helmrath MA. The human milk oligosaccharide 2'-fucosyllactose augments the adaptive response to extensive intestinal. Am J Physiol Gastrointest Liver Physiol. 2016 Mar 15;310(6):G427-38.
Short bowel syndrome caused by intestinal resection leads to a significant increase in morbidity, mortality, and cost of care. When infants with short bowel syndrome are fed human milk in lieu of formula, they have an increase in intestinal adaptation. Using a mouse model of intestinal adaptation, Dr. Mezoff and colleagues discovered that 2’-Fucosyllactose, which is the most abundant oligosaccharide found in human milk and is not a component of infant formulas, improved weight gain and intestinal crypt depth. This study suggests that 2’-Fucosyllactose supplementation after intestinal resection improves intestinal adaptation.
Miethke AG, Zhang W, Simmons J, Taylor AE, Shi T, Shanmukhappa SK, Karns R, White S, Jegga AG, Lages CS, Nkinin S, Keller BT, Setchell KD. Pharmacological inhibition of apical sodium-dependent bile acid transporter changes bile composition and blocks progression of sclerosing cholangitis in multidrug resistance 2 knockout mice. Hepatology. 2016 Feb;63(2):512-23.
Chronic fibrosing cholangiopathies, such as progressive familial intrahepatic cholestasis type 3, biliary atresia, or primary sclerosing cholangitis, carry high morbidity and mortality due to complications from progressive cholestasis and fibrosis. Dr. Miethke, MD, and his colleagues used a mouse model for chronic cholestatic disorders to show that inhibiting the apical sodium-dependent bile acid transporter resulted in an increase in bile acid excretion. Additionally, they discovered a significant reduction of liver and serum concentrations of bile acids as well as biomarkers of hepatocellular and cholestatic injury. This preclinical study demonstrates the possibility of pharmacologically blocking the apical sodium-dependent bile acid transporter to inhibit the progression of fibrosing cholangiopathies during the early phase of the disease process.
Waddell A, Vallance JE, Moore PD, Hummel AT, Wu D, Shanmukhappa SK, Fei L, Washington MK, Minar P, Coburn LA, Nakae S, Wilson KT, Denson LA, Hogan SP, Rosen MJ. ILl-33 signaling protects from murine oxazolone colitis by supporting intestinal epithelial function. Inflamm Bowel Dis. 2015 Dec;21(12):2737-46.
Inflammatory bowel disease is often described as chronic inflammation of the intestine resulting from the dysregulation of the mucosal immune response and epithelial barrier dysfunction. Dr. Rosen, MD, MSCI, and his collaborators used the oxazolone murine model to produce a type-2 cytokine mediated model of colitis with pathologic and immunologic features similar to ulcerative colitis to determine the role of interleukin 33 (IL-33). They were able to show that IL-33 deficient mice displayed an increased severity of oxazolone colitis. These results suggest that understanding the mechanisms of the protective effect of IL-33 will lead to the identification of therapeutic approaches to maintain epithelial barrier function and control inflammation in ulcerative colitis.
Xanthakos SA, Jenkins TM, Kleiner DE, Boyce TW, Mourya R, Karns R, Brandt ML, Harmon CM, Helmrath MA, Michalsky MP, Courcoulas AP, Zeller MH, Inge TH, Teen-LABS Consortium. High prevalence of nonalcoholic fatty liver disease in adolescents undergoing bariatric surgery. Gastroenterology. 2015 Sep;149(3):623-34.e8.
We know little regarding the prevalence or the factors causing the development of nonalcoholic fatty liver disease (NAFLD) in the severely obese adolescent population. Dr. Xanthakos, MD, MS, and colleagues discovered that despite high prevalence of NAFLD, severe nonalcoholic steatohepatitis (NASH) was uncommon in a multicenter cohort of adolescents who underwent bariatric surgery. Gene expression studies identified altered expression of genes that regulate macrophage chemotaxis, cholesterol absorption, and fatty acid binding among those with severe NASH. This study suggests there maybe protective factors among the severely obese that lowers the risk of developing NASH.