Lauren Barron1, Cathleen Courtney1, James Bao1, Emily Onufer1, Roheena Z Panni1, Bola Aladegbami1, Brad W Warner2. 1. Division of Pediatric Surgery, Department of Surgery, Washington University School of Medicine in St. Louis, St. Louis, MO, USA; St. Louis Children's Hospital, St. Louis, MO, USA. 2. Division of Pediatric Surgery, Department of Surgery, Washington University School of Medicine in St. Louis, St. Louis, MO, USA; St. Louis Children's Hospital, St. Louis, MO, USA. Electronic address: Brad.Warner@wustl.edu.
Abstract
BACKGROUND: Short bowel syndrome occurs following massive small bowel resection (SBR) and is one of the most lethal diseases of childhood. We have previously demonstrated hepatic steatosis, altered gut microbiome, and increased fat deposition in our murine model of SBR. These novel findings prompted us to investigate potential alterations in glucose metabolism and systemic inflammation following intestinal resection. METHODS: Male C57BL6 mice underwent 50% proximal SBR or sham operation. Body weight and composition were measured. Fasting blood glucose (FBG), glucose, and insulin tolerance testing were performed. Small bowel, pancreas, and serum were collected at sacrifice and analyzed. RESULTS: SBR mice gained less weight than shams after 10weeks. Despite this, FBG in resected mice was significantly higher than sham animals. After SBR, mice demonstrated perturbed body composition, higher blood glucose, increased pancreatic islet area, and increased systemic inflammation compared with sham mice. Despite these changes, we found no alteration in insulin tolerance after resection. CONCLUSIONS: After massive SBR, we present evidence for abnormal body composition, glucose metabolism, and systemic inflammation. These findings, coupled with resection-associated hepatic steatosis, suggest that massive SBR (independent of parenteral nutrition) results in metabolic consequences not previously described and provides further evidence to support the presence of a novel resection-associated metabolic syndrome.
BACKGROUND:Short bowel syndrome occurs following massive small bowel resection (SBR) and is one of the most lethal diseases of childhood. We have previously demonstrated hepatic steatosis, altered gut microbiome, and increased fat deposition in our murine model of SBR. These novel findings prompted us to investigate potential alterations in glucose metabolism and systemic inflammation following intestinal resection. METHODS: Male C57BL6 mice underwent 50% proximal SBR or sham operation. Body weight and composition were measured. Fasting blood glucose (FBG), glucose, and insulin tolerance testing were performed. Small bowel, pancreas, and serum were collected at sacrifice and analyzed. RESULTS: SBR mice gained less weight than shams after 10weeks. Despite this, FBG in resected mice was significantly higher than sham animals. After SBR, mice demonstrated perturbed body composition, higher blood glucose, increased pancreatic islet area, and increased systemic inflammation compared with sham mice. Despite these changes, we found no alteration in insulin tolerance after resection. CONCLUSIONS: After massive SBR, we present evidence for abnormal body composition, glucose metabolism, and systemic inflammation. These findings, coupled with resection-associated hepatic steatosis, suggest that massive SBR (independent of parenteral nutrition) results in metabolic consequences not previously described and provides further evidence to support the presence of a novel resection-associated metabolic syndrome.
Authors: Joanne F Olieman; Corine Penning; Marjolein Spoel; Hanneke Ijsselstijn; Thelma L van den Hoonaard; Johanna C Escher; Nikolaas M A Bax; Dick Tibboel Journal: Br J Nutr Date: 2011-09-15 Impact factor: 3.718
Authors: Allie E Steinberger; Maria E Tecos; Hannah M Phelps; Deborah C Rubin; Nicholas O Davidson; Jun Guo; Brad W Warner Journal: Am J Physiol Gastrointest Liver Physiol Date: 2022-06-21 Impact factor: 4.871
Authors: Cathleen M Courtney; Zeenat A Shyr; Zihan Yan; Emily Jean Onufer; Allie E Steinberger; Maria E Tecos; Lauren K Barron; Jun Guo; Maria S Remedi; Brad W Warner Journal: Am J Physiol Gastrointest Liver Physiol Date: 2020-05-28 Impact factor: 4.052