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Intestinal Failure
Published in Praveen S. Goday, Cassandra L. S. Walia, Pediatric Nutrition for Dietitians, 2022
Rashmi Patil, Elizabeth King, Jeffrey Rudolph
Nutritional therapies are the mainstay of treatment for pediatric intestinal failure. PN is largely supportive and provides substrates to meet fluid, electrolyte, and nutritional requirements and facilitate growth. Individualized PN to meet the patient’s fluid, electrolyte, energy, macronutrient, and micronutrient requirements is vital. Enteral nutrition (EN) is supportive but also therapeutic. Until the recent introduction of glucagon-like peptide-2 (GLP-2) analogs, EN was the only known therapy that directly influenced intestinal adaptation.
The Role of Growth Factor Signaling in the Development and Treatment of Necrotizing Enterocolitis
Published in David J. Hackam, Necrotizing Enterocolitis, 2021
Rita D. Shelby, Terrence M. Rager, Barrett P. Cromeens, Gail E. Besner
Glucagon-like peptide 2 (GLP-2) is derived from the precursor protein proglucagon (71) and is produced in the enteroendocrine L cells of the distal small intestine and colon. It is secreted in response to fatty acids and glucose in the intestinal lumen (72–76). GLP-2 signaling is thought to play an important role in the developing intestine. Fetal and neonatal rats have higher GLP-2 receptor (GLP-2R) transcript levels than adult rats (77). GLP-2 administration increases both the amount of and activity of intestinal enzymes in premature piglets and results in increased intestinal growth compared to those fed enterally or parenterally without GLP-2 (78). In humans, a study of GLP-2 expression in premature infants demonstrated greater baseline and postprandial levels of GLP-2 compared to adults (79, 80).
The Small Intestine
Published in Professor Sir Norman Williams, Professor P. Ronan O’Connell, Professor Andrew W. McCaskie, Bailey & Love's Short Practice of Surgery, 2018
Professor Sir Norman Williams, Professor P. Ronan O’Connell, Professor Andrew W. McCaskie
Medical management of patients with short bowel syndrome relies on the use of antidiarrhoeal agents (loperamide and codeine phosphate), drugs to reduce diarrhoea related to bile-salt malabsorption (colestyramine) and enteral and parenteral vitamin and trace element supplements. Although there has also been interest in the use of drugs to promote intestinal adaptation, such as growth hormone, glutamine and, most recently, glucagon-like peptide 2 agonists, the mainstay of treatment for short bowel syndrome remains home parenteral nutrition (HPN). The development of this treatment in the late 1960s enabled the majority of patients with short bowel syndrome to enjoy a reasonably good quality of life, with long-term survival related principally to the underlying disease. HPN is, however, expensive and demanding and patients with short bowel syndrome receiving HPN are at risk from catheter-related complications (notably catheter-related sepsis and occlusion), as well as metabolic complications (fibrotic liver disease, gallstones, metabolic bone disease and kidney stones).
Adaptation Processes of the Remaining Jejunum or Ileum after Extensive Intestinal Resection
Published in Journal of Investigative Surgery, 2022
Affonso Flávio Jorge Mussolino, Ana Cristina Aoun Tannuri, Josiane de Oliveira Gonçalves, Suellen Serafini, Uenis Tannuri
Our histomorphometric data indicate an increase in height of jejunal villi, not observed in ileal villi. However, crypt depth increased in both groups and subjectively we noticed that diarrhea, while present in both experimental groups, was more intense in the IG animals, consistent with the more evident decrease in weight gain in this group. Diarrhea is known to lead to a decrease in villi height [18], which could explain why the ileal loops did not show the same elongation of villi seen in jejunal loops. An adult mice model of SBS has shown that the increase in the villi of the residual jejunum was due to enterocyte proliferation, while in ileal loops the increased villi were due to an increase in the size of enterocytes [19]. On the other hand, the more expressive deepening in ileal crypts is consistent with the better adaptive response of the ileum. Maintenance of ileal loops seems to ensure continuity of glucagon-like peptide-2 (GLP-2) production, which is important for the intestinal adaptation process after extensive intestinal resection [20]. GLP-2 is produced by the entero-endocrine L cells from the ileum and proximal colon and is released in response to the presence of nutrients in the intestinal lumen. The direct passage of a nutrient-rich chime into the ileum of animals undergoing jejunal resection probably elicits a greater stimulus for the post-resection ileal growth.
Influence of gut microbiota and intestinal barrier on enterogenic infection after liver transplantation
Published in Current Medical Research and Opinion, 2019
Jingzhou Mu, Qiuyu Chen, Liang Zhu, Yunhong Wu, Suping Liu, Yufei Zhao, Tonghui Ma
Glucagon-like peptide-2 (GLP-2) is a newly discovered intestinal epithelial growth factor and is the primary glucagon gene in the intestinal endocrine L-cells. GLP-2 consists of 33 amino acid peptides and has a molecular weight of 3,900 kDa. Animal experiments and clinical studies have shown that GLP-2 can promote the growth of normal small intestine and the repair of pathological intestinal mucosal injury63. GLP-2 is different from the conventional polypeptide growth factors. This gene has a gut-specific role and strong growth-promoting effect. Numerous advantages of the GLP-2 show its good prospects for clinical application. GLP-2 is currently used to treat ulcerative colitis and short bowel syndrome in phase II and III clinical trials64,65. Our research also proved that GLP-2 could reduce bleeding–reperfusion injury of the small intestine (during liver transplantation, an hepatic phase exists in the intestinal injury)66.
The safety of available treatment options for short bowel syndrome and unmet needs
Published in Expert Opinion on Drug Safety, 2021
Loris Pironi, Emanuel Raschi, Anna Simona Sasdelli
The pharmacological options for SBS can be categorized as ‘symptomatic’ pharmacotherapy, including drugs registered for the treatment of diarrhea or for others GI or non-GI pathological conditions implicating an off-label use, and ‘curative’ pharmacotherapy including drugs specifically registered for SBS [5,14]. The latter group is represented by the recombinant human growth hormone (hGH), approved by Food and Drug Administration (FDA) in 1987 [15], and the glucagon-like-peptide-2 (GLP-2) analogue teduglutide, approved by FDA [16] and European Medicines Agency (EMA) [17] in 2012.