CFTR Protein Function Modulation Therapy Is Finally Targeting Cystic Fibrosis-related Gastrointestinal Disease

CFTR Protein Function Modulation Therapy Is Finally Targeting Cystic Fibrosis-related... Invited Commentaries JPGN Volume 66, Number 3, March 2018 intestinal microbiota in some subjects (8). Fecal microbiome CFTR mutations with none to minimal residual protein transplant from these 4 NNS ‘‘responders’’ transferred the glucose function clinically present with exocrine pancreas insufficiency intolerance. The mechanisms that contribute to this apparent and are classified as severe mutations (4). Already in a early phase metabolic response to NNS in some people are unclear, but of disease development, often already in utero, the exocrine pan- certainly larger randomized trials are warranted. Bacteria do have creatic tissue is structurally destroyed due to autophagic and the ability to metabolize sucralose and sucralose has been shown to autolytic activity leading up to the complete inability to excrete have a bacteriostatic effect on some bacteria. Notably other NNS the proteolytic and lipolytic digestive pancreatic enzymes. As a can alter the gut microbiome and impair glucose tolerance in result of the structural nature of the damage, the production and humans and, in the case of aspartame, in doses that are compatible secretion of exocrine pancreatic enzymes are permanently blocked with human intake (10). and stopped. Remarkably, however, this inability of CF patients to The evidence for harm from http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Journal of Pediatric Gastroenterology & Nutrition Wolters Kluwer Health

CFTR Protein Function Modulation Therapy Is Finally Targeting Cystic Fibrosis-related Gastrointestinal Disease

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Publisher
Wolters Kluwer Health
Copyright
Copyright © 2018 by European Society for Pediatric Gastroenterology, Hepatology, and Nutrition and North American Society for Pediatric Gastroenterology, Hepatology, and Nutrition
ISSN
0277-2116
eISSN
1536-4801
D.O.I.
10.1097/MPG.0000000000001868
Publisher site
See Article on Publisher Site

Abstract

Invited Commentaries JPGN Volume 66, Number 3, March 2018 intestinal microbiota in some subjects (8). Fecal microbiome CFTR mutations with none to minimal residual protein transplant from these 4 NNS ‘‘responders’’ transferred the glucose function clinically present with exocrine pancreas insufficiency intolerance. The mechanisms that contribute to this apparent and are classified as severe mutations (4). Already in a early phase metabolic response to NNS in some people are unclear, but of disease development, often already in utero, the exocrine pan- certainly larger randomized trials are warranted. Bacteria do have creatic tissue is structurally destroyed due to autophagic and the ability to metabolize sucralose and sucralose has been shown to autolytic activity leading up to the complete inability to excrete have a bacteriostatic effect on some bacteria. Notably other NNS the proteolytic and lipolytic digestive pancreatic enzymes. As a can alter the gut microbiome and impair glucose tolerance in result of the structural nature of the damage, the production and humans and, in the case of aspartame, in doses that are compatible secretion of exocrine pancreatic enzymes are permanently blocked with human intake (10). and stopped. Remarkably, however, this inability of CF patients to The evidence for harm from

Journal

Journal of Pediatric Gastroenterology & NutritionWolters Kluwer Health

Published: Mar 1, 2018

References

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