Gastrointestinal motility and glycemic control in diabetes: the chicken and the egg revisited?
Upper gastrointestinal dysfunction occurs frequently in diabetes and potentially contributes to both abdominal symptoms and impaired glycemic control; conversely, variations in blood glucose concentration reversibly affect gut motility in humans. In this issue of the JCI, Anitha et al. report apoptosis of rodent enteric neurons under hyperglycemic conditions, both in vitro and in vivo, associated with impaired PI3K activity and preventable by glial cell line-derived neurotrophic factor. These observations add to recent insights gained from animal models regarding the etiology of diabetic gastrointestinal dysfunction, but investigators must strive to translate animal data to human diabetes.
Rayner
Christopher K
CK
University of Adelaide Department of Medicine, Royal Adelaide Hospital, Adelaide, South Australia, Australia. chris.rayner@adelaide.edu.au
Horowitz
Michael
M
D000818:Animals; D001786:Blood Glucose / Q000378:metabolism*; D048909:Diabetes Complications; D003920:Diabetes Mellitus / Q000503:physiopathology*; D005767:Gastrointestinal Diseases / Q000209:etiology / Q000503:physiopathology; D005769:Gastrointestinal Motility / Q000502:physiology*; D006801:Humans; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism
D001786:Blood Glucose; D019869:Phosphatidylinositol 3-Kinases