The Role of Prostaglandins in Disrupted Gastric Motor Activity Associated with
Type 2 Diabetes.
Authors Blair PJ, Hwang SJ, Shonnard MC, Peri LE, Bayguinov Y, Sanders KM, Ward SM
Submitted By Sean Ward on 2/5/2019
Status Published
Journal Diabetes
Year 2019
Date Published 1/1/2019
Volume : Pages Not Specified : Not Specified
PubMed Reference 30626609
Abstract Patients with diabetes mellitus often develop gastrointestinal motor problems,
including gastroparesis. Previous studies have suggested this gastric motor
disorder was a consequence of an enteric neuropathy. Disruptions in interstitial
cells of Cajal (ICC) have also been reported. A thorough examination of
functional changes in gastric motor activity during diabetes has not yet been
performed. We comprehensively examined the gastric antrums of Lepob mice using
functional, morphological and molecular techniques to determine the
pathophysiological consequences in this type 2 diabetic animal model. Video
analysis and isometric force measurements revealed higher frequency and less
robust antral contractions in Lepob mice compared to controls. Electrical
pacemaker activity was reduced in amplitude and increased in frequency.
Populations of enteric neurons, ICC and PDGFRa+ cells were unchanged. Analysis
of components of the prostaglandin pathway revealed upregulation of multiple
enzymes and receptors. Prostaglandin-endoperoxide synthase-2 (PTGS2) inhibition
increased slow wave amplitudes and reduced frequency of diabetic antrums. In
conclusion, gastric pacemaker and contractile activity is disordered in type 2
diabetic mice and this appears to be a consequence of excessive prostaglandin
signaling. Inhibition of prostaglandin synthesis may provide a novel treatment
for diabetic gastric motility disorders.

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