Delayed gastric emptying in diabetic rats caused by decreased expression of cystathionine gamma lyase and H2S synthesis: in vitro and in vivo studies

Abstract

Background

This study aimed to evaluate the role of H₂S on gastric emptying rate (GER) and also to determine the effect of gastric distention on mRNA and protein expression of cystathionine β-lyase (CBS) and cystathionine γ-synthase (CSE) in diabetic-gastroparetic and normal rats.

Methods

Adult normal rats intraperitoneally received either propargylglycine (PAG), L-cysteine or NaHS 30 min prior to GER marker (acetaminophen) to investigate H₂S involvement in GER and the same protocols were performed in diabetes-induced gastroparesis rats. The role of calcitonin gene related peptide (CGRP) neurons in the prokinetic effect of endogenous H₂S on GER was determined. The level of CBS and CSE expressions in response to gastric distention were also determined. The effect of H₂S on frequency and tension of spontaneous contractions of gastric smooth muscle strips was investigated.

Key Results

Our results showed that: (i) H₂S and L-cysteine increased GER in gastroparetic and normal rats. (ii) The increased levels of CSE expression in response to gastric distention in diabetic rats were lower than in normal rats. (iii) PAG inhibited the excitatory effect of capsaicin on GER and on tension of spontaneous contractions of strips. (iv) Hydrogen sulphide increased the frequency and tension of spontaneous contractions of gastric strip muscles in normal and diabetic rats.

Conclusions & Inferences

The results showed that delayed GER in diabetic rats can be due to down-regulation of H₂S biosynthesis enzyme, CSE and suggested that a potential prokinetic role for H₂S to treat the delayed gastric emptying in diabetic patients.

The results of the present study showed that endogenous and exogenous H₂S and L-cysteine accelerate the GER in normal and diabetic rats. The molecular findings were also showed that mRNA and protein expression of cystathionine gamma lyase, the main responsible enzyme for H₂S synthesis in the rat stomach decreased in diabetic rats.

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