Published online Sep 14, 2018. doi: 10.3748/wjg.v24.i34.3821
Peer-review started: May 21, 2018
First decision: June 13, 2018
Revised: June 22, 2018
Accepted: June 27, 2018
Article in press: June 27, 2018
Published online: September 14, 2018
Recently, diabetic gastroparesis (DGP) has received much attention as its prevalence is increasing in a dramatic fashion and management of patients with DGP represents a challenge in the clinical practice due to the limited therapeutic options. DGP highlights an interrelationship between the gastric emptying and pancreatic secretory function that regulate a wide range of digestive and metabolic functions, respectively. It well documented that both gastric emptying and pancreatic secretion are under delicate control by multiple neurohormonal mechanisms including extrinsic parasympathetic pathways and gastrointestinal (GI) hormones. Interestingly, the latter released in response to various determinants that related to the rate and quality of gastric emptying. Others and we have provided strong evidence that the central autonomic nuclei send a dual output (excitatory and inhibitory) to the stomach and the pancreas in response to a variety of hormonal signals from the abdominal viscera. Most of these hormones released upon gastric emptying to provide feedback, and control this process and simultaneously regulate pancreatic secretion and postprandial glycemia. These findings emphasize an important link between gastric emptying and pancreatic secretion and its role in maintaining homeostatic processes within the GI tract. The present review deals with the neurohormonal-coupled mechanisms of gastric emptying and pancreatic secretory function that implicated in DGP and this provides new insights in our understanding of the pathophysiology of DGP. This also enhances the process of identifying potential therapeutic targets to treat DGP and limit the complications of current management practices.
Core tip: Prevalence of diabetic gastroparesis (DGP) is increasing in a dramatic fashion, however there are still gaps in our understanding of the pathophysiology of DGP. It well documented that gastric emptying and subsequent pancreatic secretion are interrelated and regulated by several neurohormonal mechanisms. Dysfunction of these mechanisms affects gastric emptying, pancreatic secretion and postprandial glycemia. Therefore, the present article reviews the neurohormonal-coupled mechanisms that control gastric emptying and pancreatic secretion and their plausible involvement in DGP. This will help in identification of novel therapeutic targets to treat DGP with minimal adverse effects on postprandial glycemia.