Gastroparesis is associated with oxytocin deficiency, oesophageal dysmotility with hyperCCKemia, and autonomic neuropathy with hypergastrinemia

Abstract

BackgroundGastrointestinal (GI) dysmotility and autonomic neuropathy are common problems among diabetics with largely unknown aetiology. Many peptides are involved in the autonomic nervous system regulating the GI tract. The aim of this study was to examine if concentrations of oxytocin, cholecystokinin (CCK), gastrin and vasopressin in plasma differ between diabetics with normal function and dysfunction in GI motility.MethodsNineteen patients with symptoms from the GI tract who had been examined with gastric emptying scintigraphy, oesophageal manometry, and deep-breathing test were included. They further received a fat-rich meal, after which blood samples were collected and plasma frozen until analysed for hormonal concentrations.ResultsThere was an increase in postprandial oxytocin plasma concentration in the group with normal gastric emptying (p = 0.015) whereas subjects with delayed gastric emptying had no increased oxytocin secretion (p = 0.114). Both CCK and gastrin levels increased after the meal, with no differences between subjects with normal respective delayed gastric emptying. The concentration of vasopressin did not increase after the meal. In patients with oesophageal dysmotility the basal level of CCK tended to be higher (p = 0.051) and those with autonomic neuropathy had a higher area under the curve (AUC) of gastrin compared to normal subjects (p = 0.007).ConclusionReduced postprandial secretion of oxytocin was found in patients with delayed gastric emptying, CCK secretion was increased in patients with oesophageal dysmotility, and gastrin secretion was increased in patients with autonomic neuropathy. The findings suggest that disturbed peptide secretion may be part of the pathophysiology of digestive complications in diabetics.

Esophageal and Gastric Dysmotilities are Associated with Altered Glucose Homeostasis and Plasma Levels of Incretins and Leptin

“…In our previous study, we found that esophageal dysmotility was associated with hyperCCKemia [22]. The elevated CCK levels may explain why the decrease in plasma leptin levels was less pronounced in the present group with esophageal dysmotility.…”

“…On the other hand, the reduced GLP-1 concentration may be a compensatory mechanism to prevent a further decrease of the emptying rate. Such a compensatory downregulating mechanism has previously been described for oxytocin, as oxytocin attenuated gastric emptying in patients with gastroparesis [22,30]. GLP-1 administration during hyperglycemia has a markedly greater impact on the gastric emptying rate compared with GLP-1 administration during euglycemia [31].…”

“…-Esophageal dysmotility was associated with hyperCCKemia. -Autonomic neuropathy was associated with hypergastrinemia [22].…”

The Effect of Oxytocin on the Gastric Emptying Rate of Liquids: The Role of Oxytocin and CCK-2 Receptors

“…Ohlsson ve ark. (20) tarafından yapılan diğer bir çalışmada, normal mide boşalma hızına sahip diabetes mellitus (DM) tanı-sı olan deneklerde OT salgılanmasında yemek sonrası artış olduğu gösterilirken, uzamış mide boşalma hızına sahip DM deneklerde yemek sonrası OT salgılamasında bu tip bir artış gösterilmemiştir. OT'nin sağlıklı kadınlarda kolon aktivitesini de arttırdığı gösterilmiş (21), ancak OT kronik konstipasyonlu hastalarda sindirim fonksiyonlarında iyileşmeye neden olmamıştır (22).…”

Effects of rehabilitation management on gastric emptying function in older adults with diabetes

“…Given the combined co-morbid conditions of disordered gastric motility and delayed gastric emptying (De Block et al, 2006;Stevens et al, 2008;Ejskjaer et al, 2009;Hyett et al, 2009;Parkman, 2010;Hejazi et al, 2012), approximately 30 to 50% of DM patients may suffer from a variety of symptoms such as pain, bloating, fullness, early satiety, anorexia, and vomiting (Ma et al, 2009;Szarka and Camilleri, 2010). Delayed gastric emptying among diabetics is closely related to poor glycemic control and cardiac autonomic neuropathy, as well as gastrointestinal hormone changes (Little et al, 2006;Chandrasekharan and Srinivasan, 2007;Mason, 2007;Huang et al, 2009Borg et al, 2009. The gastroduodenal motor dysfunctions underlying abnormally slow gastric emptying in diabetes include decreased antral contractions, impaired coordination between the antrum and duodenum, increased pyloric contractions and impaired proximal gastric relaxation (Stevens et al, 2011).…”