Upper gastrointestinal sensory-motor dysfunction in diabetes mellitus

Abstract

Gastrointestinal (GI) sensory-motor abnormalities are common in patients with diabetes mellitus and may involve any part of the GI tract. Abnormalities are frequently sub-clinical, and fortunately only rarely do severe and life-threatening problems occur. The pathogenesis of abnormal upper GI sensory-motor function in diabetes is incompletely understood and is most likely multi-factorial of origin. Diabetic autonomic neuropathy as well as acute suboptimal control of diabetes has been shown to impair GI motor and sensory function. Morphological and biomechanical remodeling of the GI wall develops during the duration of diabetes, and may contribute to motor and sensory dysfunction. In this review sensory and motility disorders of the upper GI tract in diabetes is discussed; and the morphological changes and biomechanical remodeling related to the sensory-motor dysfunction is also addressed.

Dyspeptic symptoms in patients with type 1 diabetes: endoscopic findings, Helicobacter pylori infection, and associations with metabolic control, mood disorders and nutritional factors

“…These results are in agreement with the observations of other authors (2,31). Laboratory studies in which patients were submitted to gastric distention by means of the insufflation of intragastric balloons showed that severe hyperglycemia increases the perception of nausea and bloating (30)(31)(32), suggesting that visceral hypersensitivity may also be involved in the relationship between glycemic control and dyspeptic symptoms in DM1. New studies are necessary to explore this hypothesis.…”

“…However, these results do not enable us to rule out the participation of autonomic neuropathy in the pathogenesis of dyspeptic symptoms, once the appropriate tests to investigate this change were not used in the present study. It is important to mention, however, that previous studies did not evidence good correlations between digestive symptoms and diabetic autonomic neuropathy, suggesting a multifactorial physiopathology for dyspepsia in these patients (5,30). The results of the present study seem to fit the current view that digestive symptoms in DM1 are result of a complex relationship between psychological changes, glycemic control, visceral hypersensitivity, and autonomic neuropathy (15,33).…”

“…Gastrointestinal symptoms, on their turn, may increase the levels of anxiety and depression, leading to a vicious cycle. Once the studies on diabetes already demonstrated abnormalities in the perception of visceral sensations in different parts of the gastrointestinal tract (30), it may be inferred that, similar to what was observed in functional diseases, the relationship between psychological factors and gastrointestinal symptoms in diabetes may be explained, at least in part, by visceral hypersensitivity (15). This hypothesis still needs to be confirmed by new studies.…”

To return or to discard? Randomised trial on gastric residual volume management

“…Some authors (De Boer et al, 1992;Mallampalli et al, 2000;Zhao et al, 2006) described the important role of hyperglycaemia in oesophageal motility, decreasing inferior oesophageal sphincter pressure, the speed of the oesophageal peristalsis, and in the delay of gastric emptying. In this sense, a trend has been found on detecting a higher number of hyperglycaemic episodes in patients in the intervention group and a relation between moderate and severe GED and hyperglycaemia despite the group.…”

Characteristics of Consecutive Esophageal Motility Diagnoses After a Decade of Change

“…Diabetes, specifically diabetic autonomic neuropathy, has also been associated with esophageal dysmotility, decreased amplitudes of contraction, and abnormal wave forms. 14,15 As diabetes has increased in prevalence, especially in older adults, 16 within the past decade, it is also another possible explanation for the increase in IEM prevalence.…”