Diabetic Gastroparesis: Functional/Morphologic Background, Diagnosis, and Treatment Options

Abstract

The regulation of gastrointestinal motility mainly involves the smooth muscle, neural (extrinsic and intrinsic), and hormonal elements, the glial cells, and the interstitial cells of Cajal. An orchestrated function of all these components is required for the appropriate propulsive movement of the food in the gastrointestinal tract. Gastroparesis, a pathological slowing-down of gastric emptying, is a result of the damage to the tissue elements involved in the regulation of motility. Gastroparesis is one of the well-known complications of long-standing diabetes mellitus. Although it is rarely a life-threatening complication, it has a deteriorating effect on the quality of life, leads to unpredictable oscillation of the blood glucose level, and increases the time required for the absorption of food and medicines. This review describes the clinical characteristics of diabetic gastroparesis and summarizes the organic and functional motility abnormalities caused by this complication. Finally, the currently available and potential future therapeutic approaches are summarized.

Early Assessment of Cost-effectiveness of Gastric Electrical Stimulation for Diabetic Nausea and Vomiting

“…4 The pathophysiology of diabetic GP is not fully established, but it is associated with neuropathy of extrinsic and intrinsic neurons, abnormal function of smooth muscle cells, and neuropathy of glia cells and the interstitial cells of Cajal. 5 The majority of diabetes patients with delayed gastric emptying remain asymptomatic, and severe symptoms can be present even if gastric emptying tests are normal. 6 Thus, treatment is usually initiated based on recurrent episodes of nausea and/or vomiting rather than a diagnosis of GP based on gastric emptying tests.…”

Severe gastrointestinal autonomic dysfunction in a diabetic boy

“…Gastrointestinal (GI) autonomic dysfunction may include esophageal dysmotility, gastroparesis, dysfunction of intestinal neurons, and decreased/absence of gastrocolic reflex [1,2]. We report a case of a diabetic boy who had a severe GI dysautonomia related with longstanding poorly controlled diabetes, which reverted following the restoration of glycemic control.…”

“…Gastric emptying and GI motility involve complex coordination of enteric nervous, hormonal, and smooth muscle systems [2]. The pathogenesis of GI dysautonomia is multifactorial involving cellular changes, increased oxidative stress, autoimmune and inflammatory factors, impaired hormonal regulation, and genetic predisposition [1].…”

“…Moreover, acute glycemic fluctuations may adversely affect GI function [3]. GI dysmotility may lead to unpleasant GI manifestations, deterioration of nutritional status, or unpredictable oscillations of glycemia due to irregular absorption of food/ medication [1,2]. However, rarely can be life-threatening and may lead to long periods of debilitating GI symptoms requiring prolonged hospital admissions [2,3].…”

“…GI dysmotility may lead to unpleasant GI manifestations, deterioration of nutritional status, or unpredictable oscillations of glycemia due to irregular absorption of food/ medication [1,2]. However, rarely can be life-threatening and may lead to long periods of debilitating GI symptoms requiring prolonged hospital admissions [2,3]. Gastroparesis is the commonest GI dysautonomia, but constipation, diarrhea, and more rarely megacolon or colonic pseudo-obstruction, stercoral ulcer or viscera perforation may occur [3].…”