Abnormalities of the Migrating Motor Complex in Diabetics with Autonomic Neuropathy and Diarrhea

Abstract

Diarrhea is a common symptom in long-standing diabetes. The pathogenesis of this diarrhea remains obscure, although it appears to be related to the development of autonomic neuropathy, which may cause several abnormalities including altered gut motility. We studied fasting gastrointestinal motility for a mean of 210 min in a group of 12 type-II diabetics with diarrhea. All patients had peripheral neuropathy and symptoms of autonomic neuropathy. Their motor activity was compared with that of a group of six normal volunteers. In addition, gastrointestinal transit time was assessed by the hydrogen breath test. The presence of bacterial overgrowth was assessed by the hydrogen breath test and culture of jejunal secretions. The diabetics showed grossly disordered motor activity. There was a complete absence of phase-III activity in two patients. Most phase III's commenced in the distal duodenum or jejunum. The phase-III component was often of short duration at each recording site. There was increased velocity of propagation between sites. Continuous phase-II activity was noted in some patients. Antral activity was absent or reduced during phase II. Gastrointestinal transit time was significantly prolonged in the diabetics. Bacterial overgrowth was demonstrated in three diabetic subjects. These motility abnormalities are nonspecific and are unlikely to play a major role in the pathogenesis of diabetic diarrhea.

Relationships of Upper Gastrointestinal Motor and Sensory Function With Glycemic Control

“…Pharmacologically induced inhibition of small-intestinal motility decreases absorption of glucose from the small-intestinal lumen (113). Smallintestinal motility is frequently abnormal in diabetic patients (114)(115)(116)(117) and may potentially affect glucose absorption.…”

T. gondii Infection Acquired during Pregnancy and/or after Birth may be Responsible for Development of both Type 1 and 2 Diabetes Mellitus

“…Esophagus Increased amplitude and number of peristaltic contractions [471][472][473][474] Increased number of spontaneous and non-propagated contractions [475] Decreased amplitude of lower esophageal sphincter pressure [471] Multi-peaked contractions [476,477] Stomach Decreased antral IMMC [478] Decreased postprandial antral activity and the number of antral contractions [479] Pyloric dysmotility [480] Small intestine Decreased or increased frequency and amplitude of the antropyloroduodenal contractions [481] Increased duration of MMC cycle [482] Early recurrence of the MMC and clusters of contractile activity [483] and other cells. For example, seven days after diabetes induction by streptozotocin, a significant reduction in the circumference and area of the colon (Table 29), size of the myenteric neurons and their nuclei (Table 30), and a decrease in the overall neuronal population as compared with controls, were demonstrated [504].…”

Diabetic enteropathy — still undefeated?

“…Dooley et al have determined that intestinal passage in patients with diabetes, autonomic neuropathy and unexplained diarrhoea is disturbed, and that this disturbance involves many MMC abnormalities. Most of MMC cycles had no antral component, and in the remaining phase III was absent or started in the small intestine omitting the stomach and duodenum [12]. In 25% of patients participating in the study by Dooley small intestinal bacterial overgrowth (SIBO) was diagnosed based on the hydrogen breath test and clinical improvement was obtained after antibiotic therapy.…”