There are no morphologic abnormalities of the gastric wall or abdominal vagus in patients with diabetic gastroparesis

Disordered gastric motor function in diabetes mellitus

“…In animal models of diabetes, the neural innervation and neuropeptide content of the gastrointestinal tract is abnormal [41] and in preliminary human studies a decrease in the density of unmyelinated axons in the abdominal vagus was observed [42]. However, a more detailed study found no abnormalities in the gastric wall, or abdominal vagus in patients with diabetic gastroparesis [43]. Although this latter report was not comprehensive and the techniques used were relatively insensitive, it seems clear that the absolute number of neurones in the myenteric plexus is not reduced in diabetic gastroparesis.…”

Gastrointestinal motility and glycemic control in diabetes: the chicken and the egg revisited?

“…The available information in humans is limited by the relatively small number of studies and the substantial logistical difficulties in obtaining tissue and controlling for variables, such as the type and duration of diabetes and the adequacy of glycemic control. Early studies reported no evidence of morphological changes in the vagus nerve of patients with diabetic gastroparesis (19), although vagal conduction was reportedly slowed (20) and gastric secretion in response to sham feeding was diminished, suggestive of vagal dysfunction (21). Though limited to a small number of subjects, the most convincing observations to parallel rodent data are the depletion of ICCs in the stomach (22), jejunum (23), and colon (24) of patients with longstanding diabetes and gastroparesis; absence of gastric ICCs, in particular, appears to be associated with severe upper gastrointestinal symptoms and a poor response to treatment with gastric electrical pacing (22).…”

“…It is likely that uncovering mutations in SCN5A and other ion channels will be just the beginning of determining the complex genetic basis for SIDS, and in the years ahead other genetic abnormalities may also be linked to SIDS. Current thinking emphasizes a brain stem neural network maldevelopment hypothesis for this syndrome (19). It is likely that the etiology of SIDS is heterogeneous and may result from the interaction of a number of genetic and environmental factors.…”

Gastric mucosal nerve density

“…Early studies of the vagus nerve in diabetes reported segmental demyelination and axonal degeneration, 6,7 whereas another report showed no pathology. 8 A description 9 of distended neurons in sympathetic and celiac ganglia, loss of myelinated nerves in the vagus nerve and sympathetic trunks, and inflammatory changes in autonomic ganglia remains unconfirmed. Full-thickness stomach specimens from subjects with type 2 diabetes with gastroparesis have fewer interstitial cells of Cajal 10,11 and inhibitory neurons in the myenteric plexus 11 but these are not easily available for analysis by routine endoscopic biopsy.…”