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Diabetes and the enteric nervous system.

B Chandrasekharan¹, S Srinivasan

¹Division of Digestive Diseases, Emory University, Atlanta, GA 30322, USA.

Neurogastroenterology and Motility

|November 1, 2007

Summary

This summary is machine-generated.

Diabetic gastrointestinal (GI) dysfunction stems from changes in the enteric nervous system (ENS), impacting motility. Early loss of inhibitory neurons in diabetic enteric neuropathy leads to symptoms like constipation and diarrhea.

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Area of Science:

Gastroenterology
Diabetology
Neuroscience

Background:

Diabetes mellitus is linked to significant alterations in gastrointestinal (GI) motility.
Symptoms include nausea, bloating, abdominal pain, diarrhea, and constipation.
The enteric nervous system (ENS) plays a crucial role in diabetic GI dysfunction.

Purpose of the Study:

To review current research on diabetes-related changes in the ENS.
To elucidate the mechanisms underlying altered GI motility in diabetes.
To explore potential therapeutic strategies for diabetic GI motility disorders.

Main Methods:

Review of existing research on diabetic neuropathy and the ENS.
Analysis of studies investigating neuronal changes (inhibitory and excitatory) in the ENS.
Examination of the roles of hyperglycemia, oxidative stress, and inflammation.

Main Results:

Early diabetic enteric neuropathy involves the loss of inhibitory enteric neurons.
These neuronal changes lead to altered gastric emptying, diarrhea, and constipation.
Hyperglycemia, oxidative stress, and inflammation contribute to ENS pathology.

Conclusions:

Diabetic GI motility issues are primarily driven by ENS alterations.
Antioxidants show therapeutic potential for managing diabetic GI motility problems.
Inflammation-associated neurodegeneration is a key factor in diabetes-related GI dysfunction.