Introduction

Gastrointestinal (GI) function is controlled by the extrinsic and intrinsic nervous systems. Extrinsic neural control is exerted by the parasympathetic and sympathetic nervous components of the autonomic nervous system. Intrinsic control is imposed by the enteric plexuses (the "little brain" in the digestive tract) (Fig. 1). Experimental models of gut motor function suggest a predominant modulatory role for the extrinsic nervous system, and primary control through the (intrinsic) enteric nervous system (1). Thus, derangements of the extrinsic nerves at any level may result in alteration of GI motility and secretion (2).

Intrinsic control can occur quite independently of the extrinsic control. The enteric nervous system consists of 100 million neurons that are organized in distinct ganglionated plexi including the submucous plexus (involved in absorption and secretion), the myenteric plexus (involved in motility), and the plexus of Cajal (which serves pacemaking functions). As with the somatic and autonomic nerves elsewhere, the gut's autonomic and enteric nervous system can be affected in diabetes mellitus.

The GI tract symptoms are common in patients with diabetes seen at tertiary referral centers. In the absence of structural lesions in the gut, such patients are commonly assumed to have autonomic neuropathy. This is not unreasonable since autonomic neuropathy is a common complication of diabetes. Although microvascular complications are less frequent in type 2 diabetes, as compared to people with type 1 diabetes, the prevalence of autonomic neuropathy among type 2 diabetics is still significant. The degree of glycemic control affects the incidence and progression of neuropathic complications including GI neuropathy. Moreover, since the rate of gastric emptying and the nature of the ingested meal are important determinants of postprandial glucose concentrations, altered gastric emptying may impact on the ability to achieve good glycemic control in people with diabetes.

The GI involvement is frequently associated with autonomic dysregulation of the eyes, blood pressure, heart and peripheral vessels and the urinary bladder and sexual organs. In this chapter, we aim to focus on the GI manifestations of diabetes mellitus, advances in understanding the mechanism and role of autonomic, enteric and hormonal dysfunctions, the autonomic symptoms and tests that are indicative of autonomic denervation, and management of GI manifestations of diabetes.

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