Abstract
BackgroundDiabetic neuropathy in visceral organs such as the gastrointestinal (GI) tract is still poorly understood, despite that GI symptoms are among the most common diabetic complications. The present study was designed to explore the changes in visceral sensitivity and the underlying functional and morphological deficits of the sensory nerves in short-term diabetic rats. Here, we compared the colorectal distension (CRD)-induced visceromotor response (VMR, an index of visceral pain) in vivo, the mechanosensitivity of colonic afferents ex vivo as well as the expression of protein gene product (PGP) 9.5 and calcitonin gene-related peptide (CGRP) in colon between diabetic (3–6 weeks after streptozotocin injection) and control (age-matched vehicle injection) rats.ResultsVMR was markedly decreased in the diabetic compared to the control rats. There was a significant decrease in multiunit pelvic afferent nerve responses to ramp distension of the ex vivo colon and single unit analysis indicated that an impaired mechanosensitivity of low-threshold and wide dynamic range fibers may underlie the afferent hyposensitivity in the diabetic colon. Fewer PGP 9.5- or CGRP-immunoreactive fibers and lower protein level of PGP 9.5 were found in the colon of diabetic rats.ConclusionsThese observations revealed the distinctive feature of colonic neuropathy in short-term diabetic rats that is characterized by a diminished sensory innervation and a blunted mechanosensitivity of the remnant sensory nerves.
Highlights
Diabetic neuropathy in visceral organs such as the gastrointestinal (GI) tract is still poorly understood, despite that GI symptoms are among the most common diabetic complications
Decreased visceromotor response (VMR) to CRD in diabetic rats Visceromotor responses to colorectal distension were examined in control and diabetic (3–6 weeks after fibers (Fig. 3a, b)
Low threshold (LT) units were characterized by a very low threshold (LT) to distention, reaching a maximal firing rate at about 20 mmHg
Summary
Diabetic neuropathy in visceral organs such as the gastrointestinal (GI) tract is still poorly understood, despite that GI symptoms are among the most common diabetic complications. The present study was designed to explore the changes in visceral sensitivity and the underlying functional and morphological deficits of the sensory nerves in short-term diabetic rats. Diabetic neuropathies are heterogeneous, affecting different parts of the peripheral nervous system and resulting in diverse symptoms. Somatic sensory neuropathy is known to result in neuropathic pain, loss of sensation and contribute to the development of diabetic foot ulceration. The mechanisms underlying the pathogenesis of the GI symptoms in the course of diabetes are undoubtedly multifactorial, including motor dysfunction, altered visceral sensitivity, altered gut hormone secretion, central neuroplastic changes as well as psychological and genetic factors (see references in [2]). As clinical management of these patients is often challenging, a better understanding of GI sensory processing in the diabetic condition is needed.
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