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Introduction

The GI tract is the largest endocrine organ of the body, but little is known about it.1 Traditionally, mechanisms of cell-to- cell communication have been divided into autocrine, para­crine, neurocrine, endocrine, and spermiocrine mechanisms, but this division is not entirely clear in the GI tract.

Almost all regulatory substances synthesized in the GI tract are peptides, but several of them function as endocrine, neurocrine, para­crine, and even autocrine peptides.

In 1902, secretin was discovered as the first GI hormone, and in fact the first hormone overall.1 Since then, a large number of GI regulatory peptides have been identified (Table 9.10).1,2 Many of these regulatory peptides are considered true hor­mones, although currently only six meet all the physiological criteria for a hormone: insulin, glucagon, gastrin, secretin, cholecystokinin (CCK), and motilin. The main functions of the more important regulatory peptides are listed in Ta­ble 9.11.2

In general, endocrine disorders are due to a lack (e. g., hypoad­renocorticism) or overabundance (e. g., hyperadrenocorticism) of a hormone. To date, the only syndrome known to be due to the lack of a GI hormone is diabetes mellitus, which is due to an absolute or relative insulin deficiency. Surprisingly, a lack of other GI regulatory peptides has not been identified as causing specific syndromes in any species. However, there is no reason to believe that a lack of GI regulatory peptides could not lead to clinical disease; therefore, it appears likely to be only a mat­ter of time before such syndromes are discovered. Many chronic GI diseases are considered idiopathic, and it is possible that some of these conditions are caused by GI regulatory peptide deficiency.

Disorders related to an overabundance of GI regulatory pep­tides are well recognized and are caused by neuroendocrine tumors (NETs). The prevalence of GI NETs in humans is low, with about 3-4 cases per million population. Approximately 55% of these NETs are carcinoids, 25% insulinomas, 10% gas­trinomas, 2% vasoactive intestinal polypeptidomas (VIPomas), 2% glucagonomas, less than 1% somatostatinomas, and the re­maining 5-6% non-functioning tumors or pancreatic polypep- tidomas. Similar epidemiological data are not available for dogs and cats and many of these GI NETs have not yet been described in veterinary patients. To date, GI NETs described in dogs and cats are limited to insulinomas, gastrinomas, glucagonomas, carcinoids, and a single case of a pancreatic polypeptidoma.

9.4.2

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Source: Steiner J.M. (ed.). Small Animal Gastroenterology. Schluetersche,2008. — 387 p.. 2008

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