Abnormalities of Small Intestinal Endocrine Cells in Non-Obese Diabetic Mice

• Published in: Journal of diabetes and its complications 1998-07, Vol.12 (4), p.215-223
• Main Authors: El-Salhy, M., Zachrisson, S., Spångéus, A.
• Format: Article
• Language: English
• Subjects: Animals; Associated diseases and complications; Biological and medical sciences; Diabetes Mellitus, Type 1 - pathology; Diabetes. Impaired glucose tolerance; Duodenum - chemistry; Duodenum - pathology; Endocrine pancreas. Apud cells (diseases); Endocrinopathies; Enteroendocrine Cells - chemistry; Enteroendocrine Cells - pathology; Female; Gastric Inhibitory Polypeptide - analysis; Gastrins - analysis; Humans; Islets of Langerhans - pathology; Medical sciences; Mice; Mice, Inbred BALB C; Mice, Inbred NOD; Radioimmunoassay; Secretin - analysis; Serotonin - analysis; Somatostatin - analysis; Swine
• ISSN: 1056-8727; 1873-460X
• DOI: 10.1016/S1056-8727(97)00110-4

The endocrine cells in the duodenum of pre-diabetic and diabetic female non-obese diabetic (NOD) mice aged 22–24 weeks were studied by means of immunohistochemistry and computed image analysis as well as by radioimmunoassays of tissue extracts. As controls, 12 female BALB/cJ mice of the same age as NOD mice were used. The number of secretin-immunoreactive cells increased in diabetic but not in pre-diabetic NOD mice. The level of extractable secretin was higher in both pre-diabetic and diabetic NOD mice. The number of GIP-, CCK/gastrin-, and serotonin-immunoreactive cells was significantly reduced in both pre-diabetic and diabetic NOD mice. There was no statistical difference in the number of somatostatin-immunoreactive cells between the NOD mice and controls. The level of GIP was higher and gastrin was lower in NOD mice compared to controls. There was no statistical difference in the somatostatin level between the NOD mice and controls. The cell secretory index was elevated in all the endocrine cell types except CCK/gastrin cells. It has been suggested that some of the changes in the duodenal endocrine cells could be attributed to the diabetes state, but most of the changes seem to take place before the onset of diabetes. The abnormalities in the duodenal endocrine cells observed here in an animal model for diabetes type I might have relevance for the gastrointestinal dysfunction displayed in human diabetes.