Endogenous somatostatin and the gut.

Lucey, Michael R.

doi:10.1136/gut.27.4.457

Cited by 49 publications

(20 citation statements)

References 79 publications

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“…These results are the first findings that focused on the E 2 synthesized and secreted from parietal cells in gastric mucosa during the postnatal development, and it is considered that these findings are associated with previous reports on the serum E 2 level (Germain et al 1978, Greenstein 1992. It is well known that the stomach functions not only as a gastrointestinal system but also as an endocrine system, and gastrin (Thompson 1969), somatostatin (Lucey 1986), and ghrelin (Kojima et al 1999) can be enumerated as the major gastric peptide hormones. These peptide hormones are observed in the stomach in the fetal period by immunohistochemistry (Braaten et al 1976, Hayashida et al 2002, and the speculated onset mechanism of gastric E 2 synthesis is different from that of other gastric endocrine systems.…”

Section: Discussionsupporting

confidence: 69%

Postnatal development of gastric aromatase and portal venous estradiol-17β levels in male rats

Kobayashi

Yoshida

Sun

et al. 2013

Journal of Endocrinology

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Gastric parietal cells synthesize and secrete estradiol-17b (E 2 ) into gastric veins joining the portal vein, and a large amount of gastric E 2 first binds to its receptors in the liver. However, the role of the gastric E 2 is not entirely clear during postnatal development. The objective of this study was to reveal the onset of aromatase and other steroid-synthesizing enzymes in the gastric mucosa; to determine the period of rising E 2 levels in the portal vein; and to further understand the relationship between gastric E 2 and liver estrogen receptor a (ERa). The immunoblot bands and the immunohistochemistry of gastric mucosa revealed that aromatase protein began to express itself at 20 days and then increased in the levels of aromatase protein from 20 days onward. Expression of mRNAs for gastric aromatase (Cyp19a1) and other steroid-synthesizing enzymes, 17a-Hydroxylase (Cyp17a1) and 17b-hydroxysteroid dehydrogenase (HSD17b3), also increased similar to the increment of aromatase protein. Portal venous E 2 levels were elevated after 20 days and increased remarkably between 23 and 30 days, similar to gastric aromatase mRNA levels. The E 2 level was approximately three times higher at 40 days than that at 20 days. The liver weight and Esr1 levels began to increase after 20 days and the increment was positively correlated with the change of portal venous E 2 levels. These findings suggest that some changes may occur around 20 days to regulate the gastric E 2 synthesis and secretion.

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Section: Discussionsupporting

confidence: 69%

Postnatal development of gastric aromatase and portal venous estradiol-17β levels in male rats

Kobayashi

Yoshida

Sun

et al. 2013

Journal of Endocrinology

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“…Native somatostatin is found in the periaqueductal grey matter, substantia gelatinosa, the spinal cord and in descending pathways [2][3][4][5][6][7]. Somatostatin is produced in the hypothalamus, cortex, cerebellum and spinal cord as well as in multiple organs of the gastrointestinal tract (stomach, small bowel, colon and pancreas) [2,[8][9][10][11].…”

Section: Painmentioning

confidence: 99%

The Palliative Effects of Octreotide in Cancer Patients

Dean¹

2001

Chemotherapy

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Octreotide is an extremely useful compound for palliative care physicians. It appears to be active in a number of different pain states and may be given by the spinal and intraventricular route. Its actions in reducing gut motility and secretions make it a valuable adjunct in the management of inoperable bowel obstruction. The same actions make it a potent antidiarrheal agent. Octreotide will often succeed where other antidiarrheal agents fail. Its ability to reduce gut secretions has led to its use in the treatment of fistulae. It has also been proposed as a useful drug in the management of cachexia and ascites. Most of the existing evidence is based on small numbers of case reports and further larger trials are necessary.

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“…and exerts its physiological actions as a paracrine, endocrine, and neurotransmitter ( 1 ). Its principal effects on the target organ are the inhibition of gastrointestinal hormone functions (2)(3)(4)(5), as well as the inhibition of the secretion of gastrointestinal hormones themselves, such as gastrin, cholecystokinin-pancreozymin (PZ), and secretin (6)(7)(8).…”

Section: Introductionmentioning

confidence: 99%