• 대한수의학회지
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• 제40권4호
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• pp.653-660
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• 2000

몽골리안 저빌(Meriones unguiculatus)의 위장관을 분문부, 기저부, 유문부, 십이지장, 공장, 회장, 맹장, 결장 및 직장의 9부분으로 구분하고 이들 부위에서 cholecystokinin(CCK)-8, gastrin, secretin, pancreatic polypeptide(PP), somatostatin, serotonin, glucagon 및 insulin 등 8종의 항혈청에 대한 내분비 세포의 부위별 분포 및 출현빈도를 면역조직화화적으로 관찰하였던 바, CCK-8, gastrin, somatostatin 및 serotonin 면역반응세포들이 관찰되었다. 이들 면역반응세포들은 위 부위에서는 원형에서 타원형으로 주로 위샘(gastric gland) 또는 주세포와 벽세포 사이에서 관찰되었고, 장 부위에서는 원형 또는 타원형의 면역반응세포들이 공장의 장샘(intestinal gland)에서 관찰되었으며, 타원형에서 방추형의 세포들이 장상피세포 사이에서 관찰되었다. CCK-8 면역반응세포들은 유문부와 십이지장에 국한되어 다수 또는 소수 관찰되었으며, gastrin 면역반응세포들은 유문부에 국한되어 다수 관찰되었다. Somatostatin 면역반응세포들 역시 gastrin 변역반응세포들과 유사하게 유문부에 국한되어 중등도의 출현빈도를 나타내었고, serotonin 면역반응세포들은 분문부와 맹장을 제외한 위장관 전부위에 걸쳐 중등도 또는 다수 관찰되었으나, secretin, PP, glucagon 및 insulin 면역반응세포들은 관찰되지 않았다. 이상에서 몽골리안 저빌의 위장관에 존재하는 내분비 세포들의 종류 및 출현빈도는 다른 설치류에 비해 매우 적거나 낮은 것으로 관찰되었으며, 이들 내분비 세포들의 출현부위 역시 다른 설치류에서와는 달리 일부 부분에 국한되는 것으로 관찰되었다.

• Clinical and Experimental Reproductive Medicine
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• 제23권3호
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• pp.269-275
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• 1996

Biosynthesis and secretion of anterior pituitary hormones are under the control of specific hypothalamic stimulatory and inhibitory factors. Among them, Growth Hormone Releasing Hormone (GHRH) is the major stimulator of pituitary somatotrophs activating GH gene expression and secretion. Human GHRH is a polypeptide of 44 amino acids initially isolated from pancreatic tumors, and the gene for the hypothalamic form of GHRH is organized into 5 exons spanning over 10 kilobases (kb) on genomic DNA and encodes a messenger RNA of 700-750 nucleotides. Several neuropeptides classically associated with the hypothalamus have been found in the extrahypothalamic regions, suggesting the existence of novel sources, targets and functions. GHRH-like immunoreactivity has been found in several peripheral sites, including placenta, testis, and ovary, indicating that GHRH may also have regulatory roles in peripheral reproductive organs. Furthermore, higher molecular weight forms of the GHRH transcripts were identified from these organs (1.75 kb in testis; 1.75 and >3 kb in ovary). These tissue-specific expression of GHRH gene suggest the existence of unique regulatory mechanism of GHRH expression and function in these organs. In fact, placenta-specific and testis-specific promoters for GHRH transcripts which are located in about 10 kb upstream region of hypothalamic promoter were reported. The use of unique promoters in extrahypothalamic sites could be refered in a different control of GHRH gene and different functions of the translated products in these tissues. Somatotrophs and lactotrophs have been thought to be derived from a common bipotential progenitor, the somatolactotrophs, which give origins to either phenotypes. Although the precise mechanism responsible for the lactotroph differentiation in the anterior pituitary gland has not been yet clalified, there are several candidators for the generation of lactotrophs. In human, the presence of GHRH peptides with different size from authentic hypothalamic form in the normal anterior pituitary and several types of adenoma were demonstrated. Recently our group found the existence of immunoreactive GHRH and its transcript from the normal rat anterior pituitary (gonadotroph> somatotroph> lactotroph), and the GHRH treatment evoked the increased proliferation rate of anterior pituitary cells in vitro. The transgenic mouse models clearly shown that GHRH or NGF overexpression by anterior pituitary cells induced development of pituitary hyperplasia and adenomas particularly GH-oma and prolactinoma. Taken together, we hypothesize that the pituitary GHRH could serve not only as a modulator of hormone secretion but as a paracrine or autocrine regulator of anterior pituitary cell proliferation and differentiation. Interestingly enough, the expression of Pit-1 homeobox gene (the POU class transcription factor) was confined to somatotrophs, lactotrophs and somatolactotrophs in which GHRH receptors are expressed commonly. Concerning the mechanism of somatolactotroph and lactotroph differentiation in the anterior pituitary, we have focused following two possibilities; (1) changes in the relative levels or interactions of both hypothalamic and intrapituitary factors such as dopamine, VIP, somatostatin, NGF and GHRH; (2) alterations of GHRH-GHRH receptor signaling and Pit-1 activity may be the cause of lactotroph differentiation or pituitary hyperplasia and adenoma formation. Extensive further studies will be necessary to solve these complicated questions.