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PubMed1979

Pancreatic endocrine cells of Barbus conchonius (Teleostei, Cyprinidae), and their relation to the enteroendocrine cells.

The pancreatic endocrine cells of Barbus conchonius are concentrated in a large (principal) islet, located near the gall bladder, and in a number of smaller islets. Five types of endocrine cells can be distinguished in there pancreatic islets: B cells, A1 (or D cells), 2 types of A2 cells (A2r cells with round granules; and A2fl cells with flocculent granules) and a scarce 5th cell type. The hormones produced by B and A2fl cells are probably insulin and glucagon respectively. The A2r cell contains granules with the same diameter as the granules of the enteroendocrine type III cell of the gut. Both cell types may resemble the enteroglucagon-producing EG cell of mammals. The function of the A1 cells, which are frequently found without secretory granules, and of the 5th cell type, will be discussed. The pancreastic islets of B. conchonius are strongly innervated, which suggests thatpresence of a direct nervous control system. Some intermediate or mixed cells containing exocrine and endocrine A2r granules are found continguous with the principal islet. The origin of pancreatic endocrine cells is also the subject of discussion.

Animals↗
PubMed1997

Length of metabolic normalization after rat islet cell transplantation depends on endocrine cell composition of graft and on donor age.

In vitro studies have demonstrated that beta-cell functions are negatively influenced by age and positively by the presence of glucagon producing alpha cells. This study examines whether the function of beta-cell grafts varies with the age of the donor and with the presence of other endocrine islet cells. Islet beta and endocrine non-beta-cells were purified from 10- to 30-week-old Lewis rats, and reaggregated into pure beta and mixed endocrine cell aggregates. Grafts consisted of 1.2 to 1.7 million beta cells with or without 0.6-0.7 million alpha cells. Their intraportal transplantation in 10-week-old streptozotocin-diabetic rats corrected hyperglycaemia in all experimental groups, with normal glucose tolerance curves at post-transplantation week (PT wk) 4. Recipients of mixed endocrine cell grafts from 10-week-old donors maintained a glucose tolerant state until PT wk 20, but turned glucose intolerant thereafter; only 1 of 12 animals was overtly diabetic at PT wk 64. Recipients of pure beta-cell grafts from 10-week-old donors became glucose-intolerant from PT wk 4 on, with 5 of 11 cases developing overt diabetes before PT wk 64. When grafts were prepared from 30-week-old donors, metabolic deterioration started earlier, again with a more rapid loss for pure beta-cell grafts; at PT wk 64, virtually all recipients were overtly diabetic. It is concluded that delayed graft failure can be the consequence of an insufficient number of islet endocrine non-beta-cells as well as of a higher donor age. This observation can explain late failures in animal and human islet transplantation using marginally low beta-cell numbers. The interpretation of long-term studies on islet cell transplantation can benefit from the use of standardized grafts with well defined cellular composition.

Age Factors↗
PubMed1999

Cell density of adrenomedullin-immunoreactive cells in the gastric endocrine cells decreases in antral atrophic gastritis.

AIMS: Adrenomedullin (AM) is a novel hypotensive and vasorelaxing peptide recently isolated from human phaeochromocytoma tissue, and is widely distributed in various organs. In this study we examined the localization of AM-immunoreactive (IR) cells in the gastric mucosa and AM-IR cell density in antral atrophic gastritis. METHODS AND RESULTS: Gastric mucosal tissues were taken from the gastric body and antral mucosa of 52 patients (27 men, 25 women; mean age 56.0 (range 20-86) years). Immunohistochemical analysis revealed that AM-IR cells were present in the pyloric glands, but not in the fundic glands, and that AM-IR cells were stained positively for chromogranin A and gastrin. The percentage of AM-IR cells vs chromogranin A- and gastrin-IR cells was 42 and 56%, respectively. The number of AM-IR cells decreased with the progression of severity of atrophic changes in the pyloric gland, and also of mononuclear cell infiltration. There was no correlation between the number of AM-IR cells and the degree of neutrophilic infiltration. Similar findings were also obtained for gastrin-IR cells. CONCLUSION: AM-IR cells are present in the endocrine cells including gastrin-IR cells in the pyloric glands. These results suggest that AM may contribute to gastrin secretion in the pyloric glands.

Adrenomedullin↗
PubMed1997

A simple method for purification of adult pig pancreatic endocrine cells.

Adult pig pancreatic endocrine cells were harvested by autodigestion without added enzymes. The isolated, crude cells were purified by mono-poly resolving medium (MPRM). The purity of the harvested cells was determined by dithizone staining and the number of pancreatic endocrine cells was counted. A large number of the cells were stained red with dithizone and showed a high viability and a good insulin secretory response to glucose stimulation. The average number of cells purified by MPRM was 3.40 +/- 1.32 x 10(5) cells/g pancreas and the number of dithizone-stained cells was 2.81 +/- 1.09 x 10(5) cells/g pancreas. The insulin secretion from the pancreatic endocrine cells was maintained throughout a 40-day observation period and high glucose stimulation induced an increase in insulin secretion from the cultured cells. In the cells purified by MPRM, light and electron microscopic studies showed the cells to be typical pancreatic endocrine cells. The present purification method using MPRM allowed us quickly to obtain a large amount of adult pig pancreatic endocrine cells from the unpurified preparations. It is thought to be useful for transplantation and biochemical or biological studies of adult pig pancreatic endocrine cells.

Animals↗
PubMed1995

Administration of omeprazole to rats for one year produces reciprocal effects on antral gastrin and somatostatin cells and no effect on endocrine cells in the colon.

Inhibition of acid secretion with high doses of antisecretagogues, such as omeprazole, is known to raise the plasma gastrin levels. In the present study, we examined the effect of long-term (1-year) treatment of female rats with high doses of omeprazole on the density of antral gastrin and somatostatin cells. A possible effect on the endocrine cell density (chromogranin A as marker) and mucosal thickness of the colon was also examined. The plasma gastrin level in the omeprazole-treated rats was increased 15-fold compared with the level in the controls. The gastrin cell density, on the other hand, showed only a 2-fold increase. The somatostatin cell density in the omeprazole-treated rats was half that in the controls, indicating an inverse relationship between antral gastrin and somatostatin. In the colonic mucosa, neither the mucosal thickness nor the number of chromogranin-A-containing endocrine cells were affected by the omeprazole-induced hypergastrinemia. The results indicate that long-term acid inhibition results in a sustained hypergastrinemia, a modest and stable antral gastrin cell hyperplasia, antral somatostatin cell hypoplasia and lack of trophic effects in the colon.

Animals↗
PubMed2001

Cell-specific processing of chromogranin A in endocrine cells of the rat stomach.

The rat stomach is rich in endocrine cells. The acid-producing (oxyntic) mucosa contains ECL cells, A-like cells, and somatostatin (D) cells, and the antrum harbours gastrin (G) cells, enterochromaffin (EC) cells and D cells. Although chromogranin A (CgA) occurs in all these cells, its processing appears to differ from one cell type to another. Eleven antisera generated to different regions of rat CgA, two antisera generated to a human (h) CgA sequences, and one to a bovine (b) CgA sequence, respectively, were employed together with antisera directed towards cell-specific markers such as gastrin (G cells), serotonin (EC cells), histidine decarboxylase (ECL cells) and somatostatin (D cells) to characterize the expression of CgA and CgA-derived peptides in the various endocrine cell populations of the rat stomach. In the oxyntic mucosa, antisera raised against CgA(291-319) and CGA(316-321) immunostained D cells exclusively, whereas antisera raised against bCgA(82-91) and CgA(121-128) immunostained A-like cells and D cells. Antisera raised against CgA(318-349) and CgA(437-448) immunostained ECL cells and A-like cells, but not D cells. In the antrum, antisera against CgA(291-319) immunostained D cells, and antisera against CgA(351-356) immunostained G cells. Our observations suggest that each individual endocrine cell type in the rat stomach generates a unique mixture of CgA-derived peptides, probably reflecting cell-specific differences in the post-translational processing of CgA and its peptide products. A panel of antisera that recognize specific domains of CgA may help to identify individual endocrine cell populations.

Animals↗
PubMed1995

Studies in transgenic mice reveal potential relationships between secretin-producing cells and other endocrine cell types.

We have produced transgenic mice expressing fusion genes consisting of 1.6 kilobase pairs of the secretin gene 5' flanking region to direct the expression of human growth hormone (hGH) or simian virus 40 large T antigen to secretin-producing cells. Analysis of different mouse tissues for hGH transcripts revealed expression in each of the major secretin-producing tissues, namely the intestine and endocrine pancrease. Multiple label immunohistochemistry demonstrated that the transgene was correctly directed to secretin cells in the intestinal tract, including a previously unrecognized population of secretin cells in the colon of adult and developing mice. In the small intestine, subpopulations of hGH-containing cells frequently coexpressed substance P, serotonin, and cholecystokinin, whereas in the colon, cells expressing hGH frequently coexpressed glucagon, peptide YY, or neurotensin. Transgenic mice expressing large T antigen in secretin cells developed poorly differentiated neuroendocrine tumors of the small intestine, well differentiated colonic tumors containing glucagon-expressing cells, and insulin-producing tumors in pancreas. These studies indicate that the major cis-regulatory sequences necessary for secretin expression in enteroendocrine cells and fetal islets are localized with 1.6 kilobase pairs of the transcriptional start site. Coexpression of reporter transgenes with several gastrointestinal hormones suggests a potential relationships between secretin cells and other enteroendocrine cell types, as well as pancreatic beta cells.

Animals↗
PubMed2003

Nestin-lineage cells contribute to the microvasculature but not endocrine cells of the islet.

To clarify the lineage relationship between cells that express the neural stem cell marker nestin and endocrine cells of the pancreas, we analyzed offspring of a cross between mice carrying a nestin promoter/enhancer-driven cre-recombinase (Nestin-cre) and C57BL/6J-Gtrosa26(tm1Sor) mice that carry a loxP-disrupted beta-galactosidase gene (Rosa26). In nestin-cre(+/tg);R26R(loxP/+) embryos, cre-recombinase was detected in association with nestin-positive cells in the pancreatic mesenchyme with some of the nestin-positive cells lining vascular channels. In postnatal mice, pancreatic beta-galactosidase expression was restricted to vascular endothelial cells of the islet and a subset of cells in the muscularis of arteries in a distribution identical to endogenous nestin expression. Ex vivo explants of mouse pancreatic ducts grew dense cultures that costained for nestin and beta-galactosidase, demonstrating recombination in vitro. The cultures could be differentiated into complex stereotypic structures that contain nestin- and insulin-expressing cells. Nestin-cre(+/tg);R26R(loxP/+)-derived duct cultures showed that insulin-positive cells were negative for beta-galactosidase. These results indicate that both in vivo and in vitro pancreatic endocrine cells arise independently of nestin-positive precursors. The apparent vascular nature of the nestin-positive cell population and the close association with endocrine cells suggest that nestin-positive cells play an important role in the growth and maintenance of the islet.

Animals↗
PubMed2001

Molecular cloning of the porcine insulin cDNA using a monolayer culture of pancreatic endocrine cells.

Porcine pancreatic endocrine cells are an attractive candidate for islet cell transplantation in view of the immunological properties and structural similarities of porcine insulin to human insulin. We recently established a method of isolation and a primary monolayer culture of porcine pancreatic endocrine cells. In this study, cloning of the porcine insulin cDNA was performed to clarify the genetic background of the purified isolated cells. A homology-based PCR cloning method was employed to determine the sequence using mRNA extracted from the monolayer-forming cells, and the candidate products were then determined by a homology search on the human insulin cDNA. According to the newly identified sequence, rapid amplification of cDNA ends was applied to the 5' and 3' ends, and the entire cDNA sequence was determined. Gene and protein expression was confirmed by Northern blotting, immunohistochemistry, and enzyme assay. To examine the transcriptional level, the cultured cells were incubated in a 20 mM D-glucose medium in the presence or absence of 5 microM forskolin. The porcine insulin cDNA exhibited a high homology to the human cDNA and showed 85% matching with the human amino acid sequence. D-Glucose at 20 mM stimulated the insulin secretion and mRNA expression, and further addition of 5 microM forskolin with the glucose was applied as the strongest stimulus in this culture system.

Amino Acid Sequence↗
PubMed2003

In situ analysis of human menin in normal and neoplastic pancreatic tissues: evidence for differential expression in exocrine and endocrine cells.

Multiple endocrine neoplasia type 1 (MEN1) is a hereditary syndrome linked to mutations in the MEN1 gene, which encodes a 610-amino-acid nuclear protein termed menin. Because of the lack of a suitable detection protocol, the in situ expression pattern of menin in human tissues remains to be determined. In this study, we have developed an antimenin monoclonal antibody and an indirect immunofluorescence/laser-scanning microscopy protocol for analyzing menin expression in frozen tissue sections. Because neuroendocrine pancreatic tumors represent a key feature of MEN1, we focused this study on nontumoral pancreas and a small panel of neuroendocrine pancreatic tumors. Results showed that menin was readily detected in nontumoral exocrine cells. In contrast, most islet cells expressing insulin, glucagon, or somatostatin showed considerably weaker levels of menin expression; however, a subpopulation of pancreatic polypeptide-positive cells exhibited a signal comparable with that detected in adjacent exocrine cells. Sporadic endocrine tumors showed variable levels of menin expression, whereas a MEN1-/- gastrinoma scored negative. This report thus provides the first description of the expression pattern of menin in human pancreas in situ and lays the groundwork for further studies of other tissues and tumors.

Aged↗
PubMed1989

Expression of the neural cell adhesion molecule NCAM in endocrine cells.

We examined the expression of the neural cell adhesion molecule NCAM in a number of endocrine tissues of adult rat and in an endocrine tumor cell line. NCAM was found by immunoelectron microscopy to be present on the surface of all endocrine cells in the three lobes of the hypophysis, although staining was relatively less intense in the intermediate lobe, and in pancreatic islets. Pituicytes, hypophyseal glial cells, were also labeled for NCAM. A rat insulinoma cell line (RIN A2) also expressed NCAM as judged by immunocytochemistry. Analysis of NCAM antigenic determinants (Mr 180, 140, and 120 KD) revealed large variations in the relative proportions of NCAM polypeptides present in the different tissues. Although all tissues and cell lines expressed NCAM-140, NCAM-180 was not detected in the adenohypophysis, pancreas, or adrenal medulla, and NCAM-120 was found in none of the endocrine tissues or cell lines except at low levels in the neurohypophysis. The tumor cell line expressed significant levels of NCAM-180, which was most abundant in the neurohypophysis. These results show that NCAM expression appears to be a general property of endocrine cells, although the antigenic composition differs markedly from that in brain tissue. These data are discussed with regard to the embryological origins of the different endocrine tissues, and possible functional implications are suggested.

Animals↗
PubMed2003

Centroacinar and intercalated duct cells as potential precursors of pancreatic endocrine cells in rats treated with streptozotocin.

The present study examined the possibility for regeneration of pancreatic endocrine cells from centroacinar (CA) and intercalated duct (ICD) cells in rat pancreas after 5 days of continuous streptozotocin (STZ) administration. Nine rats were divided into 3 experimental groups: 1) Control group, 2) Short term recovery group; three days after STZ administration (STZ 3), and 3) Long term recovery group; ten days post-STZ administration (STZ 10). The CA and ICD cells in the STZ 3 group had swollen cytoplasm, and sometimes contained a vesicle within the core. An insulin positive signal was detected in and around the CA and ICD cells. In the STZ 3 group, cytokeratin 20 signals were co-localized with insulin signals in both CA and ICD cells. Electron microscopically, endocrine cells and small pancreatic islets were in close contact with CA and ICD cells. Systemic biophysical serum data reflected these immunohistological results. The present results suggest that CA and ICD cells are involved in the regeneration of pancreatic B cells in rats following a lesion produced by five consecutive days of STZ administration.

Animals↗
PubMed1996

The L beta T2 clonal gonadotrope: a model for single cell studies of endocrine cell secretion.

We have used single gonadotropes from the newly derived line, LbetaT2, to investigate the modulation of Ca2+ signaling and exocytosis by the steroid hormone environment. This cell line, derived by targeted oncogenesis in transgenic mice, has recently been shown to secrete LH in response to GnRH. We have characterized the effects of both GnRH and membrane depolarization on exocytosis and intracellular [Ca2+] ([Ca2+]i) in individual LbetaT2 cells. GnRH (1-100 nM) evoked concentration-dependent increases in [Ca2+]i and secretion, as monitored by measurement of plasma membrane capacitance (Cm) using the whole-cell perforated-patch technique, and the extent of these changes were dependent upon steroid hormone background. GnRH treatment of cells cultured in medium containing charcoal-treated FBS (ct-FBS) showed smaller changes in [Ca2+]i than cells cultured in untreated FBS. However, when estradiol (E2) and dexamethasone (Dex) were added to the ct-FBS medium (E2/Dex-ct-FBS), the elevations in [Ca2+]i stimulated by GnRH increased almost 2-fold. Additionally, the rates of secretion in the E2/Dex-ct-FBS-cultured cells were greater than in either ct-FBS- or FBS-cultured cells. The increase in secretory response observed with E2/Dex-ct-FBS appeared to be due to both an increase in the peak [Ca2+]i stimulated by GnRH and a shift toward increased sensitivity of the Ca2+ dependency of exocytosis. In contrast to GnRH-evoked responses, the increases in [Ca2+]i elicited by depolarization were greater in cells cultured in ct-FBS than in E2/Dex-ct-FBS; however, the secretory rates were no different in the two groups. Likewise, there was no apparent effect of steroid treatment on the Ca2+ dependency of depolarization-evoked exocytosis. In summary, these results 1) clearly demonstrate the utility of this cell line for single-cell studies of both agonist- and depolarization-evoked secretion; 2) reveal that steroid hormone background has profound effects on LbetaT2 cells, both on stimulus-induced calcium mobilization and on the apparent Ca2+ -sensitivity of exocytosis; and 3) show that expression of the steroid hormone effect on Ca2+ -sensitivity is dependent upon receptor occupation by GnRH.

Animals↗
PubMed2003

BETA2 activates transcription from the upstream glucokinase gene promoter in islet beta-cells and gut endocrine cells.

Glucokinase (GK) gene transcription initiates in the islet (beta-cell), gut, and brain from promoter sequences residing approximately 35 kbp upstream from those used in liver. Expression of betaGK is controlled in beta-cells by cell-enriched (i.e. pancreatic duodenal homeobox 1 [PDX-1]) and ubiquitously (i.e., Pal) distributed factors that bind to and activate from conserved sequence motifs within the upstream promoter region (termed betaGK). Here, we show that a conserved E-box element also contributes to control in the islet and gut. betaGK promoter-driven reporter gene activity was diminished by mutating the specific sequences involved in E-box-mediated basic helix-loop-helix factor activator binding in islet beta-cells and enteroendocrine cells. Gel shift assays demonstrated that the betaGK and insulin gene E-box elements formed the same cell-enriched (BETA2:E47) and generally distributed (upstream stimulatory factor [USF]) protein-DNA complexes. betaGK E-box-driven activity was stimulated in cotransfection assays performed in baby hamster kidney (BHK) cells with BETA2 and E47, but not USF. Chromatin immunoprecipitation assays performed with BETA2 antisera showed that BETA2 occupies the upstream promoter region of the endogenous betaGK gene in beta-cells. We propose that BETA2 (also termed NeuroD1) regulates betaGK promoter activity.

Animals↗
PubMed2004

Altered distribution of metaplastic Paneth, gastrin and pancreatic acinar cells in atrophic gastritic mucosa with endocrine cell lesions.

The mechanism of progression from gastric endocrine cell hyperplasias (ECHs) to carcinoid tumor (GCT) is still unknown. In these lesions, the distribution of metaplastic Paneth, gastrin and pancreatic acinar cells developing due to consequences of corporal mucosal atrophy has not been investigated in detail. In this study, 33 gastric endoscopic biopsies with endocrine cell lesions were examined. In all cases except 6 with solitary GCT, complete-type (small intestine) intestinal metaplasia (IM) with Paneth cells was observed. The density of lysozyme-positive Paneth cells in IMs in cases with GCTs was less than those in ECH alone. The density of gastrin-positive cells in IMs and average number of micronodules of ECHs were similar. Pancreatic acinar metaplasia (PAM) was observed in 6 cases of GCTs with ECH. The size of GCTs with ECH was smaller than those without ECH. By image analysis, the percentage of Ki67 (MIB-1, proliferation marker) expressing cells of GCTs with ECH was 5.1+/-0.6%, and GCT without ECH 7.8+/-1%. Our results indicate that few Paneth cells and many PAMs in atrophic corporal mucosa are seen more frequently in cases of GCTs with ECH, compared to those in ECH alone. Gastrin-positive cells in the corporal IM may stimulate enterochromaffin-like (ECL) cells, which may induce hyperplasia, dysplasia or neoplasia by augmenting the effects of hypergastrinemia through a paracrine mechanism on local gastrin-sensitive cells.

Enteroendocrine Cells↗
PubMed2001

Clear cell endocrine pancreatic tumor mimicking renal cell carcinoma: a distinctive neoplasm of von Hippel-Lindau disease.

The dominantly inherited von Hippel-Lindau disease is characterized by clear cell neoplasms in various organs including the kidney and pancreas. Determination of primary versus metastatic lesion in this setting can be a diagnostic dilemma. The authors present five cases of clear cell endocrine pancreatic tumor (EPT) closely mimicking renal cell carcinomas in five patients with a family history or histologic evidence of von Hippel-Lindau disease. In fact, two of these tumors were confused with metastatic renal cell carcinoma by fine-needle aspiration. All five tumors had a component of clear cells arranged in nests, cords, and tubules with central hemorrhage separated by thin-wall vessels resembling renal cell carcinoma. However, these tumors also exhibited cords and festoons and a gyriform pattern suggestive of an endocrine neoplasm, and expressed chromogranin and synaptophysin. Vascular invasion was identified in four tumors, one of which metastasized. The concurrent primary renal cell carcinomas and the multicentric microcystic adenomas found in three patients did not show reactivity for the neuroendocrine markers. Focal clear cell change was noted in only one of 29 endocrine pancreatic tumors arising in patients without von Hippel-Lindau disease. Eleven metastatic renal cell carcinomas in the pancreas did not show immunoreactivity with the endocrine markers. Clear cell EPTs closely mimicking renal cell carcinoma are distinctive neoplasms of von Hippel-Lindau disease. In contrast to clear cell EPT, metastatic renal cell carcinoma does not express neuroendocrine markers and lacks neurosecretory granules by electron microscopy. Von Hippel-Lindau disease should be strongly suspected in patients with renal cell carcinoma, clear cell EPT, and multifocal microcystic serous adenomas.

Adenocarcinoma, Clear Cell↗
PubMed1984

Endocrine cells in the anal canal.

Endocrine cells are normal inhabitants of the anal canal. While numerous endocrine cells are distributed throughout anal ducts and crypts, few are dispersed in the anal transitional zone. All these cells were characterized as serotonin-storing cells, and this endocrine profile is quite distinctive from that of adjacent mucosae. Rectal epithelium contains serotonin, somatostatin, enteroglucagon, BPP and HPP immunoreactive cells; endocrine cells are lacking in the pectinal folds and perianal skin. It is suggested that this distinctive hormonal profile may be regarded as a specific marker of this anal territory. The same pattern is found in the fetal transitional lining of anal canal. Evidence of serotonin-storing cells in the transitional epithelium of anal glands and crypts and in the ATZ epithelium, reinforces the homology between these linings and urothelium. The presence of a similar fetal epithelium implies that ATZ epithelium in adults is not necessarily metaplastic. All derivatives of the cloaca may therefore share the same endocrine profile.

Anal Canal↗