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At least 199 records · Page 11Linked to original sources
PubMedDate not supplied

Nitric oxide biphasically modulates GH secretion in cultured cells of GH-secreting human pituitary adenomas.

BACKGROUND: Nitric oxide (NO) biphasically modulates osteoclast function, sperm motility and testosterone production by exerting a positive effect at low concentrations and a negative effect at high concentrations. In this study the effect due to administration of four NO-donors, each releasing an individual amount of NO, was studied on GH secretion from human adenomatous GH-secreting cells. METHODS: Sodium nitroprusside (SNP), diethylenetriamine NO adduct (DETA/NO), diethylamine/NO complex sodium salt (DEA/NO), and S-nitroso-N-acetylpenicillamine (SNAP) were administered at a concentration of 10-4 M to cells isolated after transsphenoidal adenomectomy from five acromegalic patients. RESULTS: SNP significantly (p < 0.01) increased GH secretion, while the other NO donors inhibited GH secretion in comparision with the amount of GH spontaneously released by unstimulated cells. Each drug showed an individual degree of inhibitory potency: DEA/NO > DETA/NO > SNAP. Nitrite accumulation in the media was measured as a marker of NO released by each individual drug and was found to be different for each drug (DEA/NO > DETA/NO > SNAP > SNP). A negative correlation (R = -0.93; p < 0.05) was found between nitrite release and GH secretion induced by each drug. CONCLUSIONS: These data show that low and quasi-physiological levels of NO, such as those released by SNP, stimulate GH secretion, while high NO levels, such as those released by the other NO-donors, inhibit GH secretion. Thus, NO is shown to be able to modulate GH secretion in a dose-dependent manner in GH adenomatous cells from human pituitary adenomas.

Adenoma↗
PubMed1991

Secretion of the cell surface lipoprotein pullulanase in Escherichia coli. Cooperation or competition between the specific secretion pathway and the lipoprotein sorting pathway.

The fatty acid-acylated enzyme pullulanase is normally found in either of two locations in Escherichia coli, depending on whether or not the producing strains also express the genes specifically required for the second step in pullulanase secretion. When they are expressed, the enzyme is localized to the cell surface, while in their absence, it is directed to an unidentified location in the cell envelope which, upon lysis, forms vesicles whose density is intermediate between those of outer and cytoplasmic membrane vesicles. In order to test the role of the putative lipoprotein sorting signal, Asp2, in pullulanase sorting and secretion, the structural gene (pulA) was subjected to site-directed mutagenesis. Replacement of the Asp2 residue by Asn, Glu, or Ser caused the enzyme to fractionate with outer membrane-derived vesicles rather than with intermediate density vesicles from E. coli cells devoid of pullulanase secretion genes. A pronounced secretion defect was observed in a two-step secretion assay in which the first (sec gene-dependent) and second (pul gene-dependent) secretion steps were uncoupled. We propose that the Asp residue increases the efficiency of pullulanase secretion by allowing the enzyme to be initially sorted to a region of the cell envelope wherein most of the pullulase-specific secretion factors are located.

Base Sequence↗
PubMed1981

Kinetics and duration of action of ranitidine on gastric secretion and its effect on pancreatic secretion in duodenal ulcer patients.

Inhibitory effects of ranitidine, a new H2-receptor antagonist, and cimetidine on histamine and pentagastrin-induced gastric secretion have been compared in duodenal ulcer patients. Compared with cimetidine, ranitidine was found to be about 6-8 times a more potent inhibitor of gastric acid secretion, the inhibition of histamine-induced secretion being competitive, whereas that of pentagastrin-induced secretion not competitive. Ranitidine was an effective inhibitor of pentagastrin-induced secretion 8-12 h after administration. When given in a dose inhibiting gastric secretion by over 90%, it did not affect pancreatic secretion induced by secretin and pancreozymin. The availability of ranitidine, a more powerful inhibitor of gastric secretion, provides an opportunity of a treatment alternative to cimetidine, for peptic ulcer and related diseases.

Adult↗
PubMed1982

[Influence of vagotomy on gastric histamine secretion and the secretion-inhibiting effect of cimetidine].

The influence of vagotomy on histamine gastric secretion and the ability of the H2-blocker cimetidine to suppress histamine gastric secretion was examined in humans and dogs. It was established that vagotomy in humans decreased histamine acid secretion. The relative ability of cimetidine to suppress gastric secretion remained unchanged. In dogs, vagotomy increased acid rather than pepsin secretion stimulated by histamine. The inhibitory effect of cimetidine on acid secretion was more profound in dogs with an intact vagus nerve. It is suggested that vagotomy in dogs but not in humans increased endogenous histamine secretion which intensified the stimulatory effect of endogenous histamine and led to the potentiation of the inhibitory action of cimetidine on histamine acid secretion.

Animals↗
PubMed1983

[Gastric secretion after major resection of the pancreas, with special reference to gut hormones and gastric acid secretion in Sandmeyer's diabetes].

The influences of major pancreas resection upon gastric acid secretion and gut hormones were studied in dogs with Heidenhain pouches. Immediately after resection of 90% or more of the entire pancreas, diabetes occurred with an abrupt decrease in insulin and glucagon secretion, and a marked increase in gastric acid output, though gastrin secretion decreased and secretin secretion increased, as after total pancreatectomy. Six weeks or more after resection of 70 to 90% of the entire pancreas, so-called Sandmeyer's diabetes occurred as a consequence of a decrease in insulin secretion and an increase in glucagon secretion from the remnant pancreas. Gastric acid output decreased markedly, and gastrin secretion also decreased. After resection of less than 70% of the entire pancreas, diabetes did not occur during 66 weeks of the longest observation period after surgery. Gastric acid output, secretion of gastrin and secretin did not change after surgery. These results suggest that gastric hypersecretion occurs after total pancreatectomy and resection of 90% or more of the entire pancreas, and it is related to pancreatic exocrine insufficiency and that gastric hyposecretion occurs after resection of 70 to 90% of the entire pancreas, and it may be related to hypersecretion of glucagon and somatostatin.

Animals↗
PubMed1994

Lysosomal enzyme secretion into pancreatic juice in rats injected with pancreatic secretagogues and augmented secretion after short-term pancreatic duct obstruction.

To examine the possible secretion of lysosomal enzymes into the pancreatic juice in rats stimulated with pancreatic secretagogues under both physiological and pathological conditions, we investigated the changes in the secretion of cathepsin B, as a lysosomal enzyme, into pancreatic juice with stimulation of 5 different doses (0.1, 0.2, 0.5, 1.0, and 1.5 micrograms/kg.hr) of caerulein. Control rats had only pancreatic duct cannulation. In other rats, the pancreatic duct was obstructed for 3 hours and secretin was infused (0.2 CU/kg.hr). Caerulein stimulated the secretion of cathepsin B into the pancreatic juice in a dose-dependent manner, as in amylase secretion, and caerulein in higher doses (1.0 and 1.5 microgram/kg.hr) inhibited cathepsin B output as it did amylase output. There was a significantly high positive correlation between cathepsin B output and amylase output after stimulation with caerulein. The secretion of several other lysosomal enzymes was also stimulated by caerulein. Blockage of the pancreatic duct for 3 hours caused a significant but moderate rise in serum amylase levels. Redistribution of cathepsin B activity in the pancreatic subcellular fractions was noted with an increase in the amount of cathepsin B recovered from zymogen-rich pellets after 15 min of centrifugation at 1300 x g. These changes after temporary pancreatic duct obstruction are very similar to those previously noted during the early stage of diet-and caerulein-induced experimental pancreatitis and suggest colocalization of lysosomal enzymes and digestive enzymes. In addition, in duct obstructed rats, the secretion of cathepsin B and other lysosomal enzymes stimulated by caerulein was significantly greater than in animals with free-flowing pancreatic juice. These results indicate that lysosomal enzymes are secreted into pancreatic juice after stimulation by gut hormones in the same manner as classical pancreatic digestive enzymes such as amylase. Moreover, lysosomal enzymes which colocalize with zymogen granules in rats with short-term pancreatic duct obstruction are also secreted into pancreatic juice together with digestive enzymes after stimulation with gut hormones. These findings suggest that lysosomal enzymes are present in zymogen granules under normal conditions and that they may play pathophysiological roles in pancreatic juice. They also contribute to an understanding of the pathogenesis of pancreatitis, since cathepsin B can activate trypsinogen.

Amylases↗
PubMedDate not supplied

Secreted products and extracellular matrix from testicular peritubular myoid cells influence androgen-binding protein secretion by Sertoli cells in culture.

Metabolic cooperation mediated by secreted factors between Sertoli cells and peritubular myoid cells has been well documented. We have confirmed that factors secreted by peritubular myoid cells modulate androgen-binding protein (ABP) secretion by Sertoli cells and shown further that this can also be achieved with peritubular myoid cell extracellular matrix (ECM). While peritubular myoid cell ECM potentiated the stimulatory effect of dibutyryl cyclic AMP on Sertoli cell ABP secretion, secreted factors did not, suggesting that the two components influence Sertoli cells through distinct mechanisms. We also tested other factors and other cell lines for effects on ABP production by Sertoli cells. The addition of human plasma fibronectin or conditioned medium from the basement membrane-producing Englebreth-Holm-Swarm sarcoma also stimulated ABP secretion by Sertoli cells. Cocultures of epithelial Sertoli cells with the cells of mesenchymal origin, such as testicular peritubular myoid cells, embryonic skin fibroblasts, and bladder smooth muscle cells, significantly stimulated ABP secretion by Sertoli cells, but coculture with the epithelial-derived Martin-Darby canine kidney cell line had no effect on Sertoli cell-secreted ABP levels. Our data further define the epithelial-mesenchymal cell interaction that exists between Sertoli cells and peritubular myoid cells in the mammalian testis.

Androgen-Binding Protein↗
PubMedDate not supplied

Sertoli cell secreted growth factor. Cellular origin, paracrine and endocrine regulation of secretion.

Rat and human Sertoli cells in culture secrete a growth factor, Sertoli cell secreted growth factor (SCSGF). The aims of the present study were (1) to evaluate other testicular cell types as additional sources of SCSGF, as well as their paracrine effect, and (2) to study the hormonal regulation of SCSGF secretion using an A431 cell growth assay. The Sertoli cell was the only testicular cell type tested that secreted SCSGF activity in vitro. Peritubular cells enhanced Sertoli cell attachment and SCSGF secretion. Spermatogenic cells had no effect. The secretion of SCSGF was specifically stimulated by follicle-stimulating hormone (FSH) and testosterone. Treatment with agents that increase intracellular cAMP levels and adenosine stimulated the secretion of mitogenic activity into Sertoli cell-conditioned medium by three- to fivefold. This growth factor, secreted by the Sertoli cell and regulated by FSH and testosterone, may play a critical role in the regulation of spermatogenesis.

Adenosine↗
PubMed1996

Effect of histone-H2A (H-H2A), platelet activating factor (PAF) and pregnancy specific protein B (PSPB) on secretion of prostaglandins E and F2 alpha (PGE; PGF2 alpha) by bovine endometrium and H-H2A on basal secretion of luteinizing hormone (LH) by bovine pituitary cells in vitro.

Effects of H-H2A, PSPB or PAF on day 16 bovine endometrial secretion of PGE and PGF2 alpha and H-H2A on basal secretion of LH by bovine pituitary cells in vitro were examined in two experiments. PAF (P < or = 0.08) and H-H2a + PAF (P < or = 0.10) treatment for two hours in an in vitro perfusion system tended to increase secretion of PGF2 alpha expressed as a proportion of the prechallenge concentrations of PGF2 alpha by day 16 bovine caruncular endometrium, which occurred during the two-hour period after treatment removal. PGF2 alpha was increased (P < or = 0.02) in the two hour period after the treatment was removed in both control and H-H2A-treated endometrium. H-H2A (P < or = 0.07) and PSPB (P < or = 0.08) tended to increase PGE, while H-H2A + PSPB (P < or = 0.05) and H-H2A + PAF (P < or = 0.03) increased secretion of PGE expressed as a proportion of the prechallenge concentrations of PGE by day 16 bovine caruncular endometrium during the challenge and postchallenge treatment periods, but did not differ (P < or = 0.05) between the two-hour challenge period and the two-hour postchallenge period after removal of the treatment. In experiment two, H-H2A decreased (P < or = 0.05) basal secretion of LH by bovine pituitary cells in vitro. These data suggest that H-H2A and PSPB preferentially stimulate secretion of PGE by bovine endometrial tissue and may play a role in maternal recognition of pregnancy, while PAF increased PGF2 alpha secretion. In addition, H-H2A may play a role in regulating secretion of LH by the pituitary. Key words: Pregnancy Specific Protein B, Histone-H2A, Prostaglandin E and F2 alpha, Platelet Activating Factor, Endometrium, Cow.

Animals↗
PubMed1997

Obesity in db and ob animals leads to impaired hepatic very low density lipoprotein secretion and differential secretion of apolipoprotein B-48 and B-100.

Dyslipidemia secondary to obesity is commonly observed in both animals and humans. As it has been hypothesized that obesity can result in overproduction of VLDL, leading to the subsequent dyslipidemia, we have examined the triglyceride and apoB secretion rates in vivo in obese C57BI/ KsJ db/db and C57BI/6J ob/ob mice and their lean littermates. In ob/ob animals, obesity resulted in significantly lower, not higher, triglyceride secretion rates in both males (3.94 +/- 0.49 mg/h per g liver vs. 5.45 +/- 0.29 mg/h per g liver in lean littermates, P < 0.001) and females (4.29 +/- 0.81 mg/h per g liver vs. 5.25 +/- 0.59 mg/h/g liver, P < 0.001). For db/db, the obese females did not show a statistically significant triglyceride secretion rate compared to their lean littermates. Only the male db/db animals showed a significantly higher triglyceride secretion rate compared with lean littermates (5.50 +/- 1.1 mg/h per g liver vs. 3.37 +/- 0.36 mg/h/g liver, P < 0.001). Examination of the apolipoprotein B (apoB) secretion rates showed that for ob/ob animals and db/db obese females, apoB48 secretion was significantly decreased compared to that of normal littermates, with a small increase in apoB-100 secretion. Total apoB secreted, however, was not increased. Our data further suggest that the predominant cause of the dyslipidemia under these conditions is a defect in removal of VLDL from the circulation.

Aging↗
PubMed1996

Effects of glucose, forskolin and tolbutamide on membrane potential and insulin secretion in the insulin-secreting cell line INS-1.

Membrane voltages (Vm) of INS-1 cells, an insulin-secreting cell line, were measured mostly using the cell-attached mode of the patch-clamp method. The cell-attached configuration allowed the cell to be kept intact. Measurement of Vm was possible because seal resistances were very high and because the membrane obviously had a sufficiently high conductance (probably via K+ channels). Resting Vm was -80 +/- 1 mV (n = 42) and was mainly determined by sulphonylurea-sensitive K+ATP channels since tolbutamide depolarized the plasma membrane in a concentration-dependent manner and generated action potentials at 50 and 100 micromol/l. D-Glucose, tested between 0.5 and 16.7 mmol/l, also depolarized the plasma membrane in a concentration-dependent manner and induced action potentials at concentrations higher than 5.6 mmol/l. Similarly, forskolin (5 micromol/l) depolarized the cells and increased the frequency of Ca2+-mediated action potentials. Insulin secretion was measured from cells growing in culture dishes, by radioimmunoassay. Glucose doubled secretion in INS-1 cells, whereas tolbutamide had no significant effect on secretion in the presence of 0.5 mmol/l and 16. 7 mmol/l glucose. At 3 mmol/l glucose, tolbutamide increased insulin release slightly. Forskolin elevated secretion twofold at a low glucose concentration. In contrast, when glucose or tolbutamide were added together with forskolin secretion was potentiated five- to tenfold. These results show that glucose induces membrane activation in INS-1 cells. Furthermore, the potent effect of tolbutamide, i.e. to depolarize the plasma membrane without inducing insulin release, leads to the conclusion that effects distal to depolarization are pivotal for secretion in INS-1 cells.

Action Potentials↗
PubMed1994

The effect of nitric oxide donors on insulin secretion, cyclic GMP and cyclic AMP in rat islets of Langerhans and the insulin-secreting cell lines HIT-T15 and RINm5F.

The aim of this study was to investigate whether short-term treatment with nitric oxide donors could mimic cytokine inhibition of insulin secretion. We tested the nitric oxide generating compounds 3-morpholinosydnonimine (SIN-1), S-nitroso-N-penicillamine (SNAP), S-nitrosoglutathione and hydroxylamine for their ability to inhibit insulin secretion, raise cyclic GMP and lower cyclic AMP levels in isolated rat islets of Langerhans and the insulin-secreting cell lines HIT-T15 and RINm5F. In islets, all nitric oxide donors inhibited glucose-induced insulin secretion and raised cyclic GMP levels. SIN-1 and S-nitrosoglutathione also reduced cyclic AMP, while SNAP and hydroxylamine had no effect. Insulin secretion in HIT-T15 cells was inhibited by SIN-1, SNAP and hydroxylamine and in RINm5F cells by hydroxylamine. Inhibition of HIT-T15 and RINm5F cell insulin secretion was not accompanied by an increase in cyclic GMP levels. The degree of inhibition of insulin secretion was unrelated to the extent of release of nitric oxide by the compounds as measured by nitrite and nitrate production. More effective inhibition by S-nitrosoglutathione and hydroxylamine versus SIN-1 and SNAP may be related to intracellular versus extracellular site of nitric oxide generation.

Animals↗
PubMed1999

Phosphatase inhibitors induce defective hormone secretion in insulin-secreting cells and entry into apoptosis.

A long-term (> or =24 h) exposure of insulin-secreting HIT T15 cells to the phosphatase inhibitor, okadaic acid (OA), at concentrations inhibiting serine/threonine phosphatases 1 (PP1) and 2A (PP2A) reduced proliferation and insulin secretion. The reduced proliferation was related to the induction of apoptosis as evidenced by morphological criteria and the occurrence of internucleosomal DNA fragmentation after 15 h in 50 nM OA. The compromised insulin secretion was not simply a consequence of a lowered hormone content and cell growth, but comprised also a complete suppression of secretion stimulated by K+ depolarisation and forskolin. K+ depolarisation of HIT cells cultured for 24 h in 50 nM OA resulted in a nearly unimpaired influx of Ca2+, but did not induce secretion. These observations suggest that the secretory defect may be localised distal to Ca2+ influx in stimulus secretion coupling of insulin-secreting cells.

Apoptosis↗
PubMed1997

Effects of all-trans-retinoic acid (ATRA) and retinoic acid receptor (RAR) expression on secretion, growth, and apoptosis of insulin-secreting RINm5F cells.

To define the functions of retinoids and their receptors in insulin secretion, we tested the effects of all-trans-retinoic acid (ATRA) and retinoic acid receptor (RAR) expression on cell growth, differentiation, and secretion using insulin-secreting RINm5F cells. Wild-type cells with a low abundance of mRNA for RAR beta were transfected with RAR beta or chloramphenicol acetyltransferase (CAT control). Cells were cultured for 2-7 days in media without (A-def) or with ATRA, 1, 10, 100, and 1,000 nM. At day 2 of culture, ATRA stimulated insulin release in wild-type and transfected cells, and this effect was dose dependent. At 7 days, ATRA stimulated insulin secretion from wild-type cells twofold at glucose concentrations of 0.5 mM (A-def, 5.1 +/- 0.27; ATRA, 1,000 nM, 10.5 +/- 1.43 ng/10(6) cells) and at 11.0 mM (A-def, 6.9 +/- 0.24; ATRA, 1,000 nM, 13.6 +/- 1.86 ng/10(6) cells). The cellular insulin content was increased about threefold (A-def, 39.2 +/- 2.95; ATRA, 1,000 nM, 118 +/- 8.54 ng/10(6) cells). ATRA inhibited growth of wild-type cells as early as 3 days, and this effect was dose dependent. Whereas in the absence of ATRA, the cell number increased over fivefold between day 3 and day 5, ATRA, 1,000 nM, inhibited cell growth completely. ATRA, 1,000 nM, increased apoptotic RINm5F cells (day 3 A-def, 0.53 +/- 0.27% of total cells, and ATRA, 2.30 +/- 1.44; day 5 A-def, 0.38 +/- 0.23, and ATRA, 2.14 +/- 0.59; day 7 A-def, 0.90 +/- 0.29, and ATRA, 6.02 +/- 1.64). RAR beta-transfected cells showed overexpression of mRNA to RAR beta and dose-dependent inhibition of growth, with almost-complete inhibition at ATRA concentrations as low as 100 nM. Overexpression of RAR beta increased insulin secretion at ATRA, 100-1,000 nM. In summary, ATRA increased the insulin secretion and content of RINm5F cells, while inhibiting growth and increasing apoptosis. Increased expression of RAR beta facilitated these effects on growth and secretion. These findings may reflect the known effect of ATRA on differentiation of cells and mediation through RAR beta.

Apoptosis↗
PubMed1986

Insulin secretion in aging: studies with sequential gating of secretion vesicle margination and lysis.

A new sequential gating perifusion technique was employed to investigate secretion vesicle margination and granule lysis in islets isolated from 2- and 18-month-old Fischer 344 rats. The technique is based on sequential perifusion (periods A, B, and C) of isolated islets with glucose (30, 165, or 300 mg/dl) in the presence of sodium isethionate, an inhibitor of granule lysis, followed thereafter by trifluoperazine, an inhibitor of secretion vesicle margination, and glucose (300 mg/dl) or isobutylmethylxanthine (IBMX; 400 microM). When glucose was employed during period A to marginate secretion vesicles to the plasma membrane, subsequent glucose- and IBMX-induced insulin release (period C) was depressed in islets from 18-month-old rats [maximal increase above the basal rate of release (delta max), 9 +/- 2 nU/micron X min] compared to that in the 2-month-old animals (delta max, -19 +/- 3 nU/micron X min). With glyburide (400 microM) used to induce secretion vesicle margination, glucose- and IBMX-induced insulin release was the same in young and old animals (delta max, 14 +/- 3 and 15 +/- 3 nU/micron X min, respectively). Insulin release was then studied as a function of secretion vesicle margination at the plasma membrane by measuring somatostatin (SRIF) receptor recruitment. The islets from older animals must be stimulated with 300 mg/dl glucose to attain the same level of SRIF binding as in islets isolated from younger animals stimulated with 150-165 mg/dl glucose. Insulin release per unit SRIF binding was identical in young and old animals (65 and 69 nU/liter fmol SRIF binding), indicating normal lysis of marginated secretion granules. These studies implicate glucose-induced secretion vesicle margination as the site of impairment in age-related insulin release.

1-Methyl-3-isobutylxanthine↗
PubMed1989

Reducing meal-stimulated acid secretion versus reducing nocturnal acid secretion for healing of duodenal ulcer.

Both meal-stimulated and nocturnal acid secretions have been shown to be abnormally increased in patients with duodenal ulcer. The relative efficacy of an acid-reducing regimen aimed specifically at controlling postprandial acid secretion compared with one that controls nocturnal acid secretion is, however, not known. The endoscopic healing rates at weeks 2, 4, 6, 8, 10, and 12 of three cimetidine regimens with identical total daily dose--bedtime (1200 mg), mealtime (400 mg three times a day with meals), and reference (200 mg three times a day with meals and 600 mg at bedtime)--were compared in a randomized study on 141 patients with endoscopically proven duodenal ulcer. Evaluating endoscopists were blinded to patients' form and duration of treatment and their clinical progress; patients were unaware of the comparative design of the study. Life-table analysis for the 12 weeks of observation revealed that the mealtime regimen resulted in significantly (P less than 0.05) better healing rates than either the bedtime or the reference regimen. The differences were accounted for largely by the significantly (P less than 0.04) better healing rate at two weeks with the mealtime regimen (68%) than with either the bedtime (47%) or the reference (45%) regimen. These findings indicate that a regimen that aims at controlling meal-stimulated acid secretion achieves a faster healing rate than one that aims at controlling nocturnal acid secretion in the treatment of duodenal ulcer, and they suggest that postprandial acid secretion plays a greater role than nocturnal acid secretion in the pathophysiology of this condition.

Cimetidine↗
PubMed1989

Somatomammotrophic cells in GH-secreting and PRL-secreting human pituitary adenomas.

A morphological study has been carried out on 20 GH-secreting adenomas removed from acromegalic normoprolactinemic patients, on 29 PRL-secreting adenomas removed from hyperprolactinemic patients without signs of acromegaly and on one normal human anterior pituitary gland collected at autopsy. The protein A-gold immunoelectron microscopic technique has been utilized in order to verify the presence of mixed cells producing both GH and PRL (somatomammotrophs) in these pituitary tissues. In the normal pituitary a considerable number of somatomammotrophs (15-20%) was found, thus supporting the idea that these cells are normal components of the human anterior pituitary gland. In 10 GH-secreting adenomas and in 10 PRL-secreting adenomas somatomammotrophs were present in a variable number (from 4 to 20% of the whole cell population in GH adenomas and from 1 to 47% in PRL tumors). It can be concluded therefore that these cells, largely present in all GH/PRL-secreting adenomas, can also be found in GH-secreting and PRL-secreting tumors without clinical evidence of a mixed secretion. Adenomatous somatomammotrophs displayed ultrastructural features of adenomatous somatotrophs and mammotrophs (prominent Golgi complexes, abundant rough endoplasmic reticulum, irregular nuclei). The size and the number of granules were variable. In some cells GH and PRL were stored in distinct secretory granules, in others in mixed granules or both in mixed and distinct granules, thus suggesting that in adenomatous somatomammotrophs the efficiency of the mechanisms of sorting of the two hormones varies from one cell to another.(ABSTRACT TRUNCATED AT 250 WORDS)

Acromegaly↗
PubMed1992

Volume-activated Cl- secretion and transepithelial vinblastine secretion mediated by P-glycoprotein are not correlated in cultured human T84 intestinal epithelial layers.

The relationship between the P-glycoprotein-mediated vinblastine secretion and cell-swelling activated Cl- secretion (conductance) in intact epithelial layers of human colonic adenocarcinoma T84 cells has been investigated. Whereas vinblastine secretion is effectively inhibited by 100 microM 1,9-dideoxy-forskolin, volume-stimulated Cl- secretion is unaffected. In contrast, 100 microM 4,4'-diisothiocyanostilbene-2,2'-disulphonic acid (DIDS) inhibited the volume-stimulated Cl- secretion, but was without effect upon transepithelial vinblastine secretion. In addition, it was noted that some epithelial layers failed to express a volume-stimulated Cl- secretion but maintained a normal level of secretory vinblastine flux.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗