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PubMed1984

Autoregulation of follicle-stimulating hormone secretion in the hamster: evidence for control at the level of the anterior pituitary gland.

Pituitary tissue obtained from proestrous, phenobarbital-treated hamsters was placed in organ culture, and the release rates of FSH and LH were monitored. Addition of LHRH to the culture medium increased gonadotropin release rates. Preincubation of pituitaries in medium that contained 1 microgram purified FSH ( NIADDK rat FSH-I-5) resulted in enhanced basal and LHRH-induced FSH release rates. Full expression of FSH hypersecretion by pituitary tissue occurred after 3-h exposure to purified FSH. This phenomenon appears to require adequate tissue calcium concentrations. Further, exposure of pituitaries to purified FSH slightly but significantly enhanced basal but not LHRH-stimulated LH release compared with that in untreated controls. Experiments that employed labeled FSH, reduced exposure time to purified FSH, or decreased calcium concentration in the medium proved that the increased FSH secretory rate was not due to contamination of the medium with the purified FSH used to stimulate the pituitary. These studies suggest that FSH has the ability to influence its own secretion by an action at the level of the anterior pituitary gland.

Animals↗
PubMed1991

Cortisone effects on growth, food efficiency, and in vitro growth hormone release.

These studies were designed to investigate the cause of growth retardation during glucocorticoid treatment in rats. In young animals, body weights and amounts of food consumed were measured at two-day intervals, beginning at 29 days of age. Average food intake and food efficiency were calculated. Animals were treated with cortisone (CORT, 5 mg/rat/day, s.c.) or saline (SAL) for eight days between 37 and 44 days. Growth hormone (GH) release by dispersed pituitary cells in response to nine concentrations of GH-releasing hormone (GHRH) were tested by in vitro perifusion at 45 and 73 days. As previously shown, CORT caused a cessation of growth during the treatment period, and body weight failed to catch up. Food efficiency was decreased during CORT treatment. All parameters of in vitro GH release including basal GH secretory rate, overall GH response to GHRH, and the GHRH concentration-response curves were significantly increased by CORT in the 45-day-old animals. An age-related increase in GH release was also observed between the 45 and 73 day saline-treated animals. These results support the hypothesis that glucocorticoids inhibit growth by induction of changes in food metabolism and GH secretion. The effect on the pituitary gland itself paradoxically involves an increase in GH secretory capacity in response to GHRH.

Animal Nutritional Physiological Phenomena↗
PubMed1995

Metabolic activation of Ca(2+)-independent phosphoinositide hydrolysis in beta-cells and its role in the control of insulin secretion.

Recent studies have led to the proposal that the oxidative metabolism of glucose leads to the generation of messengers, in addition to ATP, that are important in the ability of changes in extracellular glucose concentration to stimulate insulin secretion from pancreatic beta-cells. In particular, there is now evidence that glucose induces both a Ca(2+)-dependent and Ca(2+)-independent increase in phosphoinositide (PI) hydrolysis. To explore the relationship between oxidative metabolism and PI hydrolysis, we examined the effect of low concentrations (2.5 mM) of alpha-ketoisocaproate (KIC) and monomethylsuccinate (MMSucc) either alone or in combination on insulin secretion and PI hydrolysis in isolated rat pancreatic islets incubated with either no glucose, 5 mM glucose, or 20 mM glucose. A combination of KIC and MMSucc leads to a marked increase in largely (80%) Ca(2+)-independent PI hydrolysis in either the absence or presence of 5 mM glucose. When glucose is absent, this combination of substrates induces a very small and transient first phase of insulin secretion but no significant second phase of secretion. In the presence of 5 mM glucose, either KIC or MMSucc alone induces a first phase of insulin secretion with a peak secretory rate 10-fold greater than the basal rate but only a small second phase of secretion approximately 5-fold above control. However, in the presence of 5 mM glucose, the combination of KIC plus MMSucc induces a large biphasic increase in insulin secretion: peak first-phase secretion is increased 30-fold, and second-phase 40-fold. These response are comparable to those induced by 20 mM glucose and are completely inhibited by 0.5 microM nitrendipine. In contrast, KIC plus MMSucc do not enhance the insulin secretory response induced by 20 mM glucose. Previous data showed that when 20 mM glucose acts, the resulting increase in PI hydrolysis is only partially Ca2+ dependent. A reanalysis of these data shows that raising the glucose concentration from 5 to 7 mM causes a 2-fold increase in Ca(2+)-independent PI hydrolysis, and a further increase to 20 mM leads to a further 2-fold increase in Ca(2+)-dependent PI hydrolysis. These data show that these two pathways are regulated by different ranges of glucose concentration. They raise the interesting possibility that these distinct pathways have different signaling functions. In particular, raising the glucose concentration from 5 to 7 mM is known to alter the responsiveness of beta-cells to a variety of neurohumoral agonists and to tolbutamide.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed2005

Chronic glucocorticoid treatment alters spontaneous pulsatile parathyroid hormone secretory dynamics in human subjects.

OBJECTIVE: Spontaneous parathyroid hormone (PTH) secretory dynamics include tonic and pulsatile components. It is not known how glucocorticoids might alter these secretory dynamics. DESIGN: The aim of our study was to evaluate spontaneous fluctuations in serum PTH levels in six adult male patients (aged 31-64 years) receiving chronic (>6 months) therapy with glucocorticoids (daily dosage >7.5 mg of prednisone or dose equivalent of other corticosteroid) as compared with a control group of 10 age- and sex-matched normal subjects. METHODS: Peripheral venous blood sampling was performed every 3 min for 6 h from 0900 to 1500 h. Plasma PTH release profiles were subjected to deconvolution analysis, a method that resolves measured hormone concentrations into secretion and clearance components, and to an approximate entropy (ApEn) estimate, that in turn provides an integrated measure of the serial regularity or orderliness of the release process. RESULTS: In the glucocorticoid-treated group, the PTH tonic secretory rate was reduced (4.3+/-0.74 vs 8.8+/-1.4 pg/ml per min in controls, P = 0.017). There was, however, an increase in the fractional pulsatile PTH secretion (42+/-8.2 vs 18.3+/-3.9 pg/ml per min, P = 0.006) in glucocorticoid-treated vs normal subjects. Mean overall PTH concentration, as well as mean integrated area, was similar among normal and glucocorticoid-treated subjects. CONCLUSIONS: These results demonstrate, for the first time, that chronic glucocorticoid treatment induces a redistribution of spontaneous PTH secretory dynamics by reducing the amount released in tonic fashion and increasing the amount released as pulses.

Adult↗
PubMed1992

Effect of complete sulfation of bile acids on bile formation: role of conjugation and number of sulfate groups.

The effect of complete sulfation of conjugated cholic, chenodeoxycholic and deoxycholic acids on bile formation was investigated in rats. The sulfated bile acids were infused intravenously in stepwise increasing doses (1, 2, 3 and 4 mumol/min/100 gm body wt) in rats after 90 min of bile acid pool depletion. The effects of these bile acids on bile flow, bile salt, biliary phospholipid and cholesterol secretion rates were determined. In addition, their choleretic activity and their effect on biliary lipid secretion were calculated. Appropriate controls infused with nonsulfated bile were also performed. The sulfated bile acids increased bile flow with increasing the infusion doses, and the maximum bile flow was significantly higher than nonsulfated bile acids. Although cholestasis was developed during the infusion of nonsulfated bile acids, no cholestatic effect was observed for sulfated bile acids. With the exception of cholic acid, sulfation significantly increased the bile acid secretory rate maximum. The sulfates of chenodeoxycholic and deoxycholic acids were further hydroxylated. The choleretic activities for all the sulfated bile acids were significantly higher than the nonsulfated bile acids. All the sulfated bile acids significantly reduced the biliary lipid secretion, and a significant correlation was found between the choleretic activity and the phospholipid-dependent bile acid secretion. The data also showed that infusion of sulfated taurine-conjugated bile acids produced higher bile flow and bile acid secretion rate and was less effective when biliary lipid secretion rates were reduced compared with glycine conjugates. It is concluded that sulfated conjugated bile acids may have a role in protection during cholestasis either by stimulation of bile flow or by reduction of biliary lipid secretion, thus protecting cell membranes from the detergent properties of high concentrations of nonsulfated bile acids.

Animals↗
PubMed2002

The regulation of platelet-dense granules by Rab27a in the ashen mouse, a model of Hermansky-Pudlak and Griscelli syndromes, is granule-specific and dependent on genetic background.

The ashen (ash) mouse, a model for Hermansky-Pudlak syndrome (HPS) and for a subset of patients with Griscelli syndrome, presents with hypopigmentation, prolonged bleeding times, and platelet storage pool deficiency due to a mutation which abrogates expression of the Rab27a protein. Platelets of mice with the ashen mutation on the C3H/HeSnJ inbred strain background have greatly reduced amounts of dense granule components such as serotonin and adenine nucleotides though near-normal numbers of dense granules as enumerated by the dense granule-specific fluorescent dye mepacrine. Thus, essentially normal numbers of platelet dense granules are produced but the granule interiors are abnormal. Collagen-mediated aggregation of mutant platelets is significantly depressed. No abnormalities in the concentrations or secretory rates of 2 other major platelet granules, lysosomes and alpha granules, were apparent. Similarly, no platelet ultrastructural alterations other than those involving dense granules were detected. Therefore, Rab27a regulates the synthesis and secretion of only one major platelet organelle, the dense granule. There were likewise no mutant effects on levels or secretion of lysosomal enzymes of several other tissues. Together with other recent analyses of the ashen mouse, these results suggest a close relationship between platelet dense granules, melanosomes of melanocytes and secretory lysosomes of cytotoxic T lymphocytes, all mediated by Rab27a. Surprisingly, the effects of the ashen mutation on platelet-dense granule components, platelet aggregation, and bleeding times were highly dependent on genetic background. This suggests that bleeding tendencies may likewise vary among patients with Griscelli syndrome and HPS with Rab27a mutations.

Adenosine Diphosphate↗
PubMed1978

The control of enzyme secretion from fly salivary glands.

1. Stimulation of fluid secretion from fly salivary glands by 5-hydroxytryptamine (5-HT) is known to involve calcium and cyclic AMP. Isolated salivary glands were used to investigate the role of these second messengers in the control of enzyme (sucrase) secretion.2. The protein component of secretion from isolated glands treated with 5-HT appears to be identical to that of saliva secreted by flies during feeding.3. Stimulation of fluid secretion by 5-HT follows a definite dose-response curve, but there is no consistent relationship between the rate of enzyme secretion and the stimulating concentration of 5-HT.4. Exogenous cyclic AMP causes secretion of enzymes as well as of fluid, thus mimicking the action of 5-HT. The phosphodiesterase inhibitor theophylline enhances the rate of 5-HT-stimulated enzyme secretion.5. Removal of calcium from the bathing medium enhances enzyme secretion in response to 5 or 10 nM-5-HT but has no effect on enzyme secretion stimulated by 100 nM-5-HT or by cyclic AMP.6. Addition of 0.1 mM-lanthanum to medium containing 2 mM-calcium mimics the effect of calcium-free solution on 5-HT-stimulated enzyme secretion.7. The ionophore A 23187 causes secretion of both fluid and enzyme. The secretory rate is initially high but soon declines and ceases after about 40 min.8. Enzyme secretion in response to 5-HT or to cyclic AMP is progressively inhibited as the concentration of potassium is increased from 10 to 80 mM. Secretion in response to A 23187 is initially inhibited by 80 mM-potassium but then partially recovers.9. The rate of enzyme secretion appears to be affected by the intracellular concentrations of both calcium and cyclic AMP. It is possible that the rate of enzyme secretion increases as the intracellular calcium concentration rises, until the optimal calcium concentration is reached when further increase in the level of calcium progressively inhibits secretion. The optimal calcium concentration for enzyme secretion is lower than that for fluid secretion, and 5-HT normally causes maximal fluid secretion and submaximal enzyme secretion.

Animals↗
PubMed2000

Metabolic, cationic and secretory response to D-glucose in depolarized and Ca(2+)-deprived rat islets exposed to diazoxide.

D-glucose stimulates insulin release from islets exposed to both diazoxide, to activate ATP-responsive K+ channels, and a high concentration of K+, to cause depolarization of the B-cell plasma membrane. Under these conditions, the insulinotropic action of D-glucose is claimed to occur despite unaltered cytosolic Ca2+ concentration, but no information is so far available on the changes in Ca2+ fluxes possibly caused by the hexose. In the present experiments, we investigated the effect of D-glucose upon 45Ca efflux from islets exposed to both diazoxide and high K+ concentrations. In the presence of diazoxide and at normal extracellular Ca2+ concentration, D-glucose (16.7 mmol/l) inhibited insulin release at 5 mmol/l K+, but stimulated insulin release of 90 mmol/l K+. In both cases, the hexose inhibited 45Ca outflow. In the presence of diazoxide, but absence of Ca2+, D-glucose (8.3 to 25.0 mmol/l) first caused a rapid decrease in insulin output followed by a progressive increase in secretory rate. This phenomenon was observed both at 5 mmol/l or higher concentrations (30, 60 and 90 mmol/l) of extracellular K+. It coincided with a monophasic decrease in 45Ca efflux and either a transient (at 5 mmol/l K+) or sustained (at 90 mmol/l K+) decrease in overall cytosolic Ca2+ concentration. The decrease in 45Ca efflux could be due to inhibition of Na(+)-Ca2+ countertransport with resulting localized Ca2+ accumulation in the cell web of insulin-producing cells. A comparable process may be involved in the secretory response to D-glucose in islets exposed to diazoxide and a high concentration of K+ in the presence of extracellular Ca2+.

Animals↗
PubMed1998

Genetic and environmental influences on prolactin secretion during wake and during sleep.

To delineate the contributions of genetic and environmental factors in the regulation of human prolactin (PRL) secretion, the 24-h profile of plasma PRL was obtained at 15-min intervals in 10 pairs of monozygotic and 10 pairs of dizygotic twins. Sleep was monitored polygraphically. PRL secretory rates were derived from plasma concentrations by deconvolution. Diurnal (24-h) variations were quantified by a regression curve to define nadir, acrophase, and amplitude. Pulses of PRL secretion were identified using a computerized algorithm. A procedure specifically developed for twin studies was used to partition the variance into genetic and environmental contributions. Significant genetic effects were identified for daytime PRL concentrations, rhythm amplitude, and overall wave-shape of the daily PRL profile. In contrast, environmental effects were dominant for mean concentrations during sleep, total secretory output during sleep, overall 24-h concentrations, and total 24-h secretion. However, when interindividual variations in sleep fragmentation were taken into account, the estimates of genetic variance for PRL concentrations and secretion during sleep approached statistical significance. Significant genetic influences were identified for slow-wave sleep (SWS). Because SWS is associated with increased nocturnal PRL secretion, it is possible that genetic effects on PRL secretion during sleep reflect genetic influences on SWS. In conclusion, genetic factors determine partially both the basal daytime concentrations of PRL and the temporal organization of PRL secretion over the 24-h cycle in normal young men.

Adult↗
PubMed1991

Mechanisms of copper incorporation during the biosynthesis of human ceruloplasmin.

To examine the mechanisms of copper incorporation during ceruloplasmin biosynthesis, we developed methods to resolve and identify apo and holoceruloplasmin. The identity of holoceruloplasmin was confirmed by oxidase activity staining, immunoblotting, 67Cu-ligand exchange, and 67Cu-ligand blotting. Following metabolic labeling of human liver and lung cell lines with 67Cu, newly synthesized holoceruloplasmin was detected in the culture media as two species with apparent molecular masses of 84 and 79 kDa. Pulse-chase studies demonstrate that exogenous copper is readily available for incorporation into newly synthesized ceruloplasmin and that the kinetics of apo and holoceruloplasmin synthesis and secretion are identical. Inhibition of N-linked glycosylation did not affect the rate or amount of copper incorporated into newly synthesized ceruloplasmin but did result in the secretion of a single 68-kDa holoceruloplasmin moiety. Despite differences in the kinetics of copper uptake between cell lines a linear rate of copper incorporation into newly synthesized ceruloplasmin was observed with no evidence of copper exchange following biosynthesis. Under the conditions studied, holoceruloplasmin accounted for less than 5% of the total ceruloplasmin synthesized and secreted by each cell line. The data indicate that copper is incorporated into newly synthesized ceruloplasmin early in the course of biosynthesis by a process independent of N-linked carbohydrate addition. This process of copper incorporation results in an apparent conformational change in the ceruloplasmin molecule which does not affect the secretory rate of the protein.

Apoproteins↗
PubMed1991

Parathyroid hormone modulates angiotensin II-induced aldosterone secretion from the adrenal glomerulosa cell.

The effect of PTH on aldosterone secretion from isolated bovine adrenal glomerulosa cells was examined. PTH binding was autoradiographically localized to the adrenal cortex, suggesting a specific effect. This binding of PTH was displaceable by cold PTH, but not by ACTH. No binding was observed in the adrenal medulla. In addition, PTH was shown to stimulate aldosterone secretion in a dose-dependent manner and to potentiate aldosterone secretion in response to angiotensin-II, such that PTH (10(-9)M) elevated the secretory rate from 58.6 +/- 6.8 to 110.9 +/- 19 pg/min.million cells in the presence of 10 nM angiotensin-II. The magnitude of the synergism between the two hormones depended on the concentrations of PTH and angiotensin-II as well as the time during which aldosterone secretion was measured. Within the first 15 min of stimulation, PTH increased the sensitivity to angiotensin-II, shifting the Ka for activation from 1.0 to 0.3 nM. In contrast, between 30-45 min of angiotensin-II stimulation, PTH elevated the maximal secretory response to angiotensin-II from 109 +/- 3.4 to 219 +/- 13.3 pg/min.million cells. By itself PTH elicited only a small increase in the intracellular Ca2+ concentration, as measured by aequorin luminescence in glomerulosa cells. In cells pretreated with angiotensin-II or 15 mM potassium, the intracellular calcium response to PTH was markedly potentiated. PTH was also found to cause a small increase in the cellular cAMP content. Thus, PTH stimulates aldosterone secretion from adrenal glomerulosa cells, both alone and in combination with angiotensin-II.

Adrenal Cortex↗
PubMed1990

Rat brain natriuretic peptide--tissue distribution and molecular form.

Using an antiserum against the ring structure of rat brain natriuretic peptide (rat BNP), we have established a specific radioimmunoassay (RIA) for rat BNP and elucidated its tissue distribution and molecular form. Rat BNP-like immunoreactivity (-LI) was detected in the highest amount in cardiac extracts (574.0 +/- 138.8 pmol/g in the atrium and 4.3 +/- 1.1 pmol/g in the ventricle). The secretory rate of rat BNP-LI from the perfused whole heart was 50.0 +/- 1.9 fmol/min, about 60% of which was maintained even after atrial removal. We also detected rat BNP-LI throughout the spinal cord (134-175 fmol/g), although no detectable amount was present (less than 100 fmol/g) in other tissues including the brain. High performance-gel permeation chromatography and reverse phase-high performance liquid chromatography coupled with the RIA revealed that rat BNP with 45 amino acids is a major storage form as well as a secretory form of rat BNP-LI in the heart. The major component in the spinal cord was also rat BNP. These findings indicate that the tissue distribution and the processing pattern of rat BNP are different from those of atrial natriuretic peptide and porcine BNP, thereby suggesting the presence of complicated diversity of the natriuretic peptide system.

Animals↗
PubMed1988

Distribution of milk in the goat mammary gland and its relation to the rate and control of milk secretion.

Changes with time in the distribution of milk between different storage regions of the mammary gland were studied in goats. Milk was allowed to drain from the gland through a catheter (catheter milk); the gland was then milked by hand, before (hand milk) and after the administration of oxytocin (alveolar or residual milk). The hand-milk fraction was of negligible volume. There was an essentially linear increase in the catheter-plus hand-milk fraction from 0 to 16 h. The alveolar fraction increased up to 6 h, but thereafter remained constant to 16 h. There was considerable but consistent variation between animals in the alveolar fraction as a proportion of total milk volume. The proportion of residual milk was inversely related to milk secretory rate per unit weight of mammary tissue. The hourly administration of oxytocin without milking had no apparent effect on the distribution of milk in the gland 1 h later.

Animals↗
PubMed1983

Maximal hepatic bilirubin transport in the rat during somatostatin-induced cholestasis and taurocholate-choleresis.

A steady maximal biliary secretion of bilirubin has been produced in male Wistar rats, recovered from anesthesia, by continuous infusion of 256 nmol of unconjugated bilirubin per hour per 100 gm body weight, after priming with 3.4 mumols. The administration of somatostatin (2 micrograms/hr/100 gm body weight) produced a reversible decrease of bile flow and bile acid excretion while bilirubin output was unchanged. After discontinuation of somatostatin, a slight increase in the output of bilirubin conjugates was observed with the rapid recovery of bile flow. Administration of Na+ taurocholate at increasing rates (30 to 480 nmol/min/100 gm body weight) progressively enhanced bile flow and bile acid secretion. The rate of secretion of bilirubin conjugates increased to 18% above the values in controls at a taurocholate dose of 120 nmol/min/100 gm body weight and remained at that level with higher amounts, in spite of further increases in flow. Under Na+ taurocholate, somatostatin failed to reverse the enhancement of bilirubin output, although it still inhibited the secretion of bile acids and bile flow. A mechanism linked to osmotic flow induced by taurocholate would appear to serve as a component of the total capacity of the hepatocyte to transfer bilirubin conjugates into the canaliculus. At low bile-acid secretory rates this component seems of minor quantitative importance, whereas a major (specific) pathway seems not yet saturated.

Animals↗
PubMed1981

Cholestatic action of somatostatin in the rat: effect on the different fractions of bile secretion.

Somatostatin was administered intravenously to male Wistar rats, recovered for 3 h from an anesthesia during which the common bile duct and jugular vein were cannulated. Different bile acid-secretory rates were obtained by infusion of saline, or of Na+-taurocholate (150 nmol/min/100 g body wt), or by 8-h bile depletion. At the dose of 2 micrograms/h/100 g body wt, somatostatin causes a prompt decrease of bile flow (about 30%) and of bile acid secretion (32%-47%). The bile acid-independent fraction of canalicular bile is more decreased than the one associated with bile acid secretion. The changes are dose dependent and show a saturation pattern, with half-maximal saturation already at 2.2 ng/min/100 g body wt. Despite this cholestasis, endogenous bilirubin secretion remained unchanged, pointing to different secretory mechanisms for bilirubin and bile acids. In the isolated and perfused liver, somatostatin displays an anticholeretic effect, proportional to the amount of Na+-taurocholate present in the system. Hepatic blood flow and O2 consumption remained constant during perfusion, and were not affected by somatostatin. The hepatic transport of bile acid, and the water and electrolyte secretion are directly affected by somatostatin, and the experimentally-induced cholestasis seems a new and suitable model for studying mechanisms of bile secretion.

Animals↗
PubMed1986

Extracellular strontium substitutes for calcium in in vitro renin secretion.

It has been shown previously that ouabain, vanadate, angiotensin II and 0 and 60 mM KCl media have Ca-dependent inhibitory effects on renin secretory rates of rat renal cortical slices. In the present experiments, replacing extracellular CaCl2 with SrCl2 did not impair the inhibitory effects on renin secretion in this preparation. Moreover, methoxyverapamil antagonized the inhibitory effect of K-depolarization. The inhibitory effects and methoxyverapamil-induced antagonism of the inhibitory effect of K-depolarization, suggest that increased intracellular Sr++ can lead to inhibition of renin secretion, perhaps directly or perhaps by causing the release or mobilization of Ca++ from intracellular sites of binding or sequestration. These results add to the growing evidence that Ca++ plays an inhibitory second messenger role in the renin secretory process.

Animals↗
PubMed2000

Steroid-dependent up-regulation of adipose leptin secretion in vitro during pregnancy in mice.

Circulating leptin levels are elevated during the later stages of pregnancy in mammals, suggesting that maternal leptin may play a role in maintenance of pregnancy and/or preparation for parturition and lactation. The regulation and source of circulating leptin during pregnancy remains undetermined, but leptin mRNA levels increase in adipose tissue during this time in some species. Considerable controversy exists whether placenta is also a leptin-secreting tissue during pregnancy. Here, we directly demonstrate that leptin secretion rates from mouse adipose tissue in vitro are decreased during early pregnancy and up-regulated during late pregnancy and lactation. Changes in leptin secretion rates in vitro paralleled those of circulating leptin in vivo during gestation. Subcutaneous implants of estradiol or corticosterone into lactating mice for 48 h stimulated adipose leptin secretion rates in vitro to the level of that in pregnant mice. However, corticosterone, but not estradiol, increased leptin secretion when added to isolated adipose tissue in vitro. Placentae obtained at two stages of pregnancy did not secrete leptin in vitro, either when acutely isolated or when dissociated into cells for long-term cultures. Placental tissue (or cells) secreted progesterone, however, demonstrating placental viability. We conclude that hyperleptinemia during late pregnancy in mice primarily results from corticosterone-dependent up-regulation of leptin secretion from adipose tissue, and that the placenta does not contribute to leptin secretion. The initial decrease in leptin secretory rates from adipose tissue during early pregnancy may facilitate energy storage for the subsequent, increased metabolic demands of later pregnancy and lactation.

Adipose Tissue↗
PubMedDate not supplied

Characterization of the effects of adenosine, adenosine 5'-triphosphate and related purines on acid secretion in isolated rabbit gastric glands.

The influence of adenosine, AMP, ADP, ATP, the adenosine analogue L-PIA and the ATP analogue beta,gamma-methylene ATP, on gastric acid secretion, as measured by the aminopyrine accumulation method, in resting and histamine-stimulated glands isolated from rabbit gastric mucosa was studied. In resting glands, adenosine and its analogue L-PIA (10 microM-1 mM) caused significant concentration-related increases of the basal H+ secretion, whereas no changes were obtained in response to the other purines tested. In histamine-stimulated glands, adenosine, L-PIA and AMP (10 microM-1 mM) induced concentration-related increases of the H+ secretory rate, whereas ATP, beta,gamma-methylene ATP and ADP (10 microM-1 mM) produced concentration-related decreases of the H+ raised rate. The rank order of potency of the purine compounds in increasing the stimulated H+ secretion was: adenosine greater than L-PIA much greater than AMP, and in decreasing it was: ATP much greater than ADP greater than beta,gamma-methylene ATP. The stimulatory responses to adenosine were inhibited by theophylline (10 microM-100 microM) and caffeine (10 microM-1 mM); whereas, the inhibitory responses to ATP were significantly reduced by the well known prostaglandin synthesis inhibitor indomethacin (1 microM-100 microM). From the results it is concluded that in isolated rabbit gastric glands, purine compounds are effective modulators of the gastric H+ secretory process. The pattern of purine activity obtained suggests that the stimulatory responses, inhibited by methylxanthines, may be mediated via P1-purinoceptors, while the inhibitory responses, reduced by indomethacin, may be mediated via P2-purinoceptors.

Adenosine↗