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PubMed2000

Accurate measurement of endogenous insulin secretion does not require separate assessment of C-peptide kinetics.

The implication of beta-cell failure as an early defect in type 2 diabetes exacerbates the need for accurate but facile assessment of islet cell secretory rate, particularly in large group studies in which individual assessment of C-peptide kinetics is impractical. This study was designed to examine whether it is possible to obtain accurate secretory rates from the extended combined model, which provides insulin and C-peptide kinetics from plasma measurements of the two peptides. Equimolar intraportal infusions of insulin and C-peptide that are designed to simulate insulin secretion rates during both oral and intravenous glucose tolerance tests were used to generate plasma insulin and C-peptide data in conscious dogs that were examined under clamped glucose conditions. The plasma peptide kinetics were analyzed using the extended combined model to generate estimates of prehepatic insulin secretion that were then compared with the known intraportal infusion rates. The extended combined model was able to reproduce the known intraportal infusion profiles. The model-predicted rates were similar to those calculated with methods that require separate assessment of C-peptide kinetics. Simulation results supported lesser clearance of insulin during rapid changes of portal insulin (as measured by an intravenous glucose tolerance test) versus slow changes in portal insulin (as measured by an oral glucose tolerance test). The extended combined model accurately calculates prehepatic insulin appearance. It may be possible to apply this approach to large studies of beta-cell function designed to identify changes in islet function in subjects at risk for diabetes. Such an approach could strengthen epidemiological and genetic studies of the pathogenesis of diabetes.

Animals↗
PubMed1986

Sympathetic control of adrenal secretion of enkephalins after hemorrhage in awake dogs.

Adrenomedullary secretion of methionine (Met)-enkephalin and of leucine (Leu)-enkephalin was measured in awake trained dogs subjected to 10 or 20% hemorrhage. Enkephalin secretory rates increased in proportion to the magnitude of hemorrhage with the ratio of Met-enkephalin to Leu-enkephalin being approximately 4:1. Arterial concentrations of enkephalins reflected adrenal secretion only in dogs exhibiting the largest secretory responses to hemorrhage. Cross-correlation analysis of 12 individual experiments showed that Met-enkephalin and epinephrine secretory rates were maximally correlated at 0-min delay, suggesting that enkephalins are cosecreted with catecholamines. The molar ratio in adrenal venous blood of epinephrine to Met-enkephalin ranges from 480 +/- 50 to 570 +/- 60. Chronic denervation of the adrenal by removing thoracic and lumbar splanchnic nerves prevented the Met-enkephalin and catecholamine secretory responses to hemorrhage. These data show that the adrenal medulla secretes enkephalins in response to stimuli activated by hemorrhage. These findings suggest that secretion of opiate-like peptides into the peripheral circulation may be a component of the sympathetic response to trauma.

Adrenal Glands↗
PubMed1987

Histamine release in vivo by pentagastrin from the canine stomach.

The effect of intragastric arterial infusion of pentagastrin on gastric histamine release was evaluated in mongrel dogs in vivo. Histamine secretory rates were evaluated by measuring the arterial and gastric venous plasma histamine concentrations at 0, 5, 10, 15 and 20 min into pentagastrin infusions, and gastric blood flow was continuously monitored. Histamine secretory rates were calculated by subtracting the arterial from the venous histamine concentrations and multiplying the difference by gastric plasma flow. Two separate 20-min infusions of pentagastrin, separated by 60 min, resulted in a peak of histamine release in 5 to 10 min that returned to base line within 20 min. During the first infusion, histamine release peaked at 179 ng/min, whereas, during the second infusion, histamine peaked at 125 ng/ml. The increase in gastric blood flow to pentagastrin correlated with the increases in histamine release. Somatostatin infused into the gastric artery to attain a concentration of 10 nM, a concentration that results in the inhibition of gastric acid secretion, abolished the gastric histamine release to pentagastrin. In addition, somatostatin also attenuated the gastric vasodilation to pentagastrin. Our data indicate that, in the in vivo dog model, pentagastrin can cause a pulsed release of gastric histamine, and somatostatin inhibits this release of histamine.

Animals↗
PubMed1984

Adrenal secretion of catecholamines during hypoxemia in fetal lambs.

A new method for quantifying adrenal secretory function in chronically catheterized fetal lambs was developed. This preparation included insertion of a catheter distally into the fetal left renal vein and placement of a remotely operated, hydraulically controlled choker around the renal vein at its junction with the vena cava. With the choker open, adrenal venous blood flowed into the renal vein and then into the vena cava. With the choker closed, adrenal blood flowed into the catheter so that timed samples of adrenal venous effluent could be obtained. With this technique, left adrenal secretory rates of norepinephrine and epinephrine were determined across a spectrum of oxygen concentrations in five near-term fetal lambs. There was a rapid rise in norepinephrine secretion after induction of hypoxemia. Maximum secretory rates occurred at about 5 min, concomitantly with the lowest attained fetal arterial partial pressure of oxygen (PO2s). There was an inverse exponential relation between these catecholamine secretion rates and fetal arterial PO2 (P less than 0.001). Norepinephrine secretion appeared to increase in response to lesser degrees of hypoxemia than did epinephrine, although a longer time delay between stimulation and epinephrine response may have been a factor. Overall, norepinephrine secretion was greater than that of epinephrine. The ratios of norepinephrine to epinephrine in individual adrenal samples varied considerably and in some instances were less than one. These ratios did not correlate significantly with the degree of hypoxemia. During 25 min of a relatively steady state of hypoxemia, norepinephrine secretion declined markedly after about 5 min, although it remained above control levels throughout. Epinephrine secretion rose more gradually but then was relatively stable during the remaining period of hypoxemia.

Adrenal Glands↗
PubMed1991

Direct and indirect stimulation of pancreatic exocrine secretion by neurotensin in anaesthetized dogs.

1. The effects of neurotensin on pancreatic exocrine secretion were investigated both in the intact whole pancreas and in the isolated, blood-perfused pancreas ex vivo in anaesthetized dogs. 2. Intravenous (i.v.) injections of neurotensin (0.01-1 nmol/kg) elicited dose-dependent increases in the secretory rate of pancreatic juice without changes in plasma levels of cholecystokinin (CCK). The concentration of bicarbonate in the pancreatic juice induced by neurotensin was increased, but the protein concentration was scarcely changed. 3. The neurotensin-induced secretion was inhibited by SCH23390, a dopamine D-1 antagonist, but not by domperidone, phentolamine, propranolol, atropine, cimetidine, or L-364,718, a CCK antagonist. 4. Intra-arterial (i.a.) injections of neurotensin (0.1-3 nmol/kg) also elicited dose-dependent increases in the secretory rate of pancreatic juice flow, but did not change bicarbonate or protein concentration. The secretory activities were less effective and 1 nmol/kg of neurotensin i.a. was approximately equal to that of 0.03 nmol/kg of neurotensin i.v. 5. These results suggest that neurotensin mainly stimulates pancreatic secretion by acting indirectly. Neurotensin-induced secretion is, at least in part, mediated by endogenously released dopamine which activates dopamine D-1 receptors on the pancreas. In addition to its indirect action, neurotensin has a weak direct action to stimulate pancreatic secretion.

Animals↗
PubMed1989

Expansion of the bile acid pool changes the biliary transport characteristics of centrizonal hepatocytes.

We investigated whether acinar differences in taurocholate transport are responsible for the increased maximal secretory rate observed after expansion of the bile acid pool. The bile acid pool was expanded by cholate feeding for four days. Periportal and centrizonal hepatocytes were then probed by ante- and retrograde liver perfusion, respectively. In control animals, secretory rate constant (alpha 1) averaged 0.439 +/- 0.123 and 0.104 +/- 0.035 min-1 during ante- and retrograde perfusion, respectively, in the absence of exogenous taurocholate. These values did not significantly change when taurocholate was infused. In cholate-fed animals, alpha 1 was comparable during antegrade perfusion but was significantly reduced (0.038 +/- 0.035, p less than 0.05) during retrograde perfusion in the absence of exogenous taurocholate, presumably owing to induction of cytosolic bile acid binding proteins. During loading with exogenous taurocholate, by contrast, alpha 1 was significantly accelerated (0.252 +/- 0.026; p less than 0.01) in centrizonal hepatocytes from bile-acid fed rats. Expansion of the bile acid pool is able to change the bile salt secretory characteristics of centrizonal hepatocytes toward those of periportal ones.

Animals↗
PubMed1991

Gastric mucosal secretions and lesions by different doses of streptozotocin in rats.

The effects of various doses of streptozotocin (STZ) on gastric mucosal secretions and lesions were investigated in rats. STZ at a dose as low as 30 mg/kg significantly increased plasma glucose (P less than 0.05). The elevation of plasma glucose was dependent on the dose on STZ (30-65 mg/kg) administered. The levels of SGOT, SGPT, bilirubin and BUN also increased with the dose of STZ. The secretory rate of gastric H+ decreased whereas the degree of mucosal hyperemia increased with increasing levels of plasma glucose. Treatment with insulin improved all abnormal conditions except the gastric mucosal lesions. The lesions occurred with low H(+)-secretory rate and low gastric emptying rate. It is suggested that STZ might act directly on the gastric mucosa. Its action depended on the dose administered and was not primarily related to the insulin deficit.

Alanine Transaminase↗
PubMed2002

Effects of glucose, exogenous insulin, and carbachol on C-peptide and insulin secretion from isolated perifused rat islets.

Isolated perifused rat islets were stimulated with glucose, exogenous insulin, or carbachol. C-peptide and, where possible, insulin secretory rates were measured. Glucose (8-10 mm) induced dose-dependent and kinetically similar patterns of C-peptide and insulin secretion. The addition of 100 nm bovine insulin had no effect on C-peptide release in response to 8-10 mm glucose stimulation. The addition of 100 nm bovine insulin or 500 nm human insulin together with 3 mm glucose had no stimulatory effect on C-peptide secretion rates from perifused rat islets. Stimulation with carbachol plus 7 mm glucose enhanced both C-peptide and insulin secretion, and the further addition of 100 nm bovine insulin had no inhibitory effect on C-peptide secretory rates under this condition. Perifusion studies using pharmacologic inhibitors (genistein and wortmannin) of the kinases thought to be involved in insulin signaling potentiated 10 mm glucose-induced secretion. The results support the following conclusions. 1) C-peptide release rates accurately reflect insulin secretion rates from collagenase-isolated, perifused rat islets. 2) Exogenously added bovine insulin exerts no inhibitory effect on release to several agonists including glucose. 3) In the presence of 3 mm glucose, exogenously added bovine or human insulin do not stimulate endogenous insulin secretion.

Androstadienes↗
PubMed1995

WENDEC: a deconvolution program for processing hormone time-series.

The estimation of the glandular secretory rate from time-series of hormone concentration in plasma can be formulated as a deconvolution problem. In particular, the paper addresses the analysis of frequently sampled data collected in order to study spontaneous pulsatile secretion. Standard deconvolution methods do not allow for the non-negativity constraint and the presence of high-frequency components in the secretory rate. In order to overcome the intrinsic ill-conditioning of the problem, the maximum entropy method is used to obtain a probabilistic representation of the prior knowledge concerning the unknown secretory signal, thus leading to a White Exponential Noise (WEN) model. The deconvolution problem is then posed within a Bayesian framework and solved by means of Maximum-A-Posteriori estimation. The program that implements the algorithm handles non-negativity constraints, provides confidence intervals, and is computationally and memory efficient.

Algorithms↗
PubMed1976

Regulation of avian insulin secretion by isolated perfused chicken pancreas.

Chicken insulin secretory responses to glucose, glucagon, tolbutamide, and lack of Mg2+ were measured using isolated perfused in situ chicken pancreata. Although elevating perfusate glucose concentration from 100 to 250 mg/100 ml failed to increase insulin release, 500 mg glucose/100 ml provoked a transient 5-min insulin response. Additionally, 700 mg glucose/100 ml resulted in both a transient response and subsequent elevation in secretory rate that continued throughout the following 50-min stimulatory period. Glucagon (500 microgram/ml) and omission of perfusate Mg2+ potentiated glucose-stimulated insulin output by 6 and 25%, respectively. A faster release of insulin (less than 1 min) occurred during tolbutamide infusion (0.13 mg/ml) than with either 500 or 700 mg glucose per 100 ml (2-3 min); however, secretory rates declined to near basal levels within 5 min. Mammalian-like insulin responses to glucose, glucagon, Mg2+ lack, and tolbutamide suggest similarities between avian and mammalian beta-cell insulin secretory mechanisms. Nevertheless, the relatively high chicken insulin release threshold and low insulin output to glucose indicate that chicken pancreata are relatively glucose insensitive.

Animals↗
PubMed2002

Circadian effects on the acute responses of salivary cortisol and IgA in well trained swimmers.

OBJECTIVE: To examine whether time of day significantly affects salivary cortisol and IgA levels before and after submaximal swimming. METHODS: Fourteen male competitive swimmers (mean (SD) age 18 (3.2) years) volunteered to participate in the study. In a fully randomised, cross over design, each subject performed 5 x 400 m front crawl at 85 (1.2)% of their seasonal best time (277 (16) seconds), with one minute rest between each 400 m, at 0600 and 1800 hours on two separate days. Timed, unstimulated saliva samples were collected before and after exercise. Saliva samples were analysed for cortisol and IgA by radioimmunoassay and single radial immunodiffusion respectively. RESULTS: Significant time of day effects (am and pm respectively) were observed in IgA concentration (0.396 (0.179) v 0.322 (0.105) mg/ml, p<0.05), IgA secretory rate (0.109 (0.081) v 0.144 (0.083) mg/min, p<0.01), and saliva flow rate (0.31 (0.23) v 0.46 (0.22) ml/min, p<0.001) before exercise (all values mean (SD)). Differences in cortisol levels before exercise (1.09 (0.56) v 0.67 (0.94) microg/dl) approached significance (p = 0.059). The exercise protocol did not significantly affect IgA concentration and secretory rate (p>0.05) but, in comparison with values before exercise, caused significant alterations in cortisol (p<0.01) and saliva flow rate (p<0.01). There was no significant interaction effect of time of day by exercise on any salivary variables measured (p>0.05). However, most of the values of the salivary variables before exercise were significantly inversely related to their exercise induced response (p<0.05). CONCLUSION: These results suggest a significant circadian variation in the variables measured before exercise, without showing a significant effect on their acute responses to exercise.

Adolescent↗
PubMed1985

In vivo kinetics of radiolabeled monoclonal anti-CEA antibodies in animal models.

Studies were performed to determine the effect of the radiolabel and circulating carcinoembryonic antigen (CEA) on the pharmacodynamics of monoclonal anti-CEA antibodies (MoAbs). The studies were performed in normal BALB/c mice and in nude mice bearing human colon tumors. Three different tumors were used, each of which produced CEA levels characteristic of that particular tumor's secretory rate. The CEJ-326 MoAb labeled with either 111In or 125I was used in all studies. Circulating CEA induced the removal of 125I and 111In MoAbs from the vascular compartment. Liver concentrations of 111In increased and 125I levels decreased as the CEA secretory rate of the tumor rose. This indicates that circulating CEA complexes form in the vascular compartment which, in an animal model, are removed by the liver and spleen. This results in decreased tumor uptake of the labeled MoAb. The iodinated MoAb complexes are dehalogenated while the 111In is retained by the liver. This dehalogenation may account for the relatively low liver activity observed in radioimmunoimaging with intact radioiodinated anti-CEA MoAbs, provided the CEA complexes are similarly removed from the vascular compartment by the human liver.

Animals↗
PubMed1996

Dynamics of glucose-induced insulin release from mouse islets transplanted under the kidney capsule.

Mouse pancreatic islet grafts under the kidney capsule of syngeneic hosts were removed and perifused in vitro 1-40 weeks after the transplantation. In comparison with fresh islets, 12- to 40-week-old grafts exhibited an attenuated first phase of glucose-stimulated insulin release. In grafts 1, 12, 28, or 40 weeks old, but not in fresh islets, the mean secretory rate during the initial 10 min of stimulation was significantly lower than that during the subsequent 15 min. When expressed in relation to insulin content, the insulin output in response to 11 mmol/L glucose was no less from grafts than from fresh islets; in grafts 12 or 40 weeks old at 16.7 mmol/L glucose, the fractional output above baseline was significantly diminished during the initial 10 min, but not subsequently. Immediately on switching from basal to stimulatory glucose concentration, there was a transient drop in insulin secretion from the grafts, especially after more than 12 weeks of transplantation and in response to 16.7, as compared with 11, mmol/L glucose. When glucose was switched back from stimulatory to basal concentration, grafts also frequently exhibited a transient increase in the insulin secretory rate. Neither initial drops nor "off responses" were seen in untransplanted islets. The modifications of the secretory dynamics in islet grafts suggest that transplantation influences the balance between the stimulatory and inhibitory influences of glucose on the beta-cell's secretory machinery.

Animals↗
PubMed1987

Renin secretory effects of N6-cyclohexyladenosine: effects of dietary sodium.

Previous observations by others have shown that Na deprivation augments and Na loading attenuates the inhibitory effect of exogenous adenosine on renin secretion in vivo. The purpose of the present experiments was to test the hypothesis that Na deprivation and Na loading alter the sensitivity of the adenosine receptors (A1 subclass) that mediate the inhibitory effect. The rat renal cortical slice preparation was used. Na loading decreased and Na deprivation increased tissue renin content and the basal renin secretory rate; these two variables were directly related (r = 0.84, P less than 0.00005). N6-cyclohexyladenosine (CHA), an adenosine analogue that selectively activates the A1 subclass of adenosine receptors in the nanomolar to micromolar concentration range inhibited renin secretion over the same range of concentrations (nM-microM) and to approximately the same maximal extent (to 50% of the mean basal secretory rate) in cortical slices taken from Na-loaded, control, and Na-deprived rats. These results demonstrate that changes in the intrinsic sensitivity of adenosine receptors do not explain dietary Na-induced changes in the in vivo renin secretory response to exogenous adenosine.

Adenosine↗
PubMed1980

The effect of lithium on electrolyte transport by the in situ choroid plexus of the cat.

1. The effects of lithium on electrolyte transport were studied by using the cat choroid plexus isolated in a chamber in situ. 2. Lithium infused intravenously to produce plasma lithium concentrations up to 5 m-equiv/l. caused an increase in plasma magnesium with no effect on the concentration of magnesium in the chamber fluid. 3. When 22NaCl was infused intravenously the chamber fluid/plasma ratio of 22Na was nearly 1 in the first 30 min sample and at the steady state it was significantly greater than 1. 4. When lithium chloride (1.5 m-equiv/l.) or potassium chloride (6.6 m-equiv/l.) was added to the chamber at the start of a collection period with plasma 22Na in the steady state, the 22Na content of the chamber fluid promptly increased 118 and 68%, respectively, above the control value with no increase in secretory rate. 5. The addition of ouabain to the chamber fluid, in addition to the lithium chloride or potassium chloride, tended to stimulate or have no significant effect on 22Na uptake at a concentration of 10(-5) M and to reduce it as well as the secretory rate at 10(-3) M. 6. The date are compatible with there being two functionally separate sodium transport systems in the choroid plexus. One transports sodium accompanied by an anion and water to provide the fluid secreted into the chamber (c.s.f.) and the other operates primarily to regulate the potassium concentration of the c.s.f. by pumping potassium out in exchange for sodium. 7. Lithium can be transported by both systems to a limited extent and the presence of lithium in the c.s.f. stimulates the sodium-potassium regulating pump.

Animals↗
PubMed1988

Gonadotropin-releasing hormone (GnRH) inhibits ovulation induced with luteinizing hormone (LH) in proestrous hypophysectomized rats.

In this paper we present evidence that a single low dose of the natural synthetic gonadotropin-releasing hormone (GnRH), inhibits ovulation induced by LH in proestrous-hypophysectomized rats. Rats hypophysectomized by the parapharyngeal route in the morning of proestrus received an intravenous injection of 100 or 300 ng GnRH at 1400 h immediately followed by 1.0 microgram LH per 100 g bw. In control groups, either one or both hormones were replaced with 0.9% NaCl. Ovulation was assessed the following morning by counting the ova present in oviductal flushings. All the rats treated with LH alone ovulated, and the addition of GnRH reduced significantly the number of ovulating rats and the number of ova per ovulating rat. In other groups of rats hypophysectomized in the morning of proestrus and treated in the same way, ovarian or adrenal secretory rates of estradiol and/or progesterone were measured after cannulation of the corresponding vein, in the afternoon of proestrus. In these animals, GnRH failed to inhibit either the ovarian progesterone surge observed 2 h after LH administration, or the adrenal progesterone secretion. All hypophysectomized rats showed lower ovarian secretory rate of estradiol than intact rats; this rate was not affected by treatment with LH or LH plus GnRH. The systemic estradiol levels in plasma of hypophysectomized rats were distributed within a range of 20 pg/ml to 50 pg/ml. The number of rats whose levels were above 21 pg/ml on estrus day was significantly higher in rats receiving 300 ng GnRH as compared to those receiving 100 ng GnRH, reaching values that surpassed the concentration found in intact, untreated animals at the same time of estrus. This effect did not depend on LH administration.

Adrenal Glands↗
PubMed1986

Stimulation of gastric mucus and protein secretion by cytochalasin E in rats.

Effects of cytochalasin E on the secretion of mucus and protein were investigated in gastric fistula rats. Direct exposure of the gastric mucosa to cytochalasin E (5-20 micrograms/ml) significantly stimulated the secretory rate of soluble mucus and protein in pentagastrin-stimulated rats. The amount of surface mucus gel was also increased. The stimulatory effect was increased with increased concentrations of cytochalasin. Histological study suggests that the cytochalasin stimulated the release of mucus from the cell. The increase in secretory rate of protein was not due to an increase of pepsin secretion but rather was the consequence of the increase in mucus secretion.

Animals↗
PubMed1998

Abnormal regulation of proximal tubule renin mRNA in the Dahl/Rapp salt-sensitive rat.

BACKGROUND: The precise pathogenesis of salt-sensitive hypertension in the Dahl rat is unknown. Abnormalities in renal hemodynamics and NaCl handling have been implicated, and may relate to changes in the activity of the intrarenal renin-angiotensin system. METHODS: Circulating, juxtaglomerular and intrarenal (glomerular and proximal tubular) renin were studied in Dahl/Rapp salt-sensitive and salt-resistant rats fed with a normal (0.5%) or high (4%) NaCl diet. Circulating and juxtaglomerular renin were assessed by measurement of plasma renin activity and renin secretory rates. Glomerular and proximal tubular renin mRNA were assessed by microdissection and quantitative competitive RT-PCR. RESULTS: Circulating and juxtaglomerular renin were suppressed by high dietary NaCl in salt-sensitive rats (plasma renin activity, 0.5%, 10.9 +/- 0.7 vs. 4%, 7.9 +/- 0.3 ng/ml/hr, P < 0.05; renin secretory rate, 0.5% 220 +/- 32 vs. 4%, 58 +/- 5 ng/mg/hr, P < 0.05). Glomerular renin mRNA was also suppressed by the higher salt diet in salt-sensitive animals (0.5%, 411 +/- 84 vs. 4%, 67 +/- 22 x 103 copies/glomerulus, P < 0.05). In contrast, proximal tubular renin was not suppressed by a high NaCl diet in salt-sensitive animals (0.5%, 13.9 +/- 2.7 vs. 4%, 12.1 +/- 3.6 x 103 copies/mm tubule, P = NS), but was suppressed in salt-resistant rats (0.5%, 9.5 +/- 2.8 vs. 4%, 3.2 +/- 1.2 x 103 copies/mm, P < 0. 05). CONCLUSIONS: Failure to suppress proximal tubular renin in response to high dietary NaCl may result in increased local generation of angiotensin II and enhanced proximal tubular NaCl absorption, and thereby contribute to the generation of salt sensitive hypertension.

Animals↗