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Mental disorders and related behaviors such as suicidality and violence have been associated to dysregulation of e g carbohydrate metabolism. We hypothesized that patients after suicide attempt, compared to healthy controls, would have higher insulin and lower glucagon levels in plasma and cerebrospinal fluid and that these changes would be associated to violent behavior. Twenty-eight medication-free patients (10 women, 18 men), hospitalized after suicide attempt, and 19 healthy controls (7 women, 12 men) were recruited with the aim to study risk factors for suicidal behavior. Psychological/psychiatric assessment was performed with SCID I and II or the SCID interview for healthy volunteers respectively, the Karolinska Interpersonal Violence Scale (KIVS) for assessment of lifetime violence expression behavior, the Montgomery-Åsberg-Depression-Scale (MADRS) and the Comprehensive Psychological Rating Scale (CPRS) for symptomatic assessment of depression and appetite. Fasting levels of insulin and glucagon were measured in plasma (P) and cerebrospinal fluid (CSF). Suicide attempters had higher insulin- and lower glucagon-levels in plasma- and CSF compared to controls. Except for P-glucagon these associations remained significant after adjusting for age and/or BMI. Patients reported significantly more expressed interpersonal violence compared to healthy volunteers. Expressed violence was significantly positively correlated with P- and CSF-insulin and showed a significant negative correlation with P-glucagon in study participants. These findings confirm and extend prior reports that higher insulin and lower glucagon levels in plasma and cerebrospinal fluid are associated with suicidal behavior pointing towards a potential autonomic dysregulation in the control of insulin and glucagon secretion in suicidal patients., (Copyright © 2017 Elsevier Ltd. All rights reserved.)

The aim of the present study was to investigate the effects of repeated massage-like stroking on plasma levels of some gastrointestinal hormones, insulin included, glucose and weight gain. For this purpose, male rats were exposed to stroking on the ventral side of the abdomen for 3 or 14 times. The treatments were given every second day. Control rats were picked up at the same time but received no stroking. Body weight was measured regularly. Rats were decapitated 10 min after the last treatment. Hormone levels were radioimmunoassayed and glucose was measured by spectrophotometry. In rats exposed to 3 sessions of massage-like stroking plasma levels of insulin (p<0.05) and somatostatin (p<0.01) were significantly decreased 10 min after the last treatment. After 14 treatments of massage-like stroking, decreased plasma levels of insulin (p<0.01) and gastrin (p<0.01) as well as increased glucose levels (p<0.01) were observed 10 min after the last treatment. In addition, weight gain was significantly increased (ANOVA p<0.0001) in rats exposed to 14 treatments. In conclusion, repeated massage-like stroking decreased plasma levels of gastrin, insulin and somatostatin, increased plasma levels of glucose and promoted weight gain. The effects were influenced by the number of treatments.

The present study was designed to investigate how repeated injections of oxytocin influence plasma levels of vagally controlled hormones such as gastrin, cholecystokinin (CCK), insulin and somatostatin, as well as of endogenous oxytocin and glucose. Since oxytocin may enhance the activity of centrally located alpha2-adrenoreceptors, a second aim of this study was to explore whether these receptors are involved in the effects. For this purpose, oxytocin (1.0 mg/kg) or NaCl was given subcutaneously (s.c.) once a day during 5 days to male rats. Rats were decapitated 1, 3 and 10 days after the last injection, blood was collected and hormone levels were radioimmunoassayed. The oxytocin treatment caused an elevation of plasma levels of oxytocin 1 day (p < 0.05) but not 3 and 10 days after treatment. Gastrin levels were decreased on day 1, 3 and 10 (ANOVA; p < 0.01). In addition, both insulin and CCK levels were decreased in response to the oxytocin treatment when measured 3 and 10 days after the last injection (ANOVA; insulin p < 0.01, CCK p < 0.05). When the alpha2-adrenoreceptor agonist clonidine (2.5 microgram/kg intracerebroventricularly) was administered 3 days after the 5-day treatment period with oxytocin or saline, plasma levels of insulin and CCK increased significantly (p < 0.05) in the oxytocin-treated rats, when compared to saline-treated controls receiving clonidine only. No change in glucose or somatostatin levels was found in response to the oxytocin treatment. In conclusion, these results show that oxytocin induces long-lasting changes in plasma levels of gastrin, CCK and insulin, without affecting somatostatin or glucose levels. These effects may be mediated by changes in vagal nerve activity.

The aim of the present study was to investigate whether the 5-HT1A receptor agonist 8-OH-DPAT, which previously has been shown to release oxytocin, also influences plasma levels of gastrointestinal and pancreatic hormones, and if so, whether such an effect is mediated by an oxytocinergic mechanism. For this purpose 8-OH-DPAT (0.5 mg/kg s.c.) was injected to male rats pretreated with the oxytocin receptor antagonist 1-deamino-2-D-Tyr-(OEt)-4-Thr-8-Orn-oxytocin (1 mg/kg s.c.), or vehicle. Thirty min after injection of 8-OH-DPAT, plasma levels of oxytocin were significantly increased. 8-OH-DPAT also increased insulin and decreased CCK and somatostatin levels, effects that were blocked by pretreatment with the oxytocin antagonist. Taken together, these data suggest that the effect of 8-OH-DPAT on plasma levels of insulin, somatostatin and CCK may be mediated by oxytocin. In previous experiments, we have shown that following i.c.v. application of oxytocin, plasma levels of insulin are increased through a cholinergic mechanism. In this study, 2 ng of oxytocin decreased plasma levels of CCK, gastrin and somatostatin, effects that were blocked by pretreatment with atropine. Since oxytocinergic fibers which originate in the PVN project to the DMX, we suggest that the effect on the release of insulin, CCK and somatostatin induced by the 5 HT1A receptor agonist 8-OH-DPAT may be mediated by an oxytocinergic activation of a vagal mechanism.

Male Sprague-Dawley rats were given one of the 5-HT receptor agonists 8-OH-DPAT (0.5-2.0 mg kg-1), TFMPP (0.125-2.0 mg kg-1), DOI (0.125-2.0 mg kg-1), and m-CPBG (1.25-20.0 mg kg-1), selective for 5-HT1A, 5-HT1B, 5-HT2 and the 5-HT3 receptors, respectively, or one of the DA receptor agonists bromocriptine (2.0-32.0 mg kg-1), quinpirole (0.5-8.0 mg kg-1) and 7-OH-DPAT (0.2-3.2 mg kg-1), selective for DA D2, DA D2/D3 and DA D3 receptors, respectively. An additional group of animals was given buspirone (2.0-8.0 mg kg-1) a 5-HT1A receptor agonist and DA D2 receptor antagonist. Separate groups of rats were given both the 5-HT1A receptor antagonist pindolol and 8-OH-DPAT or both the DA D2/D3 receptor antagonist raclopride and 7-OH-DPAT. Blood samples were collected 30 min (in some cases 120 min) after drug administration and assayed for insulin, glucagon and glucose levels. The 5-HT1A receptor agonist 8-OH-DPAT produced a statistically significant decrease in plasma insulin levels and an increase in glucose, whereas glucagon levels were unaffected. The only effect observed after buspirone treatment was a small increase in plasma glucose levels. No significant effects on plasma insulin, glucagon or glucose were seen after treatment with the 5-HT1B, 5-HT2 or 5-HT3 agonists. The DA D3 receptor agonist 7-OH-DPAT produced a decrease in plasma insulin (3.2 mg kg-1, 120 min) and an increase in glucose levels. Administration of the DA D2/D3 receptor agonist quinpirole resulted only in increased plasma glucose, whereas the DA D2 receptor agonist bromocriptine had no effect. In support of a separate mediation of glucose secretion by 5-HT1A and DA D3 receptors, the effects of 8-OH-DPAT on glucose levels were antagonized by (-)pindolol pretreatment, and the 7-OH-DPAT-induced effects on glucose levels were antagonized by raclopride pretreatment. It is concluded that plasma glucose levels are under separate serotonergic and dopaminergic control, exerted via 5-HT1A and DA D3 receptors, respectively.

The effects of 24 h of fasting and refeeding on the release of oxytocin, prolactin, insulin and LH in three lactating sows were investigated. The sows were starved, but supplied with water ad libitum, from 09.00 h on day 27 of lactation until 15.00 h on day 28 of lactation, when they were refed. Blood samples were collected continuously, using an automatic collection system, at a rate of 1 ml min-1 from 09.00 to 21.00 h on day 28 (P1 = 6 h period after the 24 h fast, P2 = 6 h period after refeeding). For both P1 and P2 the mean number of nursings was 7.0 +/- 1.0. Plasma insulin and glucose decreased to very low levels during fasting and increased (P < 0.001) after refeeding (insulin, 2.5 +/- 0.7 vs. 28.9 +/- 0.7 mU l-1; glucose, 2.6 +/- 0.3 vs. 6.4 +/- 0.3 mmol l-1). Following fasting, levels of prolactin were low (2.8 +/- 0.1 micrograms l-1), and sucking did not induce significant release of prolactin. However, prolactin increased rapidly after refeeding (5.4 +/- 0.1 micrograms l-1, P < 0.001). Neither the 24 h fast nor refeeding had a marked effect on basal levels of oxytocin, the percentage of sucklings with an oxytocin peak or the size of oxytocin peak. LH release (average and basal levels and number of pulses/6 h) during fasting was similar to that measured after refeeding. Plasma CCK increased significantly after feeding. The results indicate that the release of prolactin is also regulated by feed intake.(ABSTRACT TRUNCATED AT 250 WORDS)

Twelve primiparous sows were grouped into six pairs. One sow from each pair (T) received subcutaneous injections of porcine insulin as follows: pairs 1 and 2, 0.5 IU/kg at 07.00 h; pairs 3 to 6, 0.5 IU/kg at 07.00 and 15.00 h. Insulin administration was started one day before weaning and continued until the last day of post-weaning oestrus. Control sows (C) received physiological saline solution as a sham treatment. Blood samples were collected every 3 h from 09.00 to 21.00 h and, additionally, at 07.00 h during the period of insulin treatment. Additional blood samples were collected at 15-min intervals for 6 h for 2 days before and for 3 days after weaning, and for 12 h on the day of weaning (D35 of lactation). Exogenous treatment with insulin increased plasma levels of insulin (53 v 36 mU/l, P < 0.001) and decreased plasma levels of glucose (4.6 v 5.5 mmol/l, P < 0.001) in T-sows as compared to C-sows. During the treatment period, the average levels of cortisol (31 v 35 nmol/l, P < 0.001) and non-esterified fatty acids (0.13 v 0.16 mmol/l, P < 0.01) were lower in T-than in C-sows. No differences in glucagon or urea levels were observed between the two groups. Plasma levels of LH were higher in T- than in C-sows both before and during the treatment period. However, no differences in number of LH pulses/6h were found between the two groups.(ABSTRACT TRUNCATED AT 250 WORDS)

In the present investigation it was studied whether oxytocin administered directly in the pancreas of the rat stimulates the release of insulin and glucagon. In order to study such effects in vivo, a new experimental model applying the microdialysis technique was developed. To test the validity of the method, glucose or arginine were infused i.v. and it was shown that perfusate concentrations of insulin and glucagon increased significantly to 344 and 292% of basal overflow, respectively. Administration of oxytocin via the dialysis probe into the splenic portion of the pancreas resulted in significant elevations of insulin and glucagon concentrations to 210 (P less than 0.05) and 528% (P less than 0.01), respectively. The present study also includes a combined autoradiographic and immunohistochemical investigation of binding sites for oxytocin in the rat pancreas. A high density of [3H]oxytocin binding was present in the periphery of the islets of Langerhans, corresponding to the localization of the glucagon-producing alpha-cells. Both oxytocin and arginine(A)-vasopressin displaced [3H]oxytocin. The IC50 values were 10 and 180 nM, respectively. In conclusion, the oxytocin-induced release of insulin and glucagon as previously demonstrated in a number of species, may be due to a stimulation exerted by the peptide directly within the pancreas.

The concentration of gastrin and insulin was determined in peripheral blood of 4 lactating dogs during suckling. Suckling induced an immediate rise of gastrin and insulin levels, twofold and threefold, respectively. A peak was reached at approximately 5 min after suckling was started, and basal levels were reached again within 15-20 min. The increase in gastrin and insulin levels coincided with the let-down reflex, i.e. it occurred when the puppies started to obtain milk from their mothers. Sham feeding and feeding induce a vagally mediated increase of gastrin and insulin release in dogs. We suggest that the changes in the gastrin and insulin levels observed by us in the lactating dogs, reflect a similar vagal activation induced by suckling. Possible effects of the suckling induced release of gastrin and insulin on milk ejection and secretion are discussed.

The aim of the present investigation was to study changes in insulin, glucagon and plasma glucose levels in response to suckling in lactating dogs. Blood samples were drawn from a peripheral vein during suckling in weeks 1 and 3 of lactation in 10 lactating beagles. Insulin- and glucagon-like immunoreactivity (below referred to as insulin and glucagon) were determined by radio-immunoassay, and plasma glucose levels by the glucose oxidase method. Insulin and glucagon levels rose following onset of suckling. However, only the rises recorded in week 3 of lactation were statistically significant. Plasma glucose levels were not affected. The mechanism by which suckling influences the levels of insulin and glucagon is not known. However, the release of both hormones is under vagal control and it is possible that touching of the teats reflexly elicits a vagally mediated release of these hormones. Alternatively, since oxytocin stimulates the secretion of insulin and glucagon, the effects might be secondary to the oxytocin released by suckling. The physiological function of the suckling-related release of insulin may be to stimulate milk production. Furthermore, since glucagon is also released, each suckling period may be accompanied by a transfer of glucose to the mammary glands from other maternal stores.

The aim of the present investigation was to study the effect of non-nutritive sucking on plasma levels of insulin, gastrin, and somatostatin in infants. These hormones were measured with radioimmunoassay in plasma collected from fullterm and preterm infants sucking a pacifier. In fullterm infants, sucking caused a significant increase of insulin levels from 13 +/- 10 microU/ml to 40 +/- 36 microU/ml and 21 +/- 17 microU/ml after 45 sec and 5 min respectively, from when the infants started sucking. A similar pattern was seen in preterm infants. In contrast, gastrin and somatostatin levels were not significantly affected. We suggest that sucking causes an activation of the vagal nerve, which results in the release of insulin. We also suggest that in infants, oral feeding is superior to bolus feeding, since in the latter case no vagal activation and consequently no release of hormones with anabolic properties occurs.

The objective of the present study was to investigate whether gastrointestinal hormones can be released in response to low intensity afferent activation of the sciatic nerve. Experiments were performed on anaesthetized cats in which the sciatic nerve was stimulated electrically at 3 Hz, to V and 0.2 ms. Blood samples were collected in a peripheral vein and the plasma levels of somatostatin, gastrin, glucagon, insulin and VIP-like immunoreactivity (below referred to as somatostatin, gastrin, glucagon, insulin and VIP) were recorded by radioimmunoassay. Afferent stimulation of the sciatic nerve caused immediate (approximately 15 min long) changes of the levels of all the above mentioned peptides. Somatostatin, gastrin and glucagon levels rose significantly, whereas in the case of insulin and VIP a significant relationship between the effect of sciatic nerve stimulation and basal levels was established. Thus, insulin and VIP levels decreased when basal levels were high and increased when basal levels were low. The secretion of gastrointestinal and pancreatic hormones is in part regulated by the autonomic nervous system. It is suggested that afferent stimulation of the sciatic nerve causes a reflex activation of the vagal and/or the splanchnic nerves, which in turn affects the release rate of the above-mentioned hormones. In conclusion, these data show that the release of gastrointestinal hormones can be influenced by low intensity stimulation of the sciatic nerve. The physiological trigger of these responses may be touching of the skin.

The effect of weaning on plasma levels of insulin and glucagon as well as on plasma glucose levels was studied in sows after final weaning (all the piglets removed in week 5 of lactation) and fractionated weaning (7 out of 12 piglets removed in week 3 of lactation). Insulin levels rose from 24 +/- 6 to 106 +/- 22 microU ml-1 4 days after final weaning and from 11 +/- 1 to 128 +/- 20 microU ml-1 7 days after fractionated weaning. Glucagon levels fell from 60 +/- 20 and 42 +/- 8 to 35 +/- 10 and 24 +/- 5 pm in the two groups, respectively. Plasma glucose levels increased from 4.5 +/- 0.5 to 7.2 +/- 1.2 mM after fractionated weaning and remained unchanged after final weaning. One possible mechanism that can explain this pronounced insulin increase and decrease of glucagon is the elevation of plasma glucose, since milk is no longer emptied from the mammary gland and since insulin resistance occurs after weaning in rats. Another possible explanation could be a decreased number of insulin receptors in the mammary gland, since prolactin which is known to increase insulin receptors is decreased in weaned rats.

VIP levels were measured by radioimmunoassay in peripheral venous blood of conscious dogs. Bolus injections of the dopamine agonists apomorphine, 0.05 mg/kg, and bromocriptine, 0.2 mg/kg, were found to increase VIP levels from approximately 5 pmol/l to 150 pmol/l. The release responses were abolished by pretreatment with dopamine antagonists (haloperidol 0.1 mg/kg or halopemid 0.1 mg/kg) and by hexamethonium (1 mg/kg) a blocker of ganglionic transmission. Vagotomy did not inhibit the dopamine agonist induced output of VIP. Vagal activation by means of feeding or insulin hypoglycemia caused only minor rises of VIP levels (5-10 pmol/l). It is concluded that dopamine agonists stimulate the release of VIP from populations of neurons other than those affected by vagal and sympathetic activation. Possible sites of action for the VIP releasing effect exerted by dopamine agonists are discussed. Furthermore, it is suggested that some of the peripheral effects exerted by dopaminergic drugs are exerted via a previous release of VIP.

The aim of the present study was to investigate how infusion of gastrin-17 and oxytocin affects plasma levels of insulin, glucagon and glucose in order to elucidate how the two hormones contribute to metabolic changes seen in situations where they are released, e.g. feeding and suckling during lactation. Thus, gastrin-17 (0.5 and 2.0 nmol kg-1 h-1) and oxytocin (0.11 and 1.1 nmol kg-1 h-1) were infused separately or simultaneously into conscious dogs. Both gastrin-17 and oxytocin induced significant, dose-dependent increases in insulin levels. An additive effect on insulin levels was obtained when gastrin-17 and oxytocin were infused simultaneously. Glucagon levels were not affected by gastrin-17 whereas infusion of 1.1 nmol kg-1 h-1 of oxytocin was followed by a significant increase. In contrast to a slight transient increase in the glucose level induced by oxytocin, infusion of gastrin-17 caused a sustained period of hypoglycaemia. Thus, infusion of gastrin-17 and oxytocin, respectively, gave rise to different ratios between circulating concentrations of insulin and glucagon reflected in different effects on the glucose level. The gastrin-induced hypoglycaemia could reflect that gastrin, via a release of insulin, promotes storing of glucose, e.g. in connection with feeding. That infusion of oxytocin caused a parallel increase in insulin and glucagon levels together with a slight increase in the glucose level could imply that oxytocin favours mobilization of glucose, e.g. during lactation.

The levels of growth hormone, vasopressin, prolactin, calcitonin, gastrin, insulin, epinephrine, norepinephrine and dopamine were measured in six lactating women during breast feeding. Prolactin levels increased in response to suckling as expected. In addition, insulin levels rose two-fold. No consistent changes were observed in the levels of the other hormones. It is suggested that the suckling related insulin release is either secondary to a reflexly induced activation of the vagal nerves or to the increased circulating levels of prolactin. Furthermore, it is suggested that the insulin release in response to suckling participates in the stimulation of milk production.

Blood samples were collected in peripheral venous blood of seven lactating sows, when their piglets were suckling. In four of the experiments samples were also taken when the sows were fed a meal. Gastrin, insulin, somatostatin and VIP levels were measured by radioimmunoassay. Insulin levels increased by approximately 100% for about 10 min in response to suckling, in some experiments even before the suckling occurred, i.e. when the sows saw, heard and smelled their piglets. In four of the sows suckling caused a biphasic twofold increase in gastrin levels - one immediate peak which lasted for a few min and a second peak of longer duration (about 30-60 min), whereas gastrin levels remained unchanged in three animals. Somatostatin levels usually reflected gastrin levels in a reciprocal way. Thus, a biphasic decrease of somatostatin levels occurred in the high gastrin responders. In contrast, somatostatin levels increased in the experiments, in which gastrin levels did not change. Immediate and short-lasting (a few minutes long) increases of VIP levels were also induced by suckling. Large litters and long suckling periods appeared to be related to greater changes of the levels of all the peptides measured. Feeding influenced insulin, gastrin and somatostatin levels in the same way as did suckling from both a qualitative and a quantitative point of view. In contrast, VIP levels were not increased by feeding. The possible functional effects of the suckling-induced release of gastrointestinal hormones and possible mechanisms of their release are discussed.

The aim of the present study was to investigate whether plasma levels of gastrin, somatostatin, insulin, oxytocin, VIP and blood glucose levels vary during the menstrual cycle. Therefore, 19 healthy menstruating women (5 of whom were on low-dose oral contraceptives, o.c.) were blood sampled every second to third day during the menstrual cycle. Hormone levels were measured with radio-immunoassay. Gastrin, insulin, VIP and blood sugar levels remained unchanged during the menstrual cycle. Mean somatostatin levels were significantly lower in women receiving o.c. than in women without such medication (p less than 0.05). In women on o.c., somatostatin concentrations were also significantly lower during the menstrual week, than during the rest of the period (p less than 0.01), but in women without o.c., no such change occurred. Mean oxytocin levels were significantly higher in women on o.c. (p less than 0.001) and in these women, oxytocin levels recorded during the menstrual week were significantly lower than during the rest of the period (p less than 0.02). Systolic and diastolic blood pressure values were also significantly higher in women on o.c. (p less than 0.05 and p less than 0.01). In conclusion, these data show that basal plasma concentrations of gastrin, somatostatin, VIP, insulin and glucagon do not vary during the menstrual cycle. However, ingestion of low-dose oral contraceptives causes a significant decrease of somatostatin concentrations and a significant increase in oxytocin levels, suggesting that low doses of estrogens and/or gestagens may influence digestive and metabolic processes.

The postprandial secretion of insulin, gastrin and somatostatin was studied in 23 extremely obese subjects and nine normal-weight controls after a liquid test meal. Apart from a significantly higher insulin level in the obese group, no significant intergroup difference was found. The effect of weight loss on the same hormones was studied in 18 patients 6 months after gastric banding. The mean weight loss during this period was 33 +/- 2.1 (SEM) kg. There was significant decrease in postprandial insulin secretion after gastric banding, but neither gastrin nor somatostatin levels were altered.

Plasma levels of somatostatin like immunoreactivity (SLI), below referred to as somatostatin levels, were measured in peripheral plasma of conscious dogs. Basal somatostatin levels averaged 49 +/- 10 pM. Somatostatin as well as gastrin and insulin plasma levels were measured before and after feeding with and without prior atropinization. During the first 10 min after feeding somatostatin levels fell from 49 +/- 10 to 23 +/- 9 pM, whereas gastrin and insulin levels rose from 9 +/- 2 and 140 +/- 14 pM to 48 +/- 11 and 370 +/- 91 pM respectively. Atropine 0.01 or 0.1 mg/kg did not inhibit these responses. After the initial decrease, somatostatin level rose again and peaked at around 60 min after feeding (110 +/- 24 pM). This secondary rise was completely abolished by atropine in both doses tried. Gastrin and insulin levels remained elevated throughout the experiments with and without atropine. It is suggested that gastrin release and HCl secretion are inhibited by a tonic outflow of gastric somatostatin during basal conditions. The process of feeding induces an atropine resistant, vagally mediated decrease in somatostatin release from the gastrointestinal tract and this decreased output of somatostatin facilitates initiation of meal-related endocrine and exocrine gastric secretions.

In the present study, a radioimmunoassay for oxytocin determinations is presented. In addition, we investigated whether the elevation of insulin, VIP and gastrin levels demonstrated to occur in response to suckling in lactating dogs may be induced by released oxytocin. Therefore, oxytocin was infused i.v. into conscious dogs in amounts calculated to give rise to plasma levels observed during physiological circumstances. Plasma levels of oxytocin, insulin, VIP (vasoactive intestinal polypeptide) and gastrin were measured by radioimmunoassay. When oxytocin was infused at a rate of 0.22 and 2.2 nmol kg-1 h-1, plasma oxytocin levels rose to 176 +/- 25 fmol ml-1 and to 1490 +/- 400 fmol ml-1, respectively, 10 min after the infusions were started. Plasma insulin levels rose in response to oxytocin administered at a rate of 0.22 and 2.2 nmol kg-1 h-1. A peak was recorded within 5 min of oxytocin infusion, that is, before maximal oxytocin levels were recorded, and basal levels were reached within about 20 min. The VIP levels rose slightly following infusion of oxytocin at 0.22 nmol kg-1 h-1, but a clear-cut response that lasted for 60 min was observed following infusion of oxytocin at the highest dose. In contrast, gastrin levels were not influenced by the oxytocin infusions. Suckling in dogs is followed by rapidly occurring short-lasting elevations of oxytocin levels in plasma which amount to 50-100 fmol ml-1. Since insulin and VIP were released by oxytocin when administered in amounts that give rise to plasma levels close to those levels, it is suggested that the secretion of insulin and VIP that occurs in response to suckling in lactating dogs may in part be caused by previously released oxytocin.(ABSTRACT TRUNCATED AT 250 WORDS)

Oxytocin is known to increase plasma levels of insulin, glucagon and glucose in dogs. Plasma levels of vasopressin rise during stressful conditions. Since vasopressin counteracts several oxytocin-induced effects, it was decided to study how vasopressin influences the oxytocin-induced elevation of plasma levels of insulin, glucagon and glucose. Therefore oxytocin at 0.11 (which gives rise to physiological plasma concentrations) was infused i.v. for 10 min into fasted, conscious dogs either alone or in combination with 0.033 or 0.17 nmol kg-1 h-1 of L-vasopressin. Accordingly, 1.1 nmol kg-1 h-1 of oxytocin was infused alone or in combination with 0.67 or 1.7 nmol kg-1 h-1 of L-vasopressin. Repeated blood samples were drawn during and after the infusions and insulin and glucagon levels were determined by radioimmunoassay. Plasma levels of insulin increased three- and six-fold in response to 0.11 and 1.1 nmol kg-1 h-1 of oxytocin, respectively, and the elevations were inhibited by L-vasopressin. Slight (1.5-fold) increases in plasma levels of glucagon were observed following 0.11 and 1.1 nmol kg-1 h-1 of oxytocin, although the effect was significant only after the latter dose. Concomitant infusion with L-vasopressin did not markedly influence the effect caused by oxytocin. Small, insignificant increases in blood glucose levels were induced by both doses of oxytocin. These effects were not affected by concomitant infusions of L-vasopressin. The insulin levels rose before glucose levels suggesting that oxytocin stimulates the release of insulin without a previous rise in glucose levels. In conclusion, it has been shown that vasopressin, in amounts which give rise to physiological plasma concentrations, inhibits oxytocin-induced effects on insulin levels, and that oxytocin stimulates the release of insulin via a mechanism which is independent of elevations in blood glucose levels.

The relation between the basal and stimulated gastric acid secretion, plasma gastrin, and the gastric microflora was examined in 45 patients with rheumatoid arthritis. Sixteen patients (36%) had basal achlorhydria, and of these, 10 (22%) had achlorhydria or hypochlorhydria after stimulation with pentagastrin. The peak acid output and acidity showed inverse correlation with the disease duration but were not associated with age or with the degree of physical disability. Hypergastrinaemia was found in nine patients (20%), of whom 6 (13%) had significant titres of parietal cell antibody. The acidity of the peak acid output showed negative correlation with plasma gastrin. It was confirmed that the gastric secretory state is a determinant of plasma gastrin levels and in addition influences the growth of micro-organisms in the gastric lumen. The type of microflora in the non-acid stomach was similar to that found in the saliva. A subgroup of eight females was identified who showed low gastric acid secretion rates, positive bacterial cultures, and atlantoaxial subluxation. Gastrin- and insulin-like immunoreactivities were found in joint fluid. The concentrations reflected their plasma levels, suggesting that the peptides are not released at the inflammatory site, but rather that they reach synovial fluid from circulating blood. [ABSTRACT FROM PUBLISHER]