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Biomedical subjects

I Lundquist

Publications and source records attributed to I Lundquist.

At least 127 records · Page 7Linked to original sources
PubMed1981

Single injection of terbutaline in term labor: placental transfer and effects on maternal and fetal carbohydrate metabolism.

Maternal and fetal blood glucose and insulin levels were studied in 10 women in the second stage of labor after administration of terbutaline, 250 micrograms intravenously. The transport of the drug across the placenta was also studied. Saline solution was administered to four other women who served as controls. A rise in maternal plasma insulin levels occurred in all patients but was more pronounced in patients treated with terbutaline less than 25 minutes before delivery than in those treated more than 45 minutes prior to delivery. No difference was found in maternal blood glucose levels between terbutaline-treated patients and controls. Blood glucose increased in the fetuses during the second stage of labor and paralleled that of the mothers, but on a lower level. None of the newborn infants demonstrated hypoglycemia during the first 90 minutes after birth. Terbutaline crossed the placenta rapidly, and fetal plasma levels up to 55% of the maternal plasma levels were found. The conclusion is that this form of administration of terbutaline does not seem to have any negative short-term influences on the fetal carbohydrate metabolism.

Blood Glucose↗
PubMed1981

Adrenergic innervation of pancreatic islets and modulation of insulin secretion by the sympatho-adrenal system.

Morphological changes in the adrenergic innervation of pancreatic islets after chemical sympathectomy by use of 6-hydroxydopamine and the influence of the sympatho-adrenal system on insulin secretion were investigated in the mouse and rat. Fluorescence histochemistry revealed a clear-cut reduction in the number of adrenergic nerve fibres in the pancreatic islets 2 days after administration of 6-hydroxydopamine; the reduction was more pronounced in the rat than in the mouse. In the rat, a partial regeneration was seen after 6 weeks. In the pancreas of the mouse, after administration of 6-hydroxydopamine, a severe damage of unmyelinated nerve fibres was revealed electron microscopically. However, no ultrastructural or immunohistochemical alterations could be demonstrated in the endocrine cells of the islets. 6-Hydroxydopamine induced a depression of basal plasma insulin concentrations in mice and an elevation in rats. Adrenalectomy depressed basal plasma insulin levels in mice. The alpha-adrenoceptor antagonist phentolamine enhanced insulin secretion in normal mice. The secretory response of insulin to phentolamine was diminished by chemical sympathectomy and almost abolished by adrenalectomy or the combination of chemical sympathectomy and adrenalectomy. Thus, the effect of phentolamine is probably mediated by liberated catecholamines. It is concluded that basal insulin secretion is partially regulated by the sympatho-adrenal system and that species differences exist in this respect. In addition, the results suggest that endogenous catecholamines have the ability to promote insulin secretion.

Adrenal Cortex↗
PubMed1981

Effects of vasoactive intestinal polypeptide (VIP), secretin and gastrin on insulin secretion in the mouse.

The in vivo effects of vasoactive intestinal polypeptide (VIP), secretin and two different molecular forms of gastrin, gastrin 17 and pentagastrin, on basal and stimulated insulin secretion have been investigated in the mouse. All these peptides induced a moderate dose-dependent increase in basal insulin secretion. The different polypeptides showed complex effects on insulin release stimulated by glucose, the cholinergic agonist carbachol or the beta-adrenergic agonist L-isopropylnoradrenaline (L-IPNA), these effects being dependent on the nature of the secretagogue. VIP and secretin both potentiated glucose-induced insulin release. Secretin inhibited insulin secretion induced by carbachol and L-IPNA, whereas VIP potentiated L-IPNA-induced insulin secretion and had no influence on the effect of carbachol. Gastrin 17 and pentagastrin did not affect glucose- or carbachol-induced insulin release, whereas they inhibited L-IPNA-induced insulin secretion. The results suggest that VIP, secretin and gastrin display their effects on insulin secretion through different mechanisms. The results indirectly suggest the existence of separate insulin secretory pathways which operate differently, or at least partly differently, after glucose stimulation, cholinergic stimulation, and beta-adrenergic stimulation.

Animals↗
PubMed1981

Adrenalectomy and chemical sympathectomy by 6-hydroxydopamine. Effects on basal and stimulated insulin secretion.

Influences of the sympatho-adrenal system on basal and stimulated insulin secretion were studied in vivo in the conscious mouse and rat. In the mouse, adrenalectomy or chemical sympathectomy, induced by 6-hydroxydopamine, lowered basal insulin concentrations moderately. A marked depression of basal insulin concentration (about 50%) was seen after the combined treatment of chemical sympathectomy and adrenalectomy. In short-term experiments in mice, insulin secretion stimulated by glucose or the cholinergic agonist carbachol was enhanced after chemical sympathectomy and/or adrenalectomy, whereas insulin release induced by the synthetic octapeptide of cholecystokinin (CCK-8) was inhibited. The promoting influences on the insulin secretory response to carbachol displayed a rapid development whereas those to glucose developed more slowly. In contrast, the inhibiting effect on CCK-8 stimulated insulin release vanished with time. The insulin secretory response to the beta 2-adrenoceptor stimulator, terbutaline, was increased after chemical sympathectomy, unaffected by adrenalectomy, and decreased after chemical sympathectomy plus adrenalectomy. The glucose elimination rate after 6 weeks of chemical sympathectomy was increased in mice and decreased in rats. The insulin secretory response to glucose was enhanced in mice, whereas it tended to diminish in rats after long-term sympathectomy. In conclusion, the sympatho-adrenal system is involved in regulation of basal insulin concentrations in the mouse, and apparently is of great importance for stimulated insulin secretion; the influence being dependent on the nature of the secretagogue.

Adrenalectomy↗
PubMed1981

Dietary fibre in type II diabetes.

Recent studies have indicated that diets rich in digestible carbohydrates and dietary fibre might be beneficial in the regulation of type II non insulin dependent diabetes (NIDD). Addition of the gel forming type of dietary fibre such as pectin and guar gum to meals or glucose solutions reduces post-prandial glucose and insulin response. Addition of cereal fibres in the form of bran seems to have long term beneficial effect improving glucose tolerance. Little is known, however, concerning effects of dietary fibre naturally occurring in food on postprandial glucose and hormone response. In the present study we prepared two breakfast meals which were similar regarding digestible carbohydrates but differed in their dietary fibre content. One of the meals, including whole grain bread and whole apples, contained 8.4 g of dietary fibre, and the other one, containing white bread and apple juice, 3.1 g. When given to eight NIDD, the fibre rich breakfast gave significantly lower blood glucose increment during the three hours following ingestion. The results indicate that foods rich in dietary fibre might be useful in the regulation of type II diabetes.

Blood Glucose↗
PubMed1981

Effects of autonomic blockade by methylatropine and optical isomers and propranolol on plasma insulin levels in the basal state and after stimulation.

The effects of autonomic blockade on plasma concentrations of immunoreactive insulin in the basal state and after stimulation with 4 different secretagogues were investigated in vivo in conscious mice. The muscarinic blocker methylatropine slightly depressed basal insulin, and almost totally abolished the insulin response to the cholinergic agonist carbachol, whereas the insulin response to glucose and glucagon was unaffected. Contrary to these findings, the insulin response to the beta 2-adrenoceptor agonist terbutaline was potentiated, by about 75%. The beta-adrenoceptor blocker L-propranolol depressed basal insulin by about 60%, and totally abolished the insulin responses to glucagon and terbutaline. The insulin response to glucose was slightly reduced and that to carbachol was unaffected by L-propranolol. The stereoisomer D-propranolol which is devoid of beta-adrenoceptor blocking activity but exerts local anaesthetic effect of the same potency as the Lpisomer, was without effect on basal insulin levels and the insulin responses to the different secretagogues. It is concluded that basal concentrations of immunoreactive insulin is substantially dependent on intact beta-adrenoceptors and more moderately dependent on intact muscarinic receptors. The insulin responses to terbutaline and glucagon are closely connected to beta-adrenoceptors, and the response to carbachol to the muscarinic receptors. Glucose-induced insulin response seems largely unaffected by autonomic receptor blockade although a slight reduction after beta-adrenoceptor blockade is demonstrable.

Animals↗
PubMed1981

GIP-like immunoreactivity in glucagon cells. Interactions between GIP and glucagon on insulin release.

In the present study the cellular and subcellular distribution of immunoreactive glucagon and GIP (gastric inhibitory polypeptide) were studied in the mouse. Furthermore, the effects of pure GIP and glucagon on basal and stimulated insulin secretion were investigated. Immunohistochemistry revealed that immunoreactive GIP occurred in the pancreatic glucagon cells and in endocrine cells, also displaying glucagon immunoreactivity, scattered along the small and large intestines. Electron immunocytochemistry revealed that the GIP-like material and glucagon coexisted in the secretory granules of the pancreatic glucagon cells. Pure porcine GIP and glucagon both stimulated basal insulin release. When equipotent doses of the peptides were given together, the two peptides antagonized each other's effect. Both peptides potentiated glucose- and carbachol-induced insulin release. When equipotent doses of the two peptides were given together prior to the administration of each of these secretagogues their effects on insulin release were additive.

Animals↗
PubMed1981

Insulin secretion induced by glucose and by stimulation of beta 2 -adrenoceptors in the rat. Different sensitivity to somatostatin.

The effects of somatostatin on insulin secretion stimulated by glucose or by the selective beta 2-adrenoceptor agonist terbutaline were studied in vivo in the anaesthetized rat. Infusion of low doses of glucose (5 mg/min) or terbutaline (2 microgram/min) caused slight stimulation of insulin secretion, whereas infusion of higher doses of glucose (12.5 mg/min) or terbutaline (200 microgram/min) yielded higher rates of insulin release. In both instances plasma insulin concentrations were of comparable magnitudes immediately prior to somatostatin infusion. Somatostatin (0.1 microgram/min) inhibited the insulin response to glucose and terbutaline, both at the low and high secretory rates. However, the inhibitory effect of somatostatin was much more pronounced on insulin release during glucose infusion than during infusion of terbutaline. Thus, at the high rate of insulin secretion somatostatin depressed plasma insulin by 46% during glucose and by 22% during terbutaline infusion. The results at the low rate insulin secretion were 66% and 48%, respectively. Both at high and low secretory rates somatostatin depressed plasma insulin levels more potently during glucose infusion than during terbutaline infusion (p less than 0.01 and P less than 0.05, respectively). Furthermore, the plasma insulin levels during inhibition by somatostatin following terbutaline stimulation stabilized after approximately 10 min of somatostatin infusion, whereas following glucose stimulation the insulin levels continued to decline. The results suggest that somatostatin inhibits insulin secretion via mechanisms that are more closely related to the insulin secretory pathway induced by glucose than to that induced by beta-adrenoceptor agonists.

Adrenergic beta-Agonists↗
PubMed1981

Influence of the sympatho-adrenal system and somatostatin on the secretion of insulin in the rat.

1. The effects of somatostatin on insulin secretion in anaesthetized rats subjected to different manipulations of the sympatho-adrenal system have been investigated.2. Somatostatin (0.1 mug/min) inhibited the secretion of insulin in intact rats both in the basal state and after inducing an enhanced insulin release by infusion of the alpha-adrenoceptor-blocker phentolamine.3. Combined surgical splanchnicotomy and adrenalectomy caused an increase in the basal plasma insulin concentration. Somatostatin (0.1 mug/min) inhibited basal insulin release also in these rats. After infusion of phentolamine, however, the dose of somatostatin had to be raised five fold (0.5 mug/min) to achieve a comparable inhibition of insulin release. On the other hand, a similar rate of insulin secretion induced by glucose in intact rats could be inhibited by the lower dose of somatostatin.4. Administration of the beta-adrenoceptor-blocking agent propranolol to splanchnicotomized-adrenalectomized rats lowered basal insulin secretion to the same level as seen in intact rats. In these beta-adrenoceptor-blocked rats somatostatin (0.1 mug/min) inhibited insulin release both in the presence and absence of alpha-adrenoceptor blockade.5. Rats subjected to chemical sympathectomy through pre-treatment with 6-hydroxydopamine together with adrenalectomy displayed plasma insulin concentrations slightly above the normal range, but the values were much lower than in splanchnicotomized-adrenalectomized rats. Infusion of phentolamine to the chemically sympathectomized rats did not further increase insulin secretion, and somatostatin (0.1 mug/min) depressed insulin release both in the absence and presence of alpha-adrenoceptor blockade.6. It is suggested that an inhibitory tone exerted by the splanchnic nerves modulates the basal insulin secretion in the rat. Somatostatin and the sympathoadrenal system show a complex interaction on the insulin cells in that the sensitivity to somatostatin in splanchnicotomized-adrenalectomized rats with intact beta-adrenoceptors is decreased in the presence of the alpha-adrenoceptor-blocker phentolamine. The exact mechanism behind this decreased sensitivity remains unclear.

Adrenal Glands↗
PubMed1981

Influence of hormonal stimulation by caerulein on acute experimental pancreatitis in the rat.

The influence of hormonal stimulation by caerulein administration on acute experimental pancreatitis was investigated in the rat. An experimental model of moderate acute pancreatitis was selected after injecting buffer solution containing sodium taurodeoxycholate and various concentrations of trypsin into the bile-pancreatic duct. During acute experimental pancreatitis caerulein administration increased the mortality rate, the incidence of ascites and the activity of amylase in ascites. Caerulein rendered the pancreatitis more severe also as judged from blind macroscopic evaluation. Amylase and insulin levels in serum and plasma were elevated 6 and 25 h after induction of pancreatitis irrespective of caerulein administration. In pancreatitic rats caerulein decreased the activities of digestive enzymes in pancreatic tissue. The results show that hormonal stimulation by the cholecystokinin-pancreozymin analogue caerulein during acute experimental pancreatitis is harmful.

Acute Disease↗
PubMed1981

Insulin secretory response to different secretagogues in hyper- and hypothyroid mice.

The influence of long-term changes in thyroid state on insulin secretion was investigated in vivo in mice. Hyperthyroidism was induced by daily injections of L-triiodothyronine and hypothyroidism by a single injection of 131I. Four different insulin secretagogues were used to characterize the insulin secretory response, i.e. glucose, the beta 2-adrenoceptor agonist terbutaline, the cholinergic agonist carbachol and the synthetic C-terminal octapeptide of cholecystokinin, CCK-8. In the hyperthyroid mice the plasma glucose level was moderately decreased. Despite this lower glucose level the insulin response to terbutaline and glucose were potentiated by about 200%. Insulin response to CCK-8 and carbachol was less enhanced, by about 100 and 50%, respectively. Liver and muscle glycogen levels were markedly reduced. The hypothyroid animals showed reduced insulin responses to all secretagogues; after terbutaline by 100%, after carbachol by 70%, after glucose and CCK-8 by 50%. Plasma glucose and muscle glycogen levels were normal, whereas liver glycogen levels were moderately enchanced. Insulin release induced by beta-adrenoceptor stimulation was most markedly affected by the thyroid state, which thus may be of importance for the balance between the beta- and alpha-adrenoceptors of the insulin cell. Since thyroid activity influenced the insulin response to all secretagogues it cannot be excluded that the thyroid state also exerts effects not related to the adrenoceptors.

Adrenergic beta-Agonists↗
PubMed1980

Quinacrine accumulates in certain peptide hormone-producing cells.

Quinacrine is a fluorescent anti-malarial acridine derivative which binds selectively to a population of nerves, presumably peptidergic, and to certain peptide hormone-producing cells. Among these cells are glycopeptide hormone-producing cells in the adenohypophysis, the calcitonin cells in the thyroid, the insulin, glucagon and PP cells in the pancreatic islets, and the gastrin cells in the pyloric antrum. Available evidence suggests that the fluorophore accumulates in the secretory granules. The half-life of the fluorescence varies from one cell type to another, from 6 h in the gastrin cells to 40 h in the insulin cells. It cannot be excluded that the half-life of the fluorescence reflects the turn-over rate of the secretory granules and that the disappearance rate of the fluorescence is dependent upon the secretory activity of the cell.

Adrenal Medulla↗
PubMed1980

Effects of glicentine on insulin secretion.

The glucagon-like immunoreactivity of the gastrointestinal tract is heterogeneous, probably including several different peptides. One of these peptides, glicentine, has recently been extracted and highly purified. Furthermore, by immunocytochemistry a glicentine-like peptide has been reported to occur in the glucagon cell of the pancreatic islets. In the present study we investigated the effects of pure glicentine on insulin release in vivo in mice. The effects were compared with effects of two other peptides, glucagon and GIP. It was found that glicentine had no influence on basal insulin secretion. This was in contrast to equimolar doses of glucagon and GIP, which both stimulated the secretion of insulin. Glucose-induced insulin release was partially inhibited by glicentine. D-glucose, in a dose selected to give a response of 25% of its maximal, raised the plasma insulin concentrations by 44.0 +/- 5.9 microU/ml. The corresponding rise for glicentine plus D-glucose was 22.3 +/- 3.7 microU/ml, i.e. glicentine inhibited glucose-induced insulin released by about 50% (p < 0.01). GIP, on the other hand, enhanced glucose-induced insulin release. This enhancement was diminished by glicentine, a reflection of the inhibition by glicentine of the glucose-induced insulin release. Neither glicentine nor GIP in the doses tested had any effect on insulin secretion induced by cholinergic stimulation. In conclusion, glicentine seems to have no effect on basal insulin release in the mouse, but it partially inhibits glucose-induced insulin secretion. Thus, if the recently demonstrated glicentine-like peptide in the glucagon cell is authentic glicentine, the glucagon cell of the pancreatic islets may contain peptides with stimulatory (glucagon) as well as inhibitory (glicentine) effects on insulin secretion induced by glucose.

Animals↗
PubMed1980

Effects of glucagon and pentagastrin on glibenclamide-induced insulin release.

It was recently reported that administration of sulphonylureas may lead to a stimulation of the release of glucagon and a gastrin-like peptide. These peptides may then eventually influence the insulin releasing action of the sulphonylureas. Therefore, the effects of glucagon and pentagastrin on basal and glibenclamide-induced insulin secretion were studied. It was found that at a dose of 4.25 nmol/kg the two peptides induced a significant stimulation of basal insulin secretion. However, pentagastrin at the dose of 4.25 nmol/kg did not influence the insulin release induced by glibenclamide, whereas an equimolar dose of glucagon potentiated the insulin secretory response to this sulphonylurea drug by about 40%. Glucagon in contrast to pentagastrin thus positively modulates the insulin secretory pathway stimulated by the sulphonylurea drug glibenclamide.

Animals↗
PubMed1980

Membrane and biochemical alterations after denervation and during reinnervation of mouse skeletal muscle.

Denervation of the extensor digitorum longus (EDL) muscle of the mouse by either nerve crush or nerve section produced: a reduction of the resting membrane potential (Em), alterations in the properties of muscle fibre action potentials and the development of tetrodotoxin (TTX)-resistant action potentials. These changes in membrane electrical properties were accompanied by an increase in the endocytic activity of the muscle and an increase in the activities of the lysosomal enzymes cathepsin D and N-acetylglucosaminidase (NAGA). Reinnervation of muscle was indicated at 9 days after nerve crush by the presence of miniature end-plate potentials. The recovery of membrane electrical properties, beginning with the onset of reinnervation, were not temporally related. The Em increased in two stages: an early rapid repolarization and a later slower repolarization. The muscle fibers were sensitive to the blocking action of TTX by 12 days after nerve crush, whereas the rate of rise (dV/dt) of the action potential did not approach values of innervated muscles until 21 days. Reinnervation resulted in a decrease in endocytosis and a decrease in the activities of cathepsin D and NAGA toward innervated values by 21 days after nerve crush. The results suggest that membrane alterations after denervation and during reinnervation may occur by endo- and exocytosis of membrane constituents and that the lysosomal system may play a role in the breakdown and/or recycling of these structures.

Acetylglucosaminidase↗