PubMed Health⌕ Search

Biomedical subjects

A Inui

Publications and source records attributed to A Inui.

At least 163 records · Page 9Linked to original sources
PubMed1985

[Inhibition of insulin secretion by intracerebroventricular infusion of pancreatic polypeptide in conscious dogs].

Previously, we demonstrated that peripheral infusion of pancreatic polypeptide (PP) inhibits insulin response to several stimuli through vagal innervation. Since PP is found not only in pancreas but also in brain or cerebrospinal fluid, we studied the effect of intracerebroventricular infusion of PP on insulin secretion before and after vagotomy in dogs. Mongrel dogs were settled with a chronic cannula allowing intraventricular infusions into the third (n = 4) or lateral (n = 4) cerebral ventricle. All the experiments were performed one week after the operation in a fully conscious, relaxed state. Porcine PP (pPP, 50 ng or 5 micrograms/dog in 100 microliter saline), which has the same primary structure with that of canine PP, or saline alone was infused into the cerebral ventricles for 5 minutes at the rate of 20 microliter/minutes. As stimuli of insulin secretion, modified sham feeding (MSF; sight and smell of food for 5 minutes), glucose injection (IV-Glucose; 0.5 g/kg/30 seconds, intravenously) and CCK-octapeptide infusion (IV-CCK-8; 0.07 micrograms/kg/5 minutes, intravenously) were applied immediately after (and in some experiments various intervals after) the end of pPP or saline infusion into the ventricles. Immunoreactive PP or insulin was measured by a specific radioimmunoassay. Administration of PP caused significant inhibition of insulin secretion by MSF, IV-Glucose and IV-CCK-8 without affecting basal insulin secretion. The observed effect of the peptide was most potent when infused into the third cerebral ventricle at a dose of 50 ng/dog and not in a dose-related fashion. The integrated insulin responses to MSF, IV-Glucose and IV-CCK-8 were 28, 58 and 30%, respectively, as those of controls. This effect was likely to be of central origin because an overflow of PP to the periphery could not be observed by PP radioimmunoassay. Prior transthoracic bilateral truncal vagotomy abolished the suppressive effect of PP on glucose- and CCK-8-induced insulin secretion. Furthermore, the time course study of CCK-8 suggested that PP could interact with the regions surrounding the third cerebral ventricle. These results suggest that PP affects the central nervous system to control pancreatic insulin secretion via the vagus nerve like other peptides/neuroregulators which modify physiological processes (e.g. insulin release, acid secretion, motility).

Animals↗
PubMed1985

Cross-reactivities of neuropeptide Y and peptide YY with pancreatic polypeptide antisera: evidence for the existence of pancreatic polypeptide in the brain.

Highly purified neuropeptide Y (NPY) and peptide YY (PYY) did not cross-react in our human pancreatic polypeptide (hPP) radioimmunoassay, nor did 125I-labelled NPY and PYY, even with anti-hPP serum at low dilution (1:1000). However, both [125I]NPY and [125I]PYY significantly cross-reacted with anti-bovine PP (bPP) serum at low dilution (1:1000, similar to that used in immunohistochemistry). These results suggest that radioassayable hPP-like peptide in the porcine or canine brain is probably pancreatic polypeptide itself, otherwise immunohistochemically detected bPP-like peptide may represent both NPY and PP.

Amino Acid Sequence↗
PubMed1983

[Regional distribution of pancreatic polypeptide-like immunoreactivity in the canine brain].

Recently many gut hormones have been found in the brain, and there is some evidence to suggest that pancreatic polypeptide-like immunoreactivity (PP-LI) is also present in the brain. Although in mammals, confirmative evidence is not yet shown. In the present paper we report the distribution and tissue localization of PP-LI in the canine brain by radio-immunoassay (RIA) and immunohistochemistry. Normal, fasted mongrel dogs were used. Brain tissue was extracted by boiling water. High concentrations of PP-LI were found in the pituitary gland (3.67 +/- 1.10 ng/g wet wt), substantia nigra (1.58 +/- 0.36 ng/g wet wt), hypothalamus (0.74 +/- 0.28 ng/g wet wt) and olfactory lobe (0.58 +/- 0.21 ng/g wet wt). PP-LI was not detectable in the frontal lobe, parietal lobe, striatum, thalamus, hippocampus, pons, cerebellum and medulla oblongata. The amounts of PP-LI in the brain were more less than the amounts of PP present in the pancreas (duodenal lobe, 29.3 +/- 1.1 microgram/g wet wt). The dilution curve of the brain tissue extracts showed parallelism with the standard curve of human and porcine PP on the RIA system. On Bio-Gel P-30 column chromatography, PP-LI from the pituitary gland and olfactory lobe eluted as a single peak coincided with highly purified bovine PP. In immunohistochemical study, PP-LI was found in the intermediate lobe and the stalk of the pituitary gland by means of anti-bovine PP antiserum. These findings of the specific regional localization suggest that PP or PP-LI may have a physiological role in the central nervous system.

Animals↗
PubMed1976

Acetylcholine synthesis in sympathetic human neuroblastoma.

The synthesis of acetylcholine, as well as catecholamines, was studied by assaying the activities of choline acetyltransferase (ChA) and tyrosine hydroxylase (TH) in the tumor tissues and the culture cells of human neuroblastoma. In the majority of 20 neuroblastomas of sympathetic origin, both ChA and TH activities were detected at a significantly high level. In the culture cells of five cell lines of human neuroblastoma, ChA activity was high, but TH was negative in four of the lines. However, it was observed that these enzyme activities changed significantly while in the long-term culture. ChA assay is a useful diagnostic test for neuroblastomas that synthesize acetylcholine. Future studies of neuroblastoma should consider cholinergic activity.

Acetylcholine↗
PubMedDate not supplied

The role of cholecystokinin octapeptide in the central control of food intake in the dog.

Cholecystokinin octapeptide (CCK-8, 1, 190 pmol/5 min) decreased food intake and water consumption in two models of ingestive behavior, i.e., food deprivation-induced feeding and insulin-induced feeding, when administered into the third (3V) and lateral (LV) cerebral ventricles. In fasted dogs, the suppression of food intake was more prominent after 3V CCK-8, whereas intravenously administered CCK-8 was without effect. Neuropeptide Y (NPY, 1, 190 pmol) had no significant stimulatory effect on food intake and water consumption in fasted as well as satiated dogs, and actually reduced both food and water intake in insulin-treated dogs. There was a slight but significant decrease in food and water intake after 275 nmol naloxone administration in both feeding models, and some of the dogs vomited. In insulin-treated animals, CCK-8 reversed, but NPY potentiated the hypothermic phase of temperature response observed after saline administration, whereas naloxone failed to alter rectal temperature. These results suggest that the effect of CCK-8 on feeding seems to involve central mechanisms in the dog, and that the mechanisms by which CCK-8, NPY and naloxone affect feeding behavior are different.

Animals↗
PubMedDate not supplied

Mechanism of actions of cholecystokinin octapeptide on food intake and insulin and pancreatic polypeptide release in the dog.

We investigated the mechanism by which CCK-8 injected into the third cerebral ventricle (ITV administration) inhibits food intake and stimulates insulin and pancreatic polypeptide (PP) secretion in the dog. ITV administration of CCK-8 (4.08 micrograms/5 min) resulted in a significant elevation of plasma insulin and PP concentrations. This effect was abolished by truncal vagotomy and promptly inhibited by ITV administration of atropine (20 micrograms) and proglumide (10 mg). CCK-8 was less effective in increasing insulin and PP concentrations than in reducing feeding. Thus, 1.36 micrograms of ITV CCK-8 markedly reduced food intake to 14, 15, 29 and 31% of control values at 10, 30, 60 and 120 min, respectively. Atropine and naloxone (50 micrograms) had no blocking effect on CCK-8-induced satiety, whereas proglumide antagonized it. These results indicate that ITV CCK-8 effects the endocrine pancreas and food intake through atropine-sensitive and atropine-insensitive mechanisms, respectively, both of which are likely to be mediated by CNS CCK receptors. Intravenous CCK-8 also stimulated PP and insulin release, through mechanisms that were atropine-sensitive and atropine-insensitive, respectively. However, its mode of action, especially on insulin secretion, was quite different from that of ITV CCK-8. Therefore, exogenous CCK appears to act in the brain and the periphery in concert with and independently from cholinergic systems.

Animals↗