Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Chromogranins A and B and secretogranin II have been localized in a wide spectrum of gastroenteropancreatic endocrine/paracrine cells. Chromogranin A immunoreactivity showed the widest distribution and was displayed by glucagon-, PP-, gastrin-, gastrin-CCK-, secretin-immunoreactive cells, the most intense stainings being peculiar of enterochromaffin cells. Chromogranin B immunoreactivity was detected in gastrin- and glucagon cells and in some enterochromaffin cells containing also chromogranin A. Secretogranin II was paired to chromogranin A in glucagon cells of pancreatic islets or occurred alone in glycentin/PP cells of colonic mucosa. Neither of the chromogranins nor secretogranin II have been so far detected in somatostatin-, GIP-, or motilin-immunoreactive cells. Chromogranin A but not chromogranin B or secretogranin II has been detected in the gastric argyrophilic ECL cells.
 ...
PMID:Chromogranins A and B and secretogranin II in hormonally identified endocrine cells of the gut and the pancreas. 322 65

Recent data on the immunolocalization of regulatory peptides and related propeptide sequences in endocrine cells and tumors of the gastrointestinal tract, pancreas, lung, thyroid, pituitary (ACTH and opioids), adrenals and paraganglia have been revised and discussed. Gastrin, xenopsin, cholecystokinin (CCK), somatostatin, motilin, secretin, GIP (gastric inhibitory polypeptide), neurotensin, glicentin/glucagon-37 and PYY (peptide tyrosine tyrosine) are the main products of gastrointestinal endocrine cells; glucagon, CRF (corticotropin releasing factor), somatostatin, PP (pancreatic polypeptide) and GRF (growth hormone releasing factor), in addition to insulin, are produced in pancreatic islet cells; bombesin-related peptides are the main markers of pulmonary endocrine cells; calcitonin and CGRP (calcitonin gene-related peptide) occur in thyroid and extrathyroid C cells; ACTH and endorphins in anterior and intermediate lobe pituitary cells, alpha-MSH and CLIP (corticotropin-like intermediate lobe peptide) in intermediate lobe cells; met- and leu-enkephalins and related peptides in adrenal medullary and paraganglionic cells as well as in some gut (enterochromaffin) cells; NPY (neuropeptide Y) in adrenaline-type adrenal medullary cells, etc.. Both tissue-appropriate and tissue-inappropriate regulatory peptides are produced by endocrine tumours, with inappropriate peptides mostly produced by malignant tumours.
 ...
PMID:Endocrine cells producing regulatory peptides. 329 70

The injection of trimebutine induces in the dog an increase of plasma motilin during the fasting period as well as after a meal. We studied the effect of trimebutine on several gastrointestinal hormones released into the circulation by the ingestion of a meal. The intravenous administration of trimebutine (10 mg/kg/h) in 4 dogs abolished the postprandial increase in plasma gastrin, pancreatic polypeptide, insulin, glucagon and GIP. Trimebutine could therefore, by its effects on various regulatory peptides, influence several digestive functions. Its mode of action could probably involves complex mechanisms, including paradoxical effects. The possibility that motilin is a mediator of the trimebutine effect on small bowel smooth muscle is discussed.
 ...
PMID:[Effect of trimebutine on the plasma postprandial release of gastrointestinal hormones in the dog]. 330 10

In order to examine whether hyperinsulinaemia induced glucocorticoid therapy involves alterations of the enteroinsular axis glucose, insulin, C-peptide, glucagon and GIP responses to a test meal with and without prior intake of dexamethasone (2 + 2 mg) in 13 healthy subjects were measured. Dexamethasone caused impaired glucose tolerance, which was associated with an exaggerated insulin (0.61 +/- 0.05 vs. 0.38 +/- 0.05 nmol/l; p less than 0.001). C-peptide (0.97 +/- 0.08 vs. 0.71 +/- 0.06 nmol/l; p less than 0.001) and glucagon response to a test meal. In contrast, the GIP response to the test meal was blunted after dexamethasone (126 +/- 17 vs. 177 +/- 23 pmol/l; p less than 0.001). It therefore follows that alterations in the enteroinsular axis, that is, GIP secretion, cannot be responsible for the enhancement of insulin secretion observed after dexamethasone. The mechanism(s) for the decreased GIP response after dexamethasone could involve (1) a direct inhibitory effect on GIP secretion by dexamethasone, and/or (2) a negative feedback of elevated glucose and insulin levels on GIP secretion.
 ...
PMID:The effect of dexamethasone on the enteroinsular axis. 331 Jan 95

Effects of microinjection of glucagon or GIP into the medial preoptic area on luteinizing hormone (LH) and prolactin (PRL) release were examined in unanesthetized ovariectomized rats with or without estrogen priming. Microinjection of glucagon (1.0 microgram) into the medial preoptic area of ovariectomized estrogen-primed rats significantly facilitated the circadian afternoon rise in LH secretion as compared to the hormone values in control animals microinjected with physiological saline. The timing of the afternoon LH rise was not altered by glucagon and the circadian rise of PRL secretion was not altered by glucagon injected in the preoptic area. The injection of GIP did not have any significant effect on either LH or PRL secretion. In ovariectomized estrogen-unprimed rats, on the other hand, glucagon did not affect the pulsatile LH secretion, but it inhibited PRL secretion. GIP did not affect any hormone secretion. The results show that (1) glucagon, as other secretion family peptides such as secretion and PHI, can stimulate the preoptic LH secretory mechanism that undergoes the circadian clock mechanism under the influence of estrogen, and (2) without estrogen priming, glucagon in the preoptic area inhibits PRL secretion.
 ...
PMID:Effects of preoptic injection of glucagon on luteinizing hormone secretion in ovariectomized rats with or without estrogen priming. 340 67

To determine whether the autonomic nervous system has a direct effect on GIP secretion, six normal subjects received a 4-hr intraduodenal perfusion of glucose (225 mg/min) and polyethylene glycol on four successive days. During the latter 2 hr, either normal saline, propranolol, phentolamine, or atropine were infused intravenously. Glucose absorption was calculated by measuring glucose and polyethylene glycol following luminal aspiration distal to the perfusion site. Basal and peak or nadir values in the saline study of plasma glucose, insulin, glucagon, and GIP were similar to the other three studies prior to autonomic blockade. During the latter 2 hr of the glucose perfusion, the plasma glucose and glucagon responses to saline did not differ from responses to the three blocking agents. Phentolamine but not atropine or propranolol resulted in a greater insulin response compared to saline (3247 +/- 762 vs 1348 +/- 388 microU/ml/120 min, P less than 0.01). GIP was not significantly affected by phentolamine (18,146 +/- 4574), propranolol (7585 +/- 5854), or atropine (15,797 +/- 6297) compared to saline (11,717 +/- 5204 pg/ml/120 min). Glucose absorption was unaffected by infusions of saline, phentolamine, and propranolol, but was increased following atropine infusion (5841 +/- 1120 vs 1044 +/- 808 mg/120 min, P less than 0.02). There appears to be no direct effect of the autonomic nervous system on glucose-induced secretion of GIP.
 ...
PMID:Lack of a direct effect of the autonomic nervous system on glucose-stimulated gastric inhibitory polypeptide (GIP) secretion in man. 352 48

Glucagon secretion is stimulated by cholinergic activation, and it is known that the polypeptides VIP (vasoactive intestinal polypeptide) and GIP (gastric inhibitory polypeptide) both potentiate this cholinergically induced glucagon secretion. In this study, we investigated whether secretin, which shows structural similarities to both VIP and GIP, affects basal and cholinergically induced glucagon secretion in the mouse. Secretin was injected i.v. to mice at dose levels varying from 0.53 to 17 nmol kg-1, and plasma samples were taken at 2, 6 and 10 min following injection. It was found that secretin in this wide dose range did not affect basal glucagon concentrations. When the cholinergic agonist carbachol was injected i.v. at 0.16 mumol kg-1, plasma glucagon levels were elevated; at 2 min at 0.84 +/- 0.04 ng ml-1 compared to 0.31 +/- 0.02 ng ml-1 in controls (P less than 0.001). A combination of carbachol and secretin (4.25 nmol kg-1) enhanced plasma glucagon levels to 1.22 +/- 0.07 ng ml-1. Thus, secretin potentiated carbachol-induced glucagon secretion by 70% (P less than 0.001). Concomitantly, plasma glucose levels were elevated: 10.8 +/- 0.4 mmol l-1, compared to 9.2 +/- 0.4 mmol l-1 in controls (P less than 0.001). We conclude that secretin, while being without effect on basal glucagon secretion, markedly potentiates cholinergically induced glucagon secretion in the mouse, resulting in increased plasma glucose levels.
 ...
PMID:Secretin potentiates cholinergically induced glucagon secretion in the mouse. 381 83

The role of the vagus nerve in the control of gastrin releasing peptide (GRP) stimulated gastroenteropancreatic hormone release and gastric acid secretion was investigated in four conscious gastric fistula dogs using a technique of bilateral cryogenic vagal blockade. A 90-min infusion of GRP at a dose of 400 pmol X kg-1. h-1 produced significant elevations in plasma levels of gastrin, motilin, GIP, enteroglucagon, insulin, pancreatic glucagon, pancreatic polypeptide and VIP. Vagal blockade reversibly inhibited the rise of plasma PP and significantly blunted the elevation of plasma VIP. However, the GRP stimulated response of the other hormones investigated was not modified by vagal blockade. Similarly, the substantial secretion of gastric acid observed with GRP was not influenced by vagal blockade. Thus GRP acts predominantly via mechanisms which are independent of vagal integrity, findings that are in support of a major role for the local neuromodulation of hormone release and gastric acid secretion.
 ...
PMID:The role of vagal integrity in gastrin releasing peptide stimulated gastroenteropancreatic hormone release and gastric acid secretion. 388 1

In a single-blind randomized placebo-controlled cross-over study in hypertensive patients we have examined the effects of treatment with the non-selective beta-adrenoceptor antagonist nadolol on the responses of glucose, intermediary metabolites and the hormones of the enteroinsular axis to the ingestion of a mixed meal. During treatment with nadolol the plasma insulin concentration 30 min after ingesting the meal was significantly lower than on placebo and the plasma glucose rose more slowly. Plasma concentrations of GIP tended to be higher during nadolol than placebo treatment. No significant effects of treatment with nadolol were noted on pancreatic glucagon or intermediary metabolites.
 ...
PMID:The effect of chronic treatment with a non-selective beta-adrenoceptor antagonist on the enteroinsular axis and intermediary metabolites. 390 82

Fifteen Type 2 diabetics were treated for 4-week periods with once daily (10 mg) glibenclamide, glipizide and placebo according to a double-blind cross-over protocol. Post-dose glipizide concentrations were three times higher than those of glibenclamide, due to the incomplete bioavailability of the latter. On the other hand, pre-dose drug levels were similar, as an expression of the slower absorption and/or elimination of glibenclamide. Both active treatments reduced postprandial blood glucose concentrations and 24-hour urinary glucose excretion to a similar degree, but fasting blood glucose concentrations were slightly lower during glibenclamide treatment. Both active treatments enhanced fasting and postprandial insulin and C-peptide concentrations, the C-peptide response being greater after glipizide than after glibenclamide. Plasma glucagon and GIP concentrations were not significantly affected. Insulin sensitivity was increased by glibenclamide but not by glipizide. Neither therapy affected insulin binding to erythrocytes. It appears that both glibenclamide and glipizide improved glucose metabolism by sustained stimulation of insulin secretion, which was most pronounced with glipizide. Only glibenclamide improved insulin sensitivity and was slightly more active than glipizide on fasting blood glucose levels. The differences may be consequences of the pharmacokinetics, but differences in pharmacodynamics cannot be excluded.
 ...
PMID:Pharmacokinetics and metabolic effects of glibenclamide and glipizide in type 2 diabetics. 393 84


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>