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

To examine the mechanism of the recently reported effect of an acidified intragastric test meal on insulin release and glucose homeostasis, a liver extract test meal at either pH 2 or pH 7 was instilled into the stomach of normal dogs and dogs with a chemical sympathectomy or indomethacin-induced prostaglandin deficiency, all of which had a bisected pylorus and gastric fistula. In the normal dogs the instillation of the liver meal at pH 2 elicited a significant rise in plasma glucose, glucagon and insulin levels, while in response to the meal at pH 7 only glucagon rose significantly. This was not altered in chemically sympathectomized dogs, nor during the infusion of indomethacin. In all experiments gastrin or gastric glucagon release in response to the meal at pH 2 was either lower than or similar to the response to the meal at pH 7. These data suggest that the influence of the stomach upon islet cell function and glucose homeostasis does not depend on either adrenergic innervation or the presence of prostaglandings, but rather is mediated by a yet undetermined mechanism.
Acta Endocrinol (Copenh) 1979 Dec
PMID:Sympathectomy and prostaglandin deficiency do not prevent gastrogenic hyperglycaemia and hyperinsulinaemia. 4 43

The effects of neurotensin on insulin and somatostatin release were examined in isolated pancreatic islets prepared from 3-4 days rats, and maintained in culture for 48 h before use. In the presence of 12 mM glucose, glucagon (50-2,000 ng/ml, i.e. 14-560 nM) caused a 2-fold increase in insulin and somatostatin release. Neurotensin (150 ng/ml, i.e., 100 nM) did not affect the glucagon-stimulated release, nor did it alter the release of either peptide measured at 12 mM glucose in the absence of glucagon. In contrast, neurotension markedly inhibited the release of both insulin and somatostatin that was induced by 23 mM glucose. These observations suggest that neurotensin may modulate the release of insulin and somatostatin evoked by high glucose concentrations, but not that resulting from the action of glucagon on pancreatic islets.
Diabete Metab 1979 Dec
PMID:Neurotensin inhibits glucose but not glucagon-induced insulin and somatostatin release in isolated islets. 4 73

Immunocytochemical examination of the islets of Langerhans in various animal species, including man, indicates that insulin-producing cells (B cells), glucagon-producing cells (A cells), and cells producing somatostatin or a somatostatin-like peptide (D cells) are not randomly arranged within the islet. Whenever A cells are found in the islet--i.e., mostly in its peripheral part--they are accompanied by D cells. However, most B cells, which occupy a central position, are in contact only with other B cells. In view of the inhibitory effect of somatostatin on both insulin and glucagon secretion, it is suggested that the arrangement of A, B and D cells is important to the normal and pathological functioning of the islet.
Lancet 1975 Dec 20
PMID:Functional subdivision of islets of Langerhans and possible role of D cells. 5 29

Infusion of somatostatin, an inhibitor of glucagon secretion, in insulin-dependent diabetics resulted in a 75-100% reduction in the blood-glucose rise after oral glucose administration, but did not improve intravenous glucose tolerance. Somatostatin reduced blood-xylose levels by 50-90% after ingestion of this pentose and delayed the peak increment in blood-xylose by 1-2 h. Similar effects on blood-xylose levels and a 30% reduction in splanchnic blood-flow were observed in normal subjects during infusion of somatostatin. Glucagon administration (3 ng per kg per min) or intraduodenal administration of xylose did not reverse somatostatin's effect on xylose tolerance. Somatostatin reduces postprandial hyperglycaemia in diabetes primarily by decreasing and/or delaying carbohydrate absorption rather than enhancing carbohydrate disposal. This effect may be mediated, in part, but a reduction in splanchnic blood-flow. These findings indicate that postprandial hyperglycaemia in diabetes is due primarily to insulin deficiency rather than glucagon excess.
Lancet 1976 Dec 04
PMID:Influence of somatostatin on carbohydrate disposal and absorption in diabetes mellitus. 6 40

Whole pancreases from fetal rats of 13 days and 18 days gestation were explanted onto rayon grids and grown in organ culture. Cultures were fixed in Bouin's fluid, sectioned and stained with the fluorescent antibody techniques for glucagon and insulin, aldehyde fuchsin for B cells, pseudoisocyanin for D cells and a silver technique for the fourth cell type. The 13-day explants were fixed after 10 days in culture. A, B and D and the fourth cell type were seen, indicating that precursors of all four endocrine cell types must be present in the fetal pancreas shortly after the formation of the pancreatic bud (11 days). Further, the presence of these four cell types in the walls of tubules in these cultures indicates the tubules as the site of origin of all the endocrine tissue. The 18-day explants were collected every other day of culture from 2 to 30 days in a long-term experiment. A number of large islets with well granulated B cells was still present after 30 days of culture. The relative abundance of cell types at different stages was estimated as follows: 18-day fetal controls, A greater than B=4 greater than D; after 2 to 10 days in culture, B greater than A greater than or equal to D; after 18 to 30 days in culture, B greater than D greater than A greater than 4.
In Vitro 1976 Dec
PMID:A, B, D cells and a fourth cell type in long-term cultures of fetal rat pancreas. 6 78

Implants of rabbit neonatal pancreas, encased in 'Nucleopore' chambers (0.4 micrometer) reversed streptozotocin-induced diabetes in the rat. Blood-glucose, plasma-insulin, and oral glucose-tolerance test returned to normal. An isolated, perfused, streptozotocin-treated pancreas removed from a diabetic animal did not secrete insulin and removal of implants after 6 weeks from six animals caused all animals to die in hyperglycaemia within 8 days. This shows that the implant did not lead to the re-establishment of endogenous pancreatic function. Implanted diced neonatal pancreas in three chambers removed after 6 weeks secreted glucagon, insulin, and pancreatic polypeptide in vitro. No rejection reactions were seen. Rabbit neonatal pancreatic implants may thus be feasible therapy in insulin-requiring diabetic patients. Implants of other non-syngeneic endocrine cells--i.e., pituitary, thyroid, and ovary--may be useful in other hypoendocrine syndromes.
Lancet 1977 Dec 17
PMID:Reversal of streptozotocin-induced diabetes in rats by intraperitoneal implantation of encapsulated neonatal rabbit pancreatic tissue. 7 54

An enkephalin analogue [D-Ala2, MePhe4, Met(o)-ol] enkephalin (DAMME), given intravenously to normal subjects raised serum prolactin and growth-hormone levels but lowered serum levels of luteinising hormone, follicle-stimulating hormone, cortisol, and corticotrophin. There was also a small fall in total glucagon and gastric inhibitory peptide (G.I.P.) and a rise in thyrotrophin. beta-Lipotrophin, motilin, vasoactive intestinal peptide, insulin, gastrin, and pancreatic glucagon were unchanged. Blood-glycerol increased, and blood lactate, alanine, and glucose fell. Prior administration of the opiate antagonist, naloxone, attenuated the hormonal responses to DAMME. This enkephalin analogue produces endocrine and metabolic changes in man which may be mediated through opiate-binding receptors both within and outside the brain. The enkephalins and related substances may provide an important link between perception, behaviour, and neuroendocrine regulation of hormone secretion and metabolism.
Lancet 1978 Dec 09
PMID:Hormonal and metabolic responses to an enkephalin analogue in normal man. 8 35

A procedure was developed for determination of glycogen synthase and phosphorylase activities in liver after various in vivo physiological treatments. Liver samples were obtained from anaesthetised rats by freeze-clamping in situ. Other procedures were shown to stimulate the activity of phosphorylase and depress the activity of glycogen in the liver. The direction of glycogen metabolism appears to be regulated by the relative proportions of the two enzymes, as shown by a strong positive correlation between total activities and active forms of phosphorylase and synthase. The enzyme activities responded as expected to stimuli such as insulin and glucose, which depressed phosphorylase and increased synthase activity, and glucagon, which increased phosphorylase and decreased synthase activity. In fasted animals approximately 50% of each enzyme was in the active form, which suggests the existence of a potential futile cycle for glycogen metabolism. The role for such a cycle in the regulation of glycogen synthesis and degradation is discussed.
Biochim Biophys Acta 1978 Dec 01
PMID:On the activities of glycogen phosphorylase and glycogen synthase in the liver of the rat. 10 67

"Gastric inhibitory peptide" or "glucose-dependent insulin-releasing peptide" (GIP) is a member of the gut hormone family. Its physiological action is thought to be related to its insulinotrophic effect. The occurrence and distribution of GIP was studied by immunohistochemistry. In all species examined including man, GIP immunoreactivity was found to reside in the glucagon cells of the pancrease and gut. Three pancreatic glucagonomas were found to contain numerous cells displaying GIP and glucagon immunoreactivity. The GIP antiserum used did not cross react with either pancreatic-type or gut-type glucagon (GLI).
Histochemistry 1978 Dec 13
PMID:Is GIP a glucagon cell constituent? 10 36

Glucose tolerance and insulin and glucagon secretion were examined sequentially during 6 months of calorie and carbohydrate restriction in an obese, recent-onset, ketosis-resistant diabetic adult. The subject was then followed for 9 additional months, during which some weight was regained. Fasting plasma glucose levels returned to normal after 6 week of calorie restriction and remained normal during periods of carbohydrate refeeding. Normalization of 2-h plasma glucose concentrations after a standard oral carbohydrate load required 5 months, and glucose disposal after an iv glucose load did not return to normal until the end of the study. Insulin secretion in response to oral glucose reached maximal levels during the first months of weight reduction and then decreased as glucose tolerance continued to improve. Acute phase insulin release in response to iv glucose gradually increased throughout the study. Glucagon stimulation by iv arginine and suppression by iv glucose also returned to normal levels slowly over several months. Abnormalities in glucose tolerance and glucoregulatory hormone secretion of ketosis-resistant diabetes are totally reversible with prolonged dietary therapy. Reduction in tissue resistance to the action of insulin also appeared to be of major importance in the recovery of normal glucose tolerance in this subject.
J Clin Endocrinol Metab 1979 Dec
PMID:Normalization of insulin and glucagon secretion in ketosis-resistant diabetes mellitus with prolonged diet therapy. 11 19


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