Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: HUMANGGP:034761 (insulin)
 211,843 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Intraduodenal infusion of 0.05-0.5 N hydrochloric acid dose-dependently increases serum levels of immunoreactive gastric inhibitory polypeptide (GIP) in rats. Immunoreactive GIP released by duodenal acidification is biologically active because it augments the glucose-induced release of immunoreactive insulin (IRI). This augmentation of glucose-induced IRI release by intraduodenal acid can be abolished for 30 min by simultaneous intravenous infusion of GIP-antiserum. From this it is concluded that the initial capacity to augment the glucose-induced insulin release (incretin activity) of hydrochloric acid is due to its ability to release GIP. Later on, other gut factors with incretin activity might be released by hydrochloric acid. Also, in humans, intraduodenal infusion of 0.1 N hydrochloric acid releases GIP without changing serum levels of glucose or insulin. The GIP release is a direct effect of intraduodenal acid and is not mediated via secretin release. Injection of secretin in supraphysiologic doses does not change serum levels of immunoreactive GIP. However, such secretin injections induce a short-term insulin release and a decrease in serum glucose concentration.
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PMID:Release of gastric inhibitory polypeptide (GIP) by intraduodenal acidification in rats and humans and abolishment of the incretin effect of acid by GIP-antiserum in rats. 3 54

Series of analytic experiments are presented that explore possible physiological mechanisms for the control of cardiac rate by nutritional intake in the pre-weanling rat. The essential properties of the nutrient and the first site of action were studied by using fluids of different pH, osmolality and chemical composition administered intravenously as well as intragastrically. Several probable effector pathways were explored: neuroendocrine (adrenal medullary and adrenocortical, thyroid), cholinergic and adrenergic. Pharmacological blocking agents, surgical removal of glands, replacement hormones and spinal cord trasaction were utilized. Afferent pathways such as vagus and splanchnic systems were approached surgically and the gastrointestinal hormones, histamine, insulin and glucagon, were studied by administration and pharmacological blockade. The evidence tended to rule out a number of possible mechanisms and pathways and to make it appear likely that nutrient acts initially at the gut wall, that the CNS then responds by increasing tone in the classical spinal cardioacceleratory pathways to the beta-adrenergic synapses of myocardium.
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PMID:Physiological mechanisms for cardiac control by nutritional intake after early maternal separation in the young rat. 4 39

Extrapituitary corticotropin-like peptides have been found in central nerves and in gastrointestinal and pancreatic endocrine cells. Previous biological and immunological data strongly indicate that the immunoreactivity present in the central nerves represents corticotropin (A.C.T.H.) or a closely related peptide. In some areas of the brain, the distribution of A.C.T.H. nerves parallels that of nerves containing the endogenous opioid ligand, enkephalin. Since A.C.T.H. fragments bind to the opioid receptor the two neuronal peptides may interact. The antiserum used demonstrates the COOH-terminus of the A.C.T.H. molecule, which is devoid of adrenocortical stimulatory activity. A COOH-terminal A.C.T.H.-peptide, corticotropin-like intermediate peptide (C.L.I.P.), originally isolated from the pars intermedia, has been shown to stimulate release of pancreatic insulin. The presence of C.L.I.P.-like molecules in gut and pancreatic endocrine cells may indicate that C.L.I.P.'s insulin-releasing activity is physiologically important. Further, the occurrence of A.C.T.H.-related molecules in such cells may account for the ectopic A.C.T.H. syndrome associated with some tumours of gut and pancreas.
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PMID:Corticotropin-like peptides in central nerves and in endocrine cells of gut and pancreas. 7 31

It is suggested that the early-morning growth-hormone release associated with slow-wave sleep is due to inhibition of somatostatin secretion from the hypothalamus. It is also associated with inhibition of gastrointestinal somatostatin, causing a release of gastrin and insulin. Because the levels of glucocorticoid hormones are concurrently low, the insulin effect is unopposed and increases gut motility through augmented vagal tone. This results in an increased delivery of acid to the duodenum. In duodenal-ulcer patients, whose duodenal buffering capacity is reduced because of a relative deficiency of secretin response, this leads to pain.
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PMID:Nocturnal ulcer pain associated with slow-wave sleep. 7 1

We studied serum glucose levels following a peroral glucose test in 6 healthy subjects on 2 alternate days in random order; with or without an i.v. TRH infusion for 3 hours (0.66 mg/hour). TRH infusion reduced serum glucose levels following oral glucose in all 6 subjects investigated. Serum insulin levels were reduced accordingly. Furthermore, serum xylose levels following peroral xylose were studied in the same 6 subjects. TRH infusion i.v. reduced serum xylose levels in all 6 subjects studied. I.v. glucose tolerance tests with or without an i.v. TRH infusion (0.66 mg/h) for 3 hours were studied in 4 healthy subjects. No change in serum glucose or insulin levels following TRH infusion was observed. We conclude that an i.v. infusion of TRH reduces serum levels of glucose following a peroral xylose load. TRH thus has marked actions on gastro-intestinal function in man inhibiting and/or retarding the absorption of glucose and xylose from the gut.
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PMID:Actions of thyrotropin-releasing-hormone on gastrointestinal function in man. I. Inhibition of glucose and xylose absorption from the gut. 10 Aug 66

"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).
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PMID:Is GIP a glucagon cell constituent? 10 36

Glibenclamide has been shown to stimulate an insulin releasing factor in the duodenum. The possibility that this effect is of importance in its hypoglycaemic action was investigated by studying the effect of galactose on insulin release before and after treatment with glibenclamide; galactose stimulates insulin release when given orally but has no effect when given parenterally; thus its ability to release insulin appears to reside in an action on a gut factor. Measurements of plasma glucose, insulin and glucagon were made on twelve maturity onset diabetic patients following an oral glucose tolerance test and an oral galactose tolerance test before and after one week of treatment with glibenclamide. Glibenclamide significantly reduced the blood glucose levels. Both basal insulin and basal glucagon levels were unchanged. The insulin response to oral glucose was enhanced. Glucagon levels before treatment did not suppression of glucagon levels. Galactose stimulated insulin release but insulin levels before and after treatment were identical. An effect of glibenclamide on gut insulin releasing activity was not demonstrated but the galactose tolerance test provides a useful technique by which to examine the enteroinsular axis.
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PMID:The effect of glibenclamide treatment on the insulin and glucagon responses to oral glucose and galactose in maturity onset diabetics. 11 30

The effect of insulin on the electrical activity of the small intestine was studied in both normal and alloxan induced diabetic sheep. In normal animals the migrating myoelectric complexes recur at intervals of about 90 min. In the diabetic sheep, the complexes recur at only 2 hourly intervals and administration of insulin restored the pattern to normal. Since in normal sheep, insulin slightly increases the activity and volatile fatty acids, which release insulin do likewise, one may conclude that insulin may control the activity of the gut.
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PMID:[Effect of insulin on electric activity of sheep jejunum]. 12 81

Two sibs who sustained severe hypoglycaemia in the neonatal period are reported. In spite of treatment with frequent feeds intravenous glucose, glucagon, hydrocortisone, and diazoxide, hypoglycaemia persisted, and both infants eventually required subtotal pancreatectomy. Tests for leucine toleranct were normal though the second case showed some protein sensitivity. Histological and immunohistochemical studies indicated nesidioblastosis in both specimens of pancreata. The children are presently performing at mildly retarded levels, and required diazoxide and anticonvulsant medication for some time postoperatively. Because both sexes are represetned, an autosomal recessive inheritance pattern is suggested. The theory of a gut hormone stimulating insulin production is briefly discussed.
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PMID:Idiopathic hypoglycaemia in sibs with morphological evidence of nesidioblastosis of the pancreas. 18 9

The islet cell tumors of the pancreas are now known to produce a variety of polypeptides in addition to insulin. These include glucagon, serotonin, corticotropin, melanocyte-stimulating hormone, gastrin and a secretinlike hormone that may be VIP or a combination of such polypeptides. The development and wide availability of the newer immunoassays for the various recognized hormones as well as candidate hormones of the gut will simplify the diagnosis of these challenging tumors, which up until this time have produced symptoms that were bizarre and often fatal to the patient.
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PMID:Tumors of the islets of Langerhans. 18 90


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