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)

The gastrointestinal hormones, which are continuously increasing in number, have certain effects which could play a part in the pathogenesis of infectious diarrhoea. This refers especially to VIP, motilin, and enteroglucagon, the plasma concentrations of which are elevated in acute infectious diarrhoea, cholera, and tropical malabsorption. They may act by stimulating intestinal secretion, inhibiting absorption, and altering intestinal motility. In addition, there are some hormonal effects such as those caused by glucagon on motility, by enkephalins on secretion, and by somatostatin on both, which have a therapeutic potential and deserve further investigation.
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PMID:Infectious diarrhoea and gastrointestinal hormones: potential therapeutic implications. 635 26

Acarbose, an alpha-glucosidase inhibitor, lowers the glycemic excursion following the ingestion of carbohydrates, in particular, sucrose. This was confirmed with increasing doses of acarbose (0, 50, and 100 mg) and the causes investigated. The absorption of the glucose moiety of sucrose was determined from plasma tracer concentrations when overnight-fasted normal subjects received a 100-g oral sucrose load labeled with sucrose [(1-14C]glucose and a simultaneous intravenous infusion of [3-3H]glucose. As the dose of acarbose given with the sucrose load was increased from 0 to 100 mg, the percentage of the load appearing in the peripheral circulation decreased from 90% to 62%. Malabsorption was confirmed by the appearance of breath hydrogen. Simultaneously, absorption time increased from 243 to 411 min. Maximal glycemic excursions were therefore lowered from 64 to 31 mg/dl. The plasma concentrations of gastric inhibitory polypeptide and insulin decreased with the acarbose dose so that the fractional disappearance rate of glucose also decreased. However, the concentrations of glucagon-like immunoreactivity (GLI) rose, confirming the ileal appearance of malabsorbed sucrose.
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PMID:The effects of an alpha-glucoside hydrolase inhibitor on glycemia and the absorption of sucrose in man determined using a tracer method. 636 57

Transit times were evaluated in 23 obese subjects before and 1,4 and 12 months after biliopancreatic by-pass. A modified version of the method of Hinton et al. was used to determine emptying of the stomach and partial and total transit times. Emptying of the stomach was normal preoperatively. After surgery, it was almost immediate, except in two subjects with stomitis. Both transit times were virtually unchanged. Since the segment between the stomach and the ileocaecal valve is only half as long as in the normal subject, the results show that the by-pass leads to a slowing of transit that concerns the small intestine only, is quickly established, and does not change in the course of time. Evaluation of the altered anatomical and functional situation, and the absence of a correlation between the long-term behaviour of transit times on one hand and of lipid malabsorption and weight loss on the other-hand, suggest that a slower transit time must not be regarded as a compensation mechanism, except insofar as it restricts the degree of malabsorption set up immediately after surgery. Preliminary studies of enterohormonal changes following the by-pass indicate that increased glucagon and decreased motiline values are mainly responsible for slower transit times.
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PMID:[Intestinal transit time in bilio-pancreatic bypass]. 677 38

Twenty-eight infants with persistent hyperinsulinemic hypoglycemia of infancy (PHHI) were seen during a 10-year period. There were 13 males and 15 females. Their age at time of presentation ranged from a few hours to 6 months. Consanguinity was reported in 20 cases (71.4%). One family had two affected siblings and two affected cousins, another had three affected siblings and one affected cousin, and three others had lost siblings because of hypoglycemia and seizures. The primary clinical presentation was jitters and seizures in association with hypoglycemia. The diagnosis was suspected when the therapeutic glucose requirement was found to be more than 12 mg/kg/min and also when there was a good response to glucagon after exclusion of metabolic and storage diseases. A high insulin-to-glucose ratio was noted for all patients. Twenty-two had near-total (90%) pancreatectomy; the result was excellent in all but four, who required supplemental medical therapy. Five patients were treated medically, and one patient's family refused treatment. Twelve patients sustained moderate to severe brain injury before referral. There were no deaths, and only one patient had evidence of malabsorption after the pancreatectomy. PHHI correlates well with consanguinity and family history. Clinical awareness is essential to permit early diagnosis and prompt medical and supportive therapy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Persistent hyperinsulinemic hypoglycemia of infancy: experience with 28 cases. 747 62

We examined the plasma amino acid profiles of 17 patients with pancreatic diabetes in comparison with those of 14 healthy subjects and 16 patients with primary diabetes of similarly poor glycemic control. We also measured fasting plasma glucagon and free insulin levels in patients with pancreatic diabetes and in those with primary diabetes. The fasting plasma amino acid level was highest in patients with pancreatic diabetes. Furthermore, the plasma glucagon level in patients with pancreatic diabetes was significantly low, and negative correlations were found between glucagon and glucagon-related System A and gluconeogenic amino acids. On the other hand, the levels of branched-chain amino acids (BCAA) and System L amino acids, which are subjected to change in the state of diabetes mellitus, increased in patients with pancreatic diabetes. From the above results, we determined that the amino acid profile in patients with pancreatic diabetes resembled that in patients with total pancreatectomy. It is our opinion that the increases of amino acid levels (gluconeogenic and System A amino acids) in patients with pancreatic diabetes is not dependent on maldigestion/malabsorption under treatment, but is mainly dependent on glucagon deficiency.
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PMID:Increased plasma gluconeogenic and system A amino acids in patients with pancreatic diabetes due to chronic pancreatitis in comparison with primary diabetes. 782 75

The present paper addresses the question how alpha-glucosidase inhibitors affect glucose homeostasis. To facilitate this already established data on the effects of induced malabsorption on gut hormones such as gastric inhibitory polypeptide (GIP) in connection with preliminary findings which deal with the new incretin hormone glucagon-like peptide 1 (7-36) amide (GLP-1) are discussed. To emphasize the possibly important impact of a regulated GLP-1 release in response to glucosidase inhibitor treatment we evaluate the recently introduced concept of 'glucose competence' of pancreatic beta-cells. The slowing of nutrient (i.e. glucose) absorption by therapeutic means (for example, acarbose) could supplement a new approach in the treatment of type 2 diabetics which would utilize the well-preserved insulinotropic activity of GLP-1 in these patients, its glucagon-lowering effect, and its possible inhibition of gastric emptying rates, the latter helping to reduce the requirement for rapid insulin secretory responses as is intended while using alpha-glucosidase inhibitor treatment.
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PMID:Intestinal effects of alpha-glucosidase inhibitors: absorption of nutrients and enterohormonal changes. 800 23

Plasma oxyntomodulin-like immunoreactivity (OLI) concentrations were found to be significantly elevated in 6 patients with coeliac disease when compared with those observed in 38 healthy subjects. Furthermore, OLI hypersecretion is related to the degree of malabsorption. This marker could be used as a test for detection and follow-up of patients with malabsorptive disorders.
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PMID:[Oxyntomodulin, a new hormonal marker of intestinal malabsorption syndromes]. 800 75

We report a girl with Johanson-Blizzard syndrome complicated by diabetes mellitus. She presented several characteristic malformations, such as aplasia of the alae nasi, deafness, dwarfism, absence of permanent teeth and malabsorption caused by disturbance of pancreatic exocrine function. At 11 years of age, glycosuria was detected at a routine outpatient examination. Repeated oral glucose tests showed a slowly progressive decline of insulin secretion and elevated blood glucose levels. The responsive secretion of insulin to glucagon or arginine loading was also low. The blood level of HbAlc was elevated over 9%. Based on these findings, insulin therapy was started when the patient was 13 years old. Our case suggests that diabetes mellitus might be considered as one of complications of Johanson-Blizzard syndrome.
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PMID:A case of Johanson-Blizzard syndrome complicated by diabetes mellitus. 844 11

The therapeutic effect of acarbose is generally attributed to inhibition of amylase and brush border glucosidases and consequent impaired digestion and absorption of carbohydrates. We have investigated the possibility that acarbose may also influence the rate of gastric emptying by comparing plasma glucose and gastrointestinal hormone responses to an oral sucrose load with and without acarbose in 11 healthy subjects. Gastric emptying was assessed indirectly by measuring circulating paracetamol concentrations following administration of paracetamol along with the sucrose load. Peak plasma glucose, insulin, and glucose-dependent insulinotropic polypeptide (GIP) responses were reduced when sucrose was given with acarbose. There was a significant reduction in post-sucrose paracetamol levels with acarbose suggestive of a significant delay in gastric emptying. The failure of acarbose to induce change in circulating paracetamol concentrations until after 60 min is indicative of a delay in gastric emptying rather than an osmotic malabsorption. The exaggerated and sustained release of glucagon-like peptide-1 (7-36)amide (GLP-1) seen when sucrose was given with acarbose may play a part in the inhibition of gastric emptying. This study indicates that a significant delay in gastric emptying may be an added mechanism contributing to the therapeutic effect of acarbose.
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PMID:Delayed gastric emptying occurs following acarbose administration and is a further mechanism for its anti-hyperglycaemic effect. 950 11

Necrolytic migratory erythema is characterized by waves of irregular erythema in which a central bulla develops, and subsequently erodes and becomes crusted. It usually occurs in patients with an alpha-islet cell tumor of the pancreas. However, necrolytic migratory erythema has also been observed in patients without an associated glucagonoma. We describe a woman with iatrogenic necrolytic migratory erythema. She received intravenous glucagon for hypoglycemia associated with an insulin-like growth factor II-secreting hemangiopericytoma. After chemotherapy, she developed necrolytic migratory erythema. The characteristics of the previously reported patients with nonglucagonoma-associated necrolytic migratory erythema are reviewed. In patients with nonglucagonoma-associated necrolytic migratory erythema, the dermatosis-related conditions most commonly observed were celiac disease or malabsorption, cirrhosis, malignancy, and pancreatitis; less common conditions included hepatitis, inflammatory bowel disease, heroin abuse, and odontogenic abscess. Although the pathogenesis of necrolytic migratory erythema remains unknown, hyperglucagonemia appears to have had a causative role in the development of this dermatosis in our patient. Patients who develop necrolytic migratory erythema should be evaluated for the presence of a glucagonoma; if a glucagonoma is ruled out, evaluation for other conditions known to occur with necrolytic migratory erythema, such as liver disease, malabsorptive disorders, and nonislet-cell tumors is warranted.
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PMID:Iatrogenic necrolytic migratory erythema: a case report and review of nonglucagonoma-associated necrolytic migratory erythema. 959 6


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