Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01350 (gastrin)
 9,683 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We evaluated serum gastrin responses to a test meal in normal subjects and diabetic patients with or without vagal neuropathy. Vagal neuropathy was defined as a heart rate variation during deep breathing of less than 9 beats/min. Forty-three percent (54 out of 124) of the diabetic patients had abnormal heart rate variation, compared with 5% (3 out of 53) of the normal subjects. Serum gastrin responses to a test meal were examined in 17 normal subjects, 20 out of 70 diabetic patients without vagal neuropathy and 17 out of 54 diabetic patients with vagal neuropathy. Meal-stimulated gastrin levels were significantly higher in the diabetic patients with vagal neuropathy than in the normal subjects, while the findings in the diabetic patients without vagal neuropathy were similar to those in normal subjects. These data suggest that augmented gastrin responses are due to vagal denervation induced by autonomic neuropathy.
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PMID:Augmented gastrin responses in diabetic patients with vagal neuropathy. 646 94

Basal and postprandial levels of gastrin, somatostatin, vasoactive intestinal polypeptide (VIP) and pancreatic polypeptide (PP) were followed up in 105 patients with non insulin dependent diabetes mellitus (20 with autonomic neuropathy only, 35 with peripheric neuropathy only, 30 with autonomic and peripheric neuropathy simultaneously and 20 without any sign of neuropathy) and in the control group of 40 individuals. Serum levels of gastrin, somatostatin, VIP and PP are determined by a RIA (used kits of Prof. SR Bloom, Hammersmith Hospital, London). The results of investigation showed significantly higher basal and postprandial levels of gastrin and VIP in patients with autonomic neuropathy in comparison with the group without neuropathy and with the control group (p < 0.001). The serum levels of somatostatin did not differ significantly between the groups of diabetics with and without neuropathy. Basal level of PP was significantly lower and postprandial PP levels remained low in patients with autonomic neuropathy in comparison with the group without neuropathy (p < 0.001). We postulate that basal and postprandial gastrin and VIP levels raised secondary to partial vagotomy in diabetics with autonomic neuropathy. Measuring PP serum levels in diabetics after a protein rich meal can be useful to check vagus nerve function in the gastrointestinal tract in order to detect autonomic neuropathy.
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PMID:[Association of autonomic neuropathies and gastrointestinal peptides in non-insulin dependent diabetics]. 773 57

A total of 37 subjects consisted of 10 healthy subjects (Group III), 15 diabetic patients without autonomic neuropathy (Group II), and 12 diabetic patients with autonomic neuropathy including gastroparesis in 6 cases (Group I). All three groups were comparable in age. In order to clarify the gastric function in diabetic patients with autonomic neuropathy, secretion of serum gastrin, gastric secretory function, endoscopic Congo red test of fundic glands, and coefficiency of variance of electrocardiographic beat-to-beat intervals (C.V. R-R) were examined. In Group I, 5 patients had hypergastrinemia, but its elevation was inhibited when an acid solution was injected into the stomach. Gastric secretion and C.V. R-R were markedly lower in Group I, compared with Groups II and III. In Group I, the area of fundic glands (parietal cells) was reduced considerably. The C.V. R-R was significantly correlated with fasting serum gastrin concentration and with maximal acid output. From these results, in diabetic patients with autonomic neuropathy (vagal neuropathy), gastric acid secretion in response to tetragastrin stimulation was lowered with a reduction in area of fundic gland distribution. Hypergastrinemia may reflect a negative feedback mechanism responding to decreased acidity of gastric content in the antrum.
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PMID:Decreased gastric secretory functions in diabetic patients with autonomic neuropathy. 781 84

We examined gastric acid secretion in response to various stimuli in streptozotocin (STZ) induced diabetic rats and characterized the alteration of acid secretory responses in diabetic conditions. Animals were injected STZ (70 mg/kg, intraperitoneally) and used after five weeks of diabetes with blood glucose >350 mg/dl. Under urethane anesthesia, the experiment was performed in a chambered stomach or a whole stomach preparation, and the acid secretion was measured at pH 7.0 using a pH-stat method and by adding 100 mM NaOH. The acid secretion was stimulated by intravenous infusion of either histamine (4 mg/kg/hr), pentagastrin (60 microg/kg/hr), or carbachol (20 microg/kg/hr) or by intraluminal application of peptone solution (4%), or vagal electrical stimulation (2 msec, 3 Hz, 0.5 mA). In normal rats, acid secretion was increased in response to either histamine, pentagastrin, carbachol, peptone, or electrical vagal stimulation. In STZ diabetic rats, however, changes in acid secretion varied depending on the stimuli; the acid response to histamine remained unchanged, but the responses to vagal electrical stimulation or pentagastrin and carbachol were significantly decreased or enhanced, respectively, as compared to normal rats. Likewise, the acid response to peptone was also markedly enhanced in STZ-diabetic rats, and this response was significantly blocked by atropine and YM022 (a CCKB/gastrin antagonist) as well as famotidine in both normal and diabetic rats. Both pentagastrin and carbachol increased the luminal release of histamine in normal rats, and these responses were significantly augmented in STZ-diabetic rats. The altered acid response and histamine release induced by pentagastrin in STZ diabetic rats were partially reversed by daily injection of insulin. These results suggest that STZ-diabetic rats showed different changes in gastric acid secretion in response to various stimuli. The increased acid secretory response may be associated with an enhanced release of mucosal histamine, while the decreased response may be due to vagal neuropathy.
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PMID:Acid secretory changes in streptozotocin-diabetic rats: different responses to various secretagogues. 1096 14

A case of peripheral neuropathy in a patient with diabetes who had atypical clinical findings is presented. Because of the atypical initial manifestations and short duration of insulin-dependent diabetes, another cause of the neuropathy was suspected. The presence of vitiligo, hypothyroidism, and diabetes prompted a search for evidence of pernicious anemia. Despite a normal blood cell count, the diagnosis of pernicious anemia was confirmed on the basis of an increased serum gastrin level and antiparietal cell antibody titer. Treatment with vitamin B12 resulted in an arrest, but not a reversal, of the signs of peripheral neuropathy. In patients with diabetes, vitamin B12 deficiency should be suspected; its early diagnosis and treatment are important in minimizing neurologic damage.
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PMID:Nondiabetic neuropathy in a patient with diabetes. 1525 65