Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Alteration of growth of dimethylbenz[a]anthracene-induced mammary tumors was caused by removal of estrogen (ovariectomy), or insulin (diabetes), or by inhibition of prolactin secretin (treatment with an ergoline derivative). The levels of cyclic AMP (cAMP) and cGMP were measured in carcinomas classified as growing, static, and regressing. The amount of cAMP, expressed as pmoles/mg tumor weight or pmoles/mg protein, was lowest in growing tumors, intermediate in static tumors, and highest in those regressing. No correlation was seen between tumor growth and cGMP levels. Cyclophosphamide-induced tumor stasis did not elevate cAMP levels. The data suggest a role of cAMP in arrest of hormone-induced tumor growth.
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PMID:Relationship of adenosine 3',5'-cyclic monophosphate and guanosine 3',5'-cyclic monophosphate to growth of dimethylbenz(a)anthracene-induced mammary tumors in rats. 17 3

With the advent of radioimmunoassay and immunocytochemical methods, the peptides of the gastrointestinal tract have been identified and measured. Gastrinoma and insulinoma syndromes have been wall characterized. The pancreatic cholera syndrome and some of the evidence that the major manifestations of this disease may be mediated by vasoactive intestinal peptide have been re-examined. Pancreatic polypeptide seems to be an ideal peptide for study of vagal-cholinergic mechanisms that regulate hormone release; it also appears to be a tumor marker for several types of pancreatic endocrine tumors, particularly those of pancreatic cholera. Secretin and cholecystokinin are important regulators of pancreatic exocrine secretion and have been used to test pancreatic function, but there is little evidence that they account for clinical disease. Glucagon-secreting tumors produce a clinical syndrome of diabetes mellitus and distinctive skin lesions, which can be cured by tumor resection. Hormone-secreting tumors may provide insight into normal gut physiology.
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PMID:Gastrointestinal hormones in clinical disease: recent developments. 21 42

The responses of plasma gastro-entero-pancreatic (GEP) hormones and free fatty acids (FFA) to a standard mixed meal before and after starvation have been measured. Raised insulin, glucose and FFA levels were found following refeeding after starvation and levels of secretin and C-terminal glucagon-like-immunoreactivity (C-GLI), raised by starvation, were rapidly suppressed on refeeding. The responses of gastrin and N-terminal glucagon-like-immunoreactivity (N-GLI) to a standard mixed meal were not altered by starvation. Although this study does not directly support that secretin and glucagon are responsible for the hyperglycaemia or hyperinsulinaemia of starvation diabetes, a role for both hormones in the raised FFA levels is proposed, as well as a role for glucagon in the initial hyperglycaemic response to a meal after starvation.
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PMID:The gastro-entero-pancreatic hormone secretion after a mixed meal in normal subjects before and after a 72 hour period of starvation. 44 30

Changes of an exocrine function after major resection of the canine pancreas were observed by pancreozymin-secretin test and the results were compared with an endocrine function examined by glucose tolerance test. The exocrine function of the remnant pancreas revealed characteristic changes according to the resection rate of the pancreas: 1) After removal of 50 to 70 per cent of the entire pancreas, diabetes did not develop and the exocrine function of the remnant pancreas was well maintained. 2) After 70 to 90 per cent pancreatectomy, diabetes developed six weeks or more later and the exocrine function of the remnant pancreas per body weight decreased slightly. The degree of disturbance of the exocrine function in the diabetic dogs was greater than that in the non-diabetic group, but the exocrine function per the remnant pancreas weight increased and it was greater than normal level even in the diabetic dogs. The hypersecretory state of the exocrine pancreas after surgery was verified. 3) After 90 per cent or greater resection of the pancreas, diabetes occurred immediately and disturbance of the exocrine function was remarkable. Hypersecretory state did not appear. 4) Both the endocrine and exocrine functions after major pancreatic resection were found to be related to the resection rate, but there were significant differences in the reserve capacity of the endocrine and exocrine pancreas.
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PMID:Changes of pancreatic exocrine function after major resection of the pancreas in dogs. 48 23

A follow-up investigation of 20 patients, surgically treated for acute haemorrhagic necrotising pancreatitis, was performed in an average of 2 3/4 years after the operation. Twelve patients showed manifest diabetes mellitus, four further cases had a suspicious oral glucose tolerance test. Only one patient was insulin dependent. A secretin-pancreozymin test performed in 15 patients showed a dissociated or global pancreatic insufficiency in 13 cases. The extent of the endocrine and exocrine functional disturbance did not correlate with the extent of surgery. Postoperative functional defects were readily improved therapeutically in most cases. Only in patients who continued to consume alcohol were there digestive disturbances. The results indicate that the functional state of the remaining pancreas does not only depend on the extent of surgery but also on the extent of already existing or persisting toxic inflammatory damage and on the regenerative capacity of the remaining parenchyma.
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PMID:[Long-term results after operative treatment of acute haemorrhagic necrotising pancreatitis (author's transl)]. 51 Jan 95

Endogenous insulin secretion after different stimuli was determined in insulin requiring diabetics without circulating insulin antibodies. Four groups of non-obese diabetics were investigated and compared with 111 controls. Group I: 14 patients with mild diabetes, not yet requiring insulin; diagnosis before the age of 30 years. Group II: 19 ketonuric patients just before being started on insulin treatment. Group III: 18 patients during remission after an average of 16.5 months' insulin treatment. Group IV: 13 patients with no remission period or relapse after an average of 19.5 months on insulin treatment. Blood glucose and immunoreactive insulin were measured during fasting and after iv secretin, iv tolbutamide, iv GTT, and oral GTT, followed by combined iv tolbutamide and glucagon stimulation. A considerable insulin secretion could be demonstrated in group I, whereas in group II only a very low insulin peak was obtained after secretin and the combined injection of glucagon and tolbutamide. In group III considerable insulin secretion was demonstrated, whereas in group IV only a very low insulin peak was obtained. A significant correlation between the degree of metabolic control and endogenous insulin secretion was found.
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PMID:Insulin secretion in insulin-requiring diabetics before and during insulin treatment. 57 40

The purpose of the investigations was the determination of the maximum gastric secretion during hyperglycaemia in healthy subjects as well as in patients with short-term and long-term diabetes. After the stimulation with pentagastrine, given in the dose of 6 microgram per kg of body weight in 0.9% sodium chloride solution continuous intravenous infusion, there were determined MAO, parietal and nonparietal secretions, the concentrations of sodium, potassium, chloride, calcium and magnesium, and the total secretin of these electrolytes in gastric juice. In healthy subjects hyperglycaemia was induced by intravenous infusion of 30% glucose solution. Under the influence of hyperglycaemia the decrease of MAO (p less than 0.001) in healthy subjects as well as in diabetics was found. In healthy subjects the decrease of the total potassium, chloride and magnesium secretion in gastric juice (p less than 0.001) was observed. In patients with long-term diabetes the decrease of the secretion of sodium, potassium, chloride, magnesium and calcium was observed. There were no differences in gastric secretion in both groups of diabetics. The inhibitory effect of hyperglycaemia on the parasympathetic system and the decreased release of endogenous gastrine may be the causes of these changes. Insulin may also inhibit gastric secretion.
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PMID:[Maximal gastric secretion in hyperglycemia in normal subjects and in diabetics]. 59 33

Endocine and exocrine pancreatic function were investigated in 10 patients after pancreatic trauma or traumatic pancreatitis. There were no cases of overt diabetes mellitus. Three patients had subclinical diabetes. In the secretin-pancreozymin test 5 patients had normal exocrine pancreatic function after trauma, whereas in 3 patients bicarbonate and/or enzyme secretion was diminished, to normalize during an observation time of several years. In the remaining 2 patients a secretin-pancreozymin test could not be performed; one of them had slight steatorrhoea. These results are evidence of a good reserve capacity of the endocrine pancreas, and a good regeneration capacity of the exocrine pancreas, after trauma.
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PMID:[Pancreatic function after injury to the pancreas and traumatic pancreatitis]. 62 37

Secretin releasing response to intraduodenal acid infusion was investigated in 15 cases of diseased control, 7 cases of duodenal ulcer, 5 cases of chronic pancreatitis, and 6 cases of diabetes mellitus. Plasma secretin levels in response to duodenal acidification were less in duodenal ulcer and the appearance of the maximal peak was delayed compared with that found in control. It is suggested that the secretin release was impaired in duodenal ulcer in spite of hypersecretion of gastric acids. In chronic pancreatitis, secretin releasing response to acidification was markedly impaired, in addition, inhibition of secretin release by bicarbonate was diminished due to a lack of bicarbonate flow from the pancreas. On the other hand, although the response of secretin release in diabetes mellitus was also lower compared with that in control group, the capacity of secretin response showed values in-between control subjects and chronic pancreatitis. This research was supported in part by grant from the Ministry of Education, Science and Culture in Japan.
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PMID:Secretin secretion in patients with duodenal ulcer, chronic pancreatitis and diabetes mellitus. 64 3

The prevalence of diabetes due to chronic pancreatitis would appear to be increasing. In western countries this is associated with the known increase in alcohol consumption and AIP. Malnutrition may be etiologic in tropical areas. The incidence of diabetes in chronic pancreatitis is dependent on a number of factors. It is more common in alcohol-induced pancreatitis, rarely occurs after the first attack but tends to increase with time and rises markedly in calcific pancreatitis. Abnormal glucose tolerance occurred in 91% of patients with calcific pancreatitis and 70% of patients with noncalific AIP in our follow up of five to 12 years. This stresses the importance of serial regular glucose tolerance tests in these patients (Table I). The insulin-reserve is severely depleted in most patients who do not yet demonstrate abnormal glucose tolerance, indicating that pancreatitis regularly affects the islets and that nearly all patients are potential diabetics. The beta cells appear to respond better to oral glucose, glucagon or secretin than to i.v. glucose suggesting a selective glucose receptor loss or block to hyperglycemia in chronic pancreatitis. The alpha cells seem to be more resistant to the effects of chronic pancreatitis but true hypoglucagonemia was found in 16% of patients. In addition, stimulated growth hormone secretion may be deficient in pancreatic diabetes. These last two factors, among others, may be responsible for the protracted and even fatal hypoglycemia to which some patients with AIP on insulin therapy are liable. The danger of drug-induced hypoglycemia, coupled with the infrequency of vasculopathy, retinopathy and nephropathy in pancreatic diabetes has induced us to keep these patients hyperglycemic and glycosuric rather than in a sugar-free state, as long as symptoms are contained. Recurrent abdominal pain, marked weight loss and associated steatorrhea often raise special problems in the management of the pancreatic diabetic.
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PMID:Clinical and hormonal aspects of pancreatic diabetes. 80 21


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