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

The glucagonoma syndrome is a rare disorder characterized by weight loss, necrolytic migratory erythema (NME), diabetes, stomatitis, and diarrhea. We identified 21 patients with the glucagonoma syndrome evaluated at the Mayo Clinic from 1975 to 1991. Although NME and diabetes help identify patients with glucagonomas, other manifestations of malignant disease often lead to the diagnosis. If the diagnosis is made after the tumor is metastatic, the potential for cure is limited. The most common presenting symptoms of the glucagonoma syndrome were weight loss (71%), NME (67%), diabetes mellitus (38%), cheilosis or stomatitis (29%), and diarrhea (29%). Although only 8 of the 21 patients had diabetes at presentation, diabetes eventually developed in 16 patients, 75% of whom required insulin therapy. Symptoms other than NME or diabetes mellitus led to the diagnosis of an islet cell tumor in 7 patients. The combination of NME and diabetes mellitus led to a more rapid diagnosis (7 months) than either symptom alone (4 years). Ten patients had diabetes mellitus before the onset of NME. No patients had NME clearly preceding diabetes mellitus. Increased levels of secondary hormones, such as gastrin (4 patients), vasoactive intestinal peptide (1 patient), serotonin (5 patients), insulin (6 patients, clinically significant in 1 only), human pancreatic polypeptide (2 patients), calcitonin (2 patients) and adrenocorticotropic hormone (2 patients), contributed to clinical symptoms leading to the diagnosis of an islet cell tumor before the onset of the full glucagonoma syndrome in 2 patients. All patients had metastatic disease at presentation. Surgical debulking, chemotherapy, somatostatin, and hepatic artery embolization offered palliation of NME, diabetes, weight loss, and diarrhea. Despite the malignant potential of the glucagonomas, only 9 of 21 patients had tumor-related deaths, occurring an average of 4.91 years after diagnosis. Twelve patients were still alive, with an average age follow-up of 3.67 years.
 ...
PMID:The glucagonoma syndrome. Clinical and pathologic features in 21 patients. 860 27

Endocrine disorders associated with diabetes mellitus are described. When blood glucose control deteriorates, observed endocrine abnormalities are as follows. 1) Blood GH levels increase. This elevation is small but enough to disturb insulin secretion and glucose metabolism. Plama insulin-like growth factor-1 levels decrease in spite of their strong relation with diabetic retinopathy. 2) Blood thyroid hormones show the similarity with low T3 syndrome. 3) Hyporeninemic hypoaldosteronism occurs especially with patients who have hypertension or moderate diabetic complications. 4) Plasma pancreatic glucagon levels are elevated. Amino acids induce hypersecretion but hypoglycemia fails to response normally. Glucose administration shows impaired inhibition or paradoxical hypersecretion. 5) Other plasma levels of pancreatic hormones such as gastrin, secretin, motilin and somatostatin are usually elevated.
 ...
PMID:[Endocrine disorders associated with impaired glucose tolerance]. 891 25

During a prospective screening study for recto-sigmoid adenomatous polyps, the influence of the following risk factors was evaluated: age; gender; body mass index; heredity for colorectal malignancy; diabetes; hypertension; constipation; previous gastric surgery; previous gastric acid inhibition; alcohol and cigarette consumption; serum cholesterol; serum triglycerides; and serum gastrin. Screening fibre-sigmoidoscopy of 665 patients (aged between 50 and 60 years) at a clinical rehabilitation centre for gastrointestinal and metabolic diseases showed that 146 had one or several adenomas. The study population was overweight by a mean of about 15%. Comparison of those with and those without adenoma using univariate analysis, showed that the group with adenomas had higher serum triglyceride values, drank more alcohol on a regular or excessive basis, were more frequent smokers, and had a tendency to raised fasting serum glucose. In a multivariate analysis, age, high serum triglycerides and high alcohol consumption were risk factors for recto-sigmoid adenomas. The risk factor profile identified in this study may help in the selection of individuals for screening sigmoidoscopy from a similar background population. It also identifies target conditions for primary prevention of colorectal neoplasia.
 ...
PMID:The risk factor profile of recto-sigmoid adenomas: a prospective screening study of 665 patients in a clinical rehabilitation centre. 916 11

Psammomys obesus fed a high-calorie diet develops a NIDDM-like syndrome. The use of reverse-phase high-performance liquid chromatography (HPLC) to study Psammomys insulin biosynthesis and release revealed a very delayed elution time for the Psammomys insulin peak appearing near the position of human proinsulin. This unusual peak was initially thought to represent partially processed insulin on the basis of its molecular size and susceptibility to trimming by carboxypeptidase B (CpB). However, the findings of an active carboxypeptidase E (CpE) enzyme and the normal amidated forms of gastrin and cholecystokinin octapeptide (CCK-8) in Psammomys tissues were inconsistent with CpE-related aberrant processing of insulin. Moreover, amino acid sequencing of the delayed peak of Psammomys insulin revealed fully processed insulin with amino acid sequence as predicted by the cDNA. The unique presence of a B-30 phenylalanine residue, resulting in an increased hydrophobicity of the insulin molecule, probably underlies the marked delay in elution time on HPLC. The unusual structure of Psammomys insulin does not appear to contribute to the proinsulinemia observed in diabetic Psammomys since the HPLC-purified molecule did not inhibit PC1 and PC2 convertase activities in an in vitro assay.
Diabetes 1997 Jun
PMID:Characterization of the unusual insulin of Psammomys obesus, a rodent with nutrition-induced NIDDM-like syndrome. 916 65

Gastrin influences polyamine synthesis in the enterocytes, which can lead to increased DAO activity. In diabetics with autonomic neuropathy (AN), a higher than normal gastrin concentration was found. However, in diabetics with enteropathy, a low level of plasma DAO activity was discovered. The purpose of this study was to investigate gastrin secretion and to evaluate DAO activity after i.v. injection of heparin in a group of diabetics with AN. Group I consisted of 12 diabetics with AN, group II 20 patients with diabetes without any complications and group III (the control group) 20 patients without diabetes. It was discovered that basal gastrin concentrations were significantly greater in group I (147 pg/ml +/- 76.5) that in groups II (78 pg/ml +/- 55.5)(p < 0.01) and III (61.5 pg/ml +/- 42.6)(p < 0.01). DAO activity was at its lowest in group I (247.1 pmol/min/ml +/- 104.8) and it was significantly different from group II (441 pmol/min/ml +/- 225.9)(p < 0.001) and III (540.7 pmol/min/ml +/- 171.1)(p < 0.001). There were no differences in the mean values of gastrin and DAO activity between group II and III. In group I low DAO activity was accompanied by a proportionally high concentration of the basal gastrin value (r = 0.567). In conclusion, in diabetics with AN, low postheparin plasma DAO activity was accompanied by a high basal gastrin value.
 ...
PMID:[Gastrinemia and heparin stimulated secretion of diamine oxidase on the course of diabetic autonomic neuropathy]. 929 89

Cobalamin (vitamin B12) deficiency is more common in the elderly than in younger patients. This is because of the increased prevalence of cobalamin malabsorption in this age group, which is mainly caused by (autoimmune) atrophic body gastritis. Cobalamin supplementation is affordable and nontoxic, and it may prevent irreversible neurological damage if started early. Elderly individuals with cobalamin deficiency may present with neuropsychiatric or metabolic deficiencies, without frank macrocytic anaemia. An investigation of symptoms and/or signs includes the diagnosis of deficiency as well as any underlying cause. Deficiency states can still exist even when serum cobalamin levels are higher than the traditional lower reference limit. Cobalamin-responsive elevations of serum methylmalonic acid (MMA) and homocysteine are helpful laboratory tools for the diagnosis. The health-related reference ranges for homocysteine and MMA appear to vary with age and gender. Atrophic body gastritis is indirectly diagnosed by measuring serum levels of gastrin and pepsinogens, and it may cause dietary cobalamin malabsorption despite a normal traditional Schilling's test. The use of gastroscopy may also be considered to diagnose dysplasia, bacterial overgrowth and intestinal villous atrophy in healthy patients with atrophic body gastritis or concomitant iron or folic acid deficiency. Elderly patients respond to cobalamin treatment as fully as younger patients, with complete haematological recovery and complete or good partial resolution of neurological deficits. Chronic dementia responds poorly but should, nevertheless, be treated if there is a metabolic deficiency (as indicated by elevated homocysteine and/or MMA levels). Patients who are at risk from cobalamin deficiency include those with a gastrointestinal predisposition (e.g. atrophic body gastritis or previous partial gastrectomy), autoimmune disorders [type 1 (insulin-dependent) diabetes mellitus and thyroid disorders], those receiving long term therapy with gastric acid inhibitors or biguanides, and those undergoing nitrous oxide anaesthesia. To date, inadequate cobalamin intake has not proven to be a major risk factor. Intervention trials of cobalamin, folic acid and pyridoxine (vitamin B6) in unselected elderly populations are currently under way.
 ...
PMID:Age-related changes in cobalamin (vitamin B12) handling. Implications for therapy. 957 92

The antral endocrine cells were investigated in nonobese diabetic (NOD) mice by means of immunohistochemistry, image analysis, and radioimmunoassays (RIA). As controls BALB/CJ mice of the same age and sex as the NOD mice were used. The number of gastrin- and somatostatin-immunoreactive cells was significantly decreased in both prediabetic and diabetic mice. There was no statistical difference between the NOD mice and controls regarding the serotonin-immunoreactive cells. Somatostatin levels as revealed by RIA in the antrum of both prediabetic and diabetic NOD mice were lower than those of the controls. There was no statistical difference in the level of antral gastrin between NOD mice and the controls. It was concluded that the changes in antral cells are primary to the onset of diabetes, and that the abnormalities observed in the antral cells in an animal model for diabetes type I might have relevance for the upper gastrointestinal dysfunction displayed in human diabetes.
 ...
PMID:Antral endocrine cells in nonobese diabetic mice. 959 Apr 18

The endocrine cells in the duodenum of pre-diabetic and diabetic female non-obese diabetic (NOD) mice aged 22-24 weeks were studied by means of immunohistochemistry and computed image analysis as well as by radioimmunoassays of tissue extracts. As controls, 12 female BALB/cJ mice of the same age as NOD mice were used. The number of secretin-immunoreactive cells increased in diabetic but not in pre-diabetic NOD mice. The level of extractable secretin was higher in both pre-diabetic and diabetic NOD mice. The number of GIP-, CCK/gastrin-, and serotonin-immunoreactive cells was significantly reduced in both pre-diabetic and diabetic NOD mice. There was no statistical difference in the number of somatostatin-immunoreactive cells between the NOD mice and controls. The level of GIP was higher and gastrin was lower in NOD mice compared to controls. There was no statistical difference in the somatostatin level between the NOD mice and controls. The cell secretory index was elevated in all the endocrine cell types except CCK/gastrin cells. It has been suggested that some of the changes in the duodenal endocrine cells could be attributed to the diabetes state, but most of the changes seem to take place before the onset of diabetes. The abnormalities in the duodenal endocrine cells observed here in an animal model for diabetes type I might have relevance for the gastrointestinal dysfunction displayed in human diabetes.
J Diabetes Complications
PMID:Abnormalities of small intestinal endocrine cells in non-obese diabetic mice. 964 40

Overt diabetic gastroparesis is a rare long-term complication of diabetes, probably resulting from autonomic neuropathy of vagus nerve. It is now clear that neural damage plays a pivotal role in the pathogenesis of the disease. Some studies showed high basal gastrin levels in patients with diabetic gastroparesis, but the clinical meaning of this observation is still unclear. We report the case of a young woman with Insulin Dependent Diabetes Mellitus (IDDM) who was referred to evaluate nausea and vomiting associated to ketoacidosis. Our hypothesis of autonomic neuropathy with gastroparesis was confirmed. We observed a progressive increase in fasting gastrin concentration (20-fold normal values) in the absence of any clinical and laboratory signs of Zollinger-Ellison (ZE) syndrome. The increasing vomiting induced a severe state of cachexia, which required total parenteral nutrition for a long period. All therapeutic approaches were unsuccessful, and the patient rapidly died, suggesting a possible link between the severity of the clinical picture and the gastrin plasma levels.
 ...
PMID:Extreme but asymptomatic hypergastrinemia with gastroparesis in a young woman with insulin dependent diabetes mellitus. 964 55

Infection by viral or bacterial pathogens has been suspected in playing a role in the development of autoimmune thyroid disease. Because Helicobacter pylori might be involved in the development of nongastrointestinal conditions such as rosacea, ischemic heart disease, and diabetes mellitus, we evaluated the prevalence of H. pylori infection in patients with autoimmune thyroid disease. Fifty-nine patients with autoimmune thyroid disease were included: autoimmune atrophic thyroiditis (n=21), Hashimoto's thyroiditis (n=18), and Graves' disease (n=20). Twenty patients with nontoxic multinodular goiter served as controls for nonautoimmune thyroid disease, and 11 patients with Addison's disease served as controls for nonthyroid endocrine autoimmune disease. The levels of anti-H. pylori immunoglobulin G (IgG) were determined, and a radiolabeled urea breath test were performed. The prevalence of H. pylori infection was markedly increased in the patients with autoimmune atrophic thyroiditis (85.7%), compared with the controls with nontoxic multinodular goiter (40%) and Addison's disease (45.4%). Infection by H. pylori resulted in increased levels of gastrin, pepsinogen I, and pepsinogen II in the H. pylori-positive groups, compared with the H. pylori-negative groups. A positive linear regression was found between the levels of microsomal autoantibodies and those of anti-H. pylori IgG in patients with autoimmune atrophic thyroiditis (n=21; r=0.79; p < 0.01). Finally, and although the overall prevalence of H. pylori infection was not increased, the anti-H. pylori IgG levels and the results from the breath test were higher in the patients with Graves' disease and Hashimoto's thyroiditis patients than in the controls. Clearly, the prevalence of H. pylori infection is increased in autoimmune atrophic thyroiditis and results in abnormalities of gastric secretory function. The strong relation between the levels of anti-H. pylori IgG and the levels of microsomal antibodies suggests that H. pylori antigens might be involved in the development of autoimmune atrophic thyroiditis or that autoimmune function in autoimmune atrophic thyroiditis may increase the likelihood of H. pylori infection.
 ...
PMID:Helicobacter pylori infection is markedly increased in patients with autoimmune atrophic thyroiditis. 964 6


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>