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)

The gastric inhibitory polypeptide (GIP) is the main hormone of the incretin type acting on the entero-insular axis. It is released after fat, glucose or meal ingestion. The variations of this secretion are described in obesity and in some pancreatic and gastrointestinal diseases: it is increased in maturity onset diabetes mellitus, obesity or duodenal ulcer, variable according to the food taken and the severity of the pancreatic lesion in chronic pancreatitis and cystic fibrosis, normal in insulinoma and decreased in celiac disease. The impaired absorption of the food-stuffs and the defective feed-back regulation of GIP secretion by insulin are the major causes of these variations. To a lesser degree, gastric acid secretion, gastric emptying and vagal control may also influence GIP secretion.
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PMID:Clinical aspects of GIP secretion. 628 Apr 23

A case of polymyositis associated with scleroderma, adult coeliac disease, diabetes mellitus and IgA nephropathy is reported in a 33-year-old male.
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PMID:Polymyositis associated with several immunological disorders. 652 90

The DR-locus controlled B-cell antigens were studied in 163 unrelated Spanish coeliac children and 68 families of this group, nine of them with more than one coeliac patient, to obtain more information about the association between these antigens and coeliac disease. The results show that the most common coeliac phenotypes are DR3/DR7, DR7/DR5, DR3/other DR, and DR3/DR3. The family study confirmed the segregation of the disease with the above mentioned phenotypes. In eight of the nine multiple case families, all coeliac children shared both HLA-DR antigens. These findings make it unlikely that a single dominant gene linked to HLA-DR controls the susceptibility to coeliac disease. The phenotypes in the patients were not distributed according to the Hardy-Weinberg equilibrium. Thus, a model based on one recessive susceptibility gene linked to HLA-DR is not probable either. The complexity of the genetics of coeliac disease and some of the features shared with the HLA-DR pattern in juvenile insulin-dependent diabetes are discussed.
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PMID:HLA-DR phenotypes in Spanish coeliac children: their contribution to the understanding of the genetics of the disease. 660 84

Diabetic diarrhea and steatorrhea occur predominantly in young adult males who have juvenile-onset diabetes mellitus complicated by neuropathy. The presentation is often severe, with nocturnal or postprandial watery diarrhea and tenesmus. Massive malabsorption of fat may occur; however, malabsorption of other nutrients and generalized wasting are quite rare. Because the symptoms are relatively refractory to treatment, it is important to rule out other, more easily treatable causes of this presentation. Bacterial overgrowth, exocrine pancreatic insufficiency, and celiac disease are also associated with diabetes mellitus and can mimic this process. Although the mechanism of diabetic diarrhea and steatorrhea remains unclear, neuropathy, gastrointestinal motor abnormalities, bacterial overgrowth, and bile acid abnormalities have been implicated in the pathogenesis.
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PMID:Small intestinal manifestations of diabetes mellitus. 665 61

The clinical features of 24 patients with coeliac disease and insulin-dependent diabetes mellitus were reviewed. The HLA types of 17 of these patients were compared with those of 44 normal subjects, 49 patients with diabetes only and 58 patients with coeliac disease only. The diagnosis of coeliac disease was made after the diagnosis of diabetes in 14 patients, before diabetes in five and simultaneously in five. In established diabetics, coeliac disease was recognized relatively late (mean age 31 years) but the average duration of symptoms attributable to coeliac disease prior to a jejunal biopsy was five months. Gluten restriction was generally followed by a marked improvement in diabetic control. The frequency of HLA-DR3 in patients with coeliac disease and diabetes mellitus (88 per cent), patients with coeliac disease only (88 per cent), and patients with insulin-dependent diabetes mellitus only (69 per cent), was significantly greater than in normal subjects (44 per cent). The subtype of diabetes related to DR4/B15 does not appear to predispose to coeliac disease. The mechanism of the association between coeliac disease and insulin-dependent diabetes is discussed and the importance of coeliac disease in the differential diagnosis of 'diabetic diarrhoea' is emphasized.
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PMID:Coeliac disease and diabetes mellitus: a study of 24 patients with HLA typing. 675 30

A test of linkage that is exact even in small samples is developed for multiple case families, together with large-sample theory for estimation and supplementary tests. Hemochromatosis, insulin-dependent diabetes, and celiac disease are compatible with an intermediate model biased toward recessivity on the penetrance scale, whereas multiple sclerosis favors dominance and unlinked modifiers. Alternatives to the model are complex, and comparison of affected sib pairs with larger sets of relatives provides no critical evidence of epistasis. Problems of sampling and inference are discussed.
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PMID:An exact linkage test for multiple case families. 688 87

The features of 41 proven or suspected cases of pancreatic glucagonoma and one possible case of renal glucagonoma have been reviewed. Glucagonoma is one form of islet cell neoplasm and involves pancreatic alpha cells. It may occur more frequently in women and is more likely to be malignant than insulinoma. Patients may present with glucose intolerance, an erythematous, eczematous dermatitis, glossitis, stomatitis, vaginitis and unexplained weight loss. Anemia, hypoproteinemia, hypoaminoacidemia and hypolipidemia may also be present. Malignant glucagonoma metastasizes frequently to liver. An evaluation for possible glucagonoma may be considered in a patient with the characteristic eczematous dermatitis, glossitis or stomatitis and glucose intolerance, an unusual or atypical history of diabetes mellitus, or hepatomegaly with other characteristics of glucagonoma. Initial evaluation may include measurement of fasting plasma glucagon concentration, and an oral glucose tolerance test with measurements of plasma glucose and glucagon levels. Extreme fasting hyperglucagonemia, and a paradoxical rise in plasma glucagon concentrations after glucose ingestion should strongly suggest the presence of glucagonoma. Radiographic demonstration of pancreatic glucagonoma is best carried out by celiac arteriography. Surgical excision of the tumor is the treatment of choice. Nonresectable lesions may respond to chemotherapy with streptozotocin. Treatment for the various dermatologic or metabolic complications of glucagonoma which include glucose intolerance, hypoproteinemia, hypocholesterolemia and anemia may not be satisfactory. Glucose intolerance is usually mild and may be adequately treated with dietary or insulin therapy. Rarely, glucagonoma with massive destruction of the pancreas or other factors may induce severe glucose intolerance. In contrast, the anemia, skin rash, and hypoproteinemia do not respond to conservative therapies tested thus far. Glucagonoma is a model for studying the importance of glucagon in causing the hyperglycemia of diabetes mellitus. Study of patients with glucagonoma does suggest that glucagon has some role in the etiology of hyperglycemia in diabetic states; however, as in studies on diabetes, investigations on glucagonoma do not demonstrate that glucagon has a primary role in producing severe glucose intolerance.
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PMID:Clinical and metabolic aspects of glucagonoma. 698 81

The presence of autoantibodies detected by immunofluorescence to single endocrine cells, of human duodenum is described in three groups of patients and two control groups. Of 173 coeliac cases, four had GIP cell antibodies, one had secretin cell antibodies and twenty-one reacted with both cell types. Of twelve tropical sprue sera, four reacted with the same two cells. Among fifty elderly diabetics treated with hypoglycaemic drugs, seven sera gave a positive cytoplasmic IFL on duodenal substrate. Four were identified as GIP cells by use of the appropriate hormone antiserum and three reactions were against cells distinct from those stained by anti-GIP, -secretin, -somatostatin, -glucagon and -gastrin. Additional gut hormone antisera will have to be tested to identify these APUD cells. Thirty blood donors and seventy-three sera from autoimmune endocrine patients gave entirely negative results on unfixed cryostat sections of duodenal mucosa. Although impaired GIP and secretin responses have been reported in coeliac disease, and abnormal GIP values were found in Type II diabetes, there is as yet no data to correlate these metabolic dificiencies with the presence of endocrine cell antibodies in the serum. These studies are in progress.
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PMID:Autoantibodies to duodenal gastric-inhibitory-peptide (GIP) cells and to secretin (S) cells in patients with coeliac disease, tropical sprue and maturity-onset diabetes. 700 90

The incidences of symptomatic coeliac disease (CD) and pyloric stenosis (PS) in children born 1960-1979 were studied retrospectively in Northern Finland. The total incidence of CD was 42.3, and of PS 122.7 per 100,000 live births. The figure for CD was lower than in studies from other industrial countries during the same period. The incidence of CD was highest in the early 1970s, and has decreased significantly, at least in children under two years of age, during the late 1970s. In the city of Oulu the incidence of CD was significantly higher than that in the surrounding countryside. Active search, with small intestinal biopsies, should reveal over 90% of cases with CD before the age of two years. Of 78 children diagnosed as having CD during the observation period, 75% were breast-fed for less than three months, 18% had signs of allergy at the time of diagnosis and seven % had IgA deficiency. In four patients CD was associated with diabetes. The incidence of PS varied from 107 per 100,000 live births in the early 1960S to 153 per 100,000 in the late 1960s. No significant seasonal variance was observed in the analysis of 226 children with PS in the study.
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PMID:The incidence of coeliac disease and pyloric stenosis in children in Northern Finland. 713 81

A case of coeliac disease accompanied by serum-negative rheumatoid arthritis and (subsequently) by diabetes mellitus is described. The appearance of a similar clinical and sympatomatological enteric and articular picture in one of the patient's brothers is seen as evidence that the link between the components of the three-fold syndrome is to be found in common genetic factors, with an onset in the form of a cellular and biohumoral immunological disorder.
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PMID:[Celiac disease: association with rheumatoid arthritis and diabetes mellitus. Apropos of a clinical case]. 743 43


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