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)

A 59 year old woman with insulin-dependent diabetes mellitus and chronic diarrhea was found to have mild steatorrhea, selective plasma IgA deficiency and adrenal insufficiency. Significant adrenal secretion of corticosteroids resulted only after prolonged stimulation with large doses of exogenous ACTH. Plasma ACTH levels were not elevated during clinical adrenal insufficiency or after metyrapone administration but did respond normally to vasopressin and insulin-induced hypoglycemia. These studies were interpreted as showing both primary adrenal insufficiency and impaired pituitary reserve for ACTH secretion in response to the feedback stimulus. No deficiency was found in secretion of other pituitary tropic hormones. Jejunal biopsy showed a lack of IgA-containing plasma cells. With cortisone replacement, diarrhea subsided and a malabsorption pattern on a film of the small bowel was no longer seen. IgA deficiency has been noted frequently with steatorrhea but rarely with diabetes and only once previously with adrenal insufficiency.
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PMID:Atypical adrenal insufficiency with failure of the pituitary feedback receptor. A case with associated diabetes mellitus and selective IgA deficiency with steatorrhea. 17 48

The effect of a new complex oligosaccharide exhibiting potent inhibitory action on alpha-glucoside hydrolases on intestinal absorption of sucrose in man was tested by constant in vivo perfusion of the jejunum. At concentrations of 4.65 or 15.5 X 10(-6)M the alpha-glucosidehydrolase inhibitor (alpha-GHI) markedly inhibited absorption of glucose from sucrose and absorption of sodium and water. Oral administration of the alpha-GHI resulted as well in depression of solute, sodium, and water absorption. This new compound can serve as an interesting tool to induce carbohydrate malabsorption by inhibition of final digestion and may possibly be of beneficial therapeutic effect in dietary control of diabetes or obesity.
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PMID:Effect of alpha-glucosidehydrolase inhibition and intestinal absorption of sucrose, water, and sodium in man. 38 40

The effect of a new complex oligosaccharide (Bay g 5421) of microbial origin on human intestinal alpha-glucosidehydrolase activity was tested in mucosal homogenate from human small bowel biopsy specimens. The alpha-glucosidehydrolase inhibitor (alpha-GHI) exerted a potent inhibitory effect on glucoamylase, sucrase, and maltase, was minimally effective on isomaltase, and did not affect trehalase and lactase activity. Kinetic analysis revealed a fully competitive type of inhibition with a Ki of 1.3 x 10(-6) M; thus the inhibitor had a 15,000-fold higher affinity to the enzyme sucrase than its natural substrate sucrose. The new compound may prove to be useful in the study of carbohydrate maldigestion and malabsorption and may possibly be of therapeutic benefit in diabetes and obesity.
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PMID:Inhibition of human intestinal alpha-glucosidehydrolases by a new complex oligosaccharide. 44 22

Follow-up of 25 cases of pancreatitis in childhood ascertained from the Hospital Activity Analysis in Newcastle and Wales showed that the majority of the children thrived after their illness. Only one child died. Only 2 children developed diabetes mellitus and 3 had significant malabsorption. There were 13 idiopathic cases (9 acute, 4 chronic relapsing), 3 of which were obese girls of pubertal age. It is speculated that obesity, puberty and female sex together may predispose to acute pancreatitis.
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PMID:Pancreatitis in childhood. 46 Dec 79

Experimentally diabetic rats have low serum 1,25-dihydroxyvitamin D, intestinal malabsorption of calcium, secondary hyperparathyroidism, and bone loss. To examine the hypothesis that abnormalities similar to those in the diabetic rat might explain human diabetic osteopenia, we studied calcium metabolism in 40 healthy control and 82 diabetic patients aged 18--75 yr [47 untreated: fasting plasma glucose (mean +/- SE), 267 +/- 8 mg/dl; 19 treated but hyperglycemic: glucose 305 +/- 24 mg/dl; 16 treated and in better control: glucose, 146 +/- 8 mg/dl]. Serum total calcium, ionic calcium, immunoreactive parathyroid hormone (Arnaud method, GP-1M and CH-12M antisera), 25-hydroxyvitamin D (Haddad method), and 1,25-dihydroxyvitamin D (Lambert method) concentrations were normal in all 3 groups of diabetics and were not significantly different from values in the control group. We determined absorption of calcium from the intestine by a double isotope method (100 mg Ca carrier; normal range, 40--80%) in 11 control and 13 untreated, uncontrolled diabetics (mean plasma glucose, 285 +/- 17 mg/dl). Absorption of calcium in controls was 60 +/- 3% and in diabetics was 56 +/- 3% (not significantly different). We have found no derangement of calcium metabolism in adults with insulin-requiring juvenile- and adult-onset diabetes regardless of treatment status. The experimental diabetic rat model does not appear to be useful for determining the pathogenesis of adult human diabetic osteopenia.
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PMID:Calcium homeostasis in diabetes mellitus. 46 80

The authors discuss the main features of the complex pathophysiology of patients subjected to duodenocephalopancreatectomy, and particularly the difficulties inherent in clinical assessment of the digestive and metabolic impairment consequent upon the duodeno-gastro-pancreatic mutilation. Out of a total of 57 cases of this description, they singled out for recheck 23 patients who had undergone duodenocephalopancreatectomy not less than six months and not more than seven years before (chronic pancreatitis, 11 cases; various malignancies of the periampullar area, 10 cases; Zollinger-Ellison syndrome, 1 case; retroperitoneal lymphoma, 1 case). Seventy-six per cent of patients who had been gainfully employed were able to resume their jobs after surgery. Steatorrhea, assessed in terms of fecal fats, was present in all cases; notwithstanding, 70% of the patients gained weight (average increase 7 kg). All patients were on enzyme replacement therapy. Only 4% developed diabetes, and none developed postoperative peptic ulcers. Conversely there was a high incidence (65%) of bone structure reshuffling, signally osteoporosis, probably imputable to steatorrhea and vitamin D malabsorption, plus the often associated increase of serum alkaline phosphatase activity.
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PMID:[The biological results of duodenocephalopancreatectomy. Clinical evaluations based on a long-term follow-up]. 53 2

Three persons in a kindred of 43 had variable expression of a syndrome consisting of immunoglobulin A deficiency, diabetes mellitus, malabsorption, and a common HLA haplotype. Findings from the proband included life-threatening malabsorption; idiopathic intestinal mucosal atrophy with infalmmation; IgA deficiency and antibodies to multiple endocrine organs; insulin-dependent diabetes mellitus; and the major histocomptability antigens HLA-A2, B8, and DW3. In addition to the described syndrome other conditions present in the family include Graves' disease, vitiligo, hypocomplementemia, rheumatic fever, multiple sclerosis, and a high frequency of antibodies to endocrine tissue. Since Graves' disease, diabetes mellitus, and idiopathic Addison's disease have all been described in association with HLS-B8 and DW3, we believe that the occurrence of these diseases in this family suggests that a single immune response gene or gene complex is linked with HLA-B8 and DW3.
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PMID:A syndrome of immunoglobulin A deficiency, diabetes mellitus, malabsorption, a common HLA haplotype. Immunologic and genetic studies of forty-three family members. 57 75

Information from 72 patients from 7 families in England and Wales confirms that hereditary pancreatitis is inherited as an autosomal dominant conditions with limited penetrance. The degree of penetrance is approximately 80%. These patients have had recurrent attacks of abdominal pain starting from childhood or young adult life. The mean age of onset in the 7 families studied was 13.6 years. There were two peaks, with maximum numbers at 5 years and 17 years. The second peak was thought to represent genetically susceptible individuals having pain brought on by alcohol rather than representing evidence of genetic heterogeneity. Five of the 7 families had members with both childhood and adult ages of onset. Only 4 patients out of 72 had life-threatening disease and in the majority of cases the attacks of pain were of nuisance value only. Hereditary pancreatitis was implicated in only 1 patient's death and this was not definite. Patients appear to get better after a period of symptoms usually as they approach middle age, or after a severe attack. In older patients alcohol, emotional upsets, and fatty food appear to precipitate attacks. Pancreatic insufficiency (5.5%), diabetes mellitus (12.5%), pseudocysts (5.5%), and haemorrhagic pleural effusion are uncommon complications. Portal vein thrombosis occurred definitely in 2 patients and was suspected in 3 others. Carcinoma of the pancreas was not found in any of 72 patients studied in detail; however, 2 members from a family not visited personally had chronic pancreatitis and malabsorption going on to carcinoma. They may have suffered from a different disease. Genetic linkage information was too slight for many definite conclusions. However, there was no suggestion of linkage with any of the markers tested.
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PMID:Hereditary pancreatitis in England and Wales. 67 83

Fourteen adults in whom diabetes mellitus and coeliac disease coexist, are described. In no patient was coeliac disease diagnosed (biopsy proven) before the age of 28 years. Diabetes was recognized before coeliac disease in all except one. Diabetic control was very unstable and hypoglycaemia particularly troublesome before treatment with a gluten free diet. Following gluten restriction, insulin requirement increased in six patients, and diabetic control became more stable. Diarrhoea due to coeliac disease in a patient with coexisting diabetes, may be mistakenly diagnosed as 'diabetic diarrhoea'. However, certain clinical and laboratory features should arouse suspicion that the diarrhoea is not of diabetic origin. These included a history of gastrointestinal symptoms preceding the diagnosis of diabetes, the occurrence of repeated hypoglycaemia, absence of neuropathy, anaemia, low serum folate, low serum albumin and a malabsorption pattern on small bowel radiography. A definitive diagnosis of coeliac disease can be made only jejunal biopsy. The opportunity to diagnose coeliac disease in adult diabetics will usually fall to the diabetologist and wider use of jejunal biopsy in diabetics with chronic or recurrent diarrhoea is suggested.
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PMID:Diabetes mellitus and coeliac disease: a clinical study. 67 52

Since kappa-chain deficiency is an unusual condition, we studied the clinical and laboratory findings in a patient with this deficiency. The patient had cystic fibrosis with concurrent malabsorption, diabetes mellitus and IgA deficiency. The serum levels of IgM and IgG were 0.85 and 7.22 mg per milliliter, respectively. Kappa type IgM and IgG was not present in serum and external secretions; gamma, mu and lambda chains were probably polyclonal in character. Antibodies against kappa chains were not detected in either the patient or the mother. Plasma cells containing kappa-type immunoglobulins were absent in jejunum samples and bone marrow; kappa-chainbearing B lymphocytes could not be detected in blood and bone marrow. The serum of one of the patient's sisters contained trace amounts of kappa-type immunoglobulins. The patient displays a complete absence of kappa-type immunoglobulins, probably owing to a genetic defect.
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PMID:Kappa-chain deficiency. An immunoglobulin disorder. 81 19


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