Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011854 (type 1 diabetes)
 20,749 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In this study we report, for the first time, the molecular analysis of HLA-DR and DQ gene frequencies in a large cohort of well-characterized type 1 (insulin-dependent) diabetes mellitus (IDDM) patients (n = 72), and ethnically matched controls (n = 59) collected in sub-Saharan Africa. High molecular mass DNA was prepared and analysed in Southern blots and by oligonucleotide typing. We have shown a strong positive association between IDDM and the Asp 57- DQB1 allele *0201 (DQw2). A rare DR4, DQw2 haplotype was also identified at high frequency in the IDDM cohort. We can now confirm that the association between Asp 57- DQB1 alleles and IDDM, previously reported in ethnically diverse cohorts collected in Western Europe, North America, and South Asia, is also present in an IDDM cohort collected in Africa.
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PMID:Identification of genetic susceptibility loci for insulin-dependent diabetes in Sudan. 135 6

A paradoxical growth hormone (GH) response to thyrotropin-releasing hormone (TRH) has been observed in type 1 diabetic patients and was hypothetically attributed to a reduced hypothalamic somatostatin tone. We have previously reported that corticotropin-releasing hormone (CRH) inhibits GH response to growth hormone-releasing hormone (GHRH) in normal subjects, possibly by an increased release of somatostatin. To study the effect of CRH on anomalous GH response to TRH, we tested with TRH (200 micrograms intravenously [IV]) and CRH (100 micrograms IV) + TRH (200 micrograms IV) 13 patients (six males and seven women) affected by insulin-dependent diabetes mellitus. A paradoxical GH response to TRH was observed in seven of 13 patients, one man and six women. In these subjects, the simultaneous administration of CRH and TRH significantly reduced the GH response to TRH, as assessed by both the maximal GH mean peak +/- SE (2.18 +/- 0.67 v 9.2 +/- 1.26 micrograms/L, P less than 0.005) and the area under the curve (AUC) +/- SE (187 +/- 32 v 567 +/- 35 micrograms.min/L, P less than .001). CRH had no effect on TRH-induced thyroid-stimulating hormone (TSH) release. Our data demonstrate that the paradoxical GH response to TRH in patients with type 1 diabetes mellitus is blocked by CRH administration. This CRH action may be due to an enhanced somatostatin release. Our data also show that exogenous CRH has no effect on TSH response to TRH, thus suggesting the existence of separate pathways in the neuroregulation of GH and TSH secretion.
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PMID:Corticotropin-releasing hormone inhibition of paradoxical growth hormone response to thyrotropin-releasing hormone in insulin-dependent diabetics. 135 81

Atherosclerosis, presenting as macrovascular complications of diabetes mellitus, produces approximately 80% of all diabetic mortality, whether the patient has Type I insulin-dependent diabetes (IDDM) or Type II non-insulin dependent diabetes mellitus (NIDDM). Specifically, 75% of this atherosclerotic macrovascular mortality flows as the outcome of coronary atherosclerosis, which is increased approximately two-fold in men and four-fold in women with diabetes as compared with otherwise matched populations with entirely normal carbohydrate tolerance. The remaining 25% of this atherosclerotic mortality in patients with diabetes mellitus is the result either of accelerated cerebrovascular or of peripheral vascular complications of diabetes, both of which are increased four-fold and five-fold, respectively, in patients with diabetes mellitus, regardless of type. Furthermore, atherosclerosis is the principal cause of hospitalizations for patients with diabetes mellitus. Admissions for this complication account for approximately 77% of total hospitalizations for diabetes owing to complications. Aside from mortality data alone, atherosclerosis is obviously a leading cause of diabetic disability, since it produces patients who are chronic cardiovascular, peripheral or cerebrovascular cripples, perhaps for many years before their ultimate demise. Small blood vessel or microvascular complications of diabetes mellitus, while formerly thought to be the end-stage in the unfolding of the diabetic process, do not appear to have the potential for mortality as do the atherosclerotic large blood vessel complications.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effective treatment of hypertension in patients with diabetes mellitus. 135 76

Calcitonin concentration (CT) was measured in 52 children with insulin-dependent diabetes (IDDM). All the patients studied were divided into three groups. The first group consisted of children with freshly diagnosed diabetes remaining in the condition of ketonemic acidosis. The second group was composed of children with the well controlled diabetes during the first two years od duration of the disease. The third group included the patients with poorly controlled diabetes of the duration longer than ten years having the accompanying vascular complications. The control values were determined in children without metabolic disturbances of either diabetic or other origin. CT concentration was significantly elevated both in the patients of the first group and those of the third group. In the second group the concentration of this hormone was close to normal. It is known that calcitonin participates in the homeostasis of calcium and is an important regulator of insulin secretion. The results obtained suggest that calcitonin may play a role both in the pathogenesis of diabetes and in developing of diabetic osteopenia.
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PMID:[Level of calcitonin in blood serum of children with insulin dependent diabetes]. 136 94

The levels of glycosylated hemoglobin (HbA1c) and glycosylated keratin were studied along the hair length in 17 patients with newly detected insulin dependent diabetes mellitus (IDDM) aged 7 to 33, in 14 patients with newly detected noninsulin dependent diabetes mellitus (NIDDM) aged 46 to 73, and in 41 healthy subjects. The level of glycosylated keratin in healthy hairs along the entire length varied within 0.094-0.124 mumol of fructosamine per 100 mg of hair. In 10 of 17 patients of the IDDM group measurements of glycosylated keratin levels made it possible to determine the time of appearance of diabetes mellitus, in 13 patients of the NIDDM group these levels along the entire hair length were elevated. The determination of these levels permitted the estimation of the time of appearance of IDDM. Its manifestation followed a long period (1-2 yrs.) of latent derangements of carbohydrate metabolism. In NIDDM patients the time of appearance of disease is difficult to determine because of the limited hair length and a long latent period of disease (over 2-3 yrs.).
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PMID:[Determining the time of diabetes mellitus onset by the level of glycosylated keratin in hair]. 138 Oct 94

The autoimmune phenomena associated with destruction of the beta cell in pancreatic islets and development of type 1 (insulin-dependent) diabetes mellitus (IDDM) include circulating islet cell antibodies. We have immortalized peripheral blood lymphocytes from prediabetic individuals and patients with newly diagnosed IDDM by Epstein-Barr virus transformation. IgG-positive cells were selected by anti-human IgG-coupled magnetic beads and expanded in cell culture. Supernatants were screened for cytoplasmic islet cell antibodies using the conventional indirect immunofluorescence test on cryostat sections of human pancreas. Six islet cell-specific B-cell lines, originating from a patient with newly diagnosed IDDM, could be stabilized on a monoclonal level. All six monoclonal islet cell antibodies (MICA 1-6) were of the IgG class. None of the MICA reacted with human thyroid, adrenal gland, anterior pituitary, liver, lung, stomach, and intestine tissues but all six reacted with pancreatic islets of different mammalian species and, in addition, with neurons of rat cerebellar cortex. MICA 1-6 were shown to recognize four distinct antigenic epitopes in islets. Islet cell antibody-positive diabetic sera but not normal human sera blocked the binding of the monoclonal antibodies to their target epitopes. Immunoprecipitation of 35S-labeled human islet cell extracts revealed that a protein of identical size to the enzyme glutamate decarboxylase (EC 4.1.1.15) was a target of all MICA. Furthermore, antigen immunotrapped by the MICA from brain homogenates showed glutamate decarboxylase enzyme activity. MICA 1-6 therefore reveal glutamate decarboxylase as the predominant target antigen of cytoplasmic islet cell autoantibodies in a patient with newly diagnosed IDDM.
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PMID:Human monoclonal islet cell antibodies from a patient with insulin-dependent diabetes mellitus reveal glutamate decarboxylase as the target antigen. 138 89

There has been a dramatic reduction in perinatal mortality and the incidence of malformation among the offspring of mothers with IDDM, current perinatal infant mortality now being no worse among mothers treated at the best Scandinavian diabetes centres than among non-diabetic mothers (Table 1). Such improvement is dependent upon very well organised care facilities and information services, close cooperation with the diabetic gravida, and the availability of good medical treatment that does not unduly burden her economy. Among diabetic women, careful planning for pregnancy improves the chances of giving birth to healthy offspring.
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PMID:[Pregnancy in insulin-dependent diabetic patients]. 138 22

Two patients, a 28-year-old male and a 70-year-old female, with chronic insulin dependent diabetes mellitus and evidence of autonomic neuropathy were studied using cortical evoked responses following esophageal balloon and electrical stimulation. Both patients had symptomatic gastroparesis, poor gastric emptying, and reduced gastroduodenal motility including abnormal results of scintigraphy and manometry. There was slowing of afferent vagal conduction but good evoked potential responses were recorded even though one patient could not feel electrical stimulation of either the proximal or distal esophagus. It is improbable that the gastric symptoms are due to an afferent autonomic neuropathy, but symptoms may well be related to impairment of motor vagal pathways. Nevertheless, afferent vagal pathways are involved in severe diabetes mellitus. The clinical significance of this delay in conduction velocity of afferent pathways remains to be established.
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PMID:Evidence of impaired afferent vagal function in patients with diabetes gastroparesis. 138 75

Current knowledge of the phenotype of mononuclear cells accumulating in pancreatic islets in insulin-dependent diabetes (IDDM) and factors determining their homing into the pancreas is limited. Therefore, a pancreas obtained at the onset of IDDM was studied in detail. Cryostat sections were stained for mononuclear cell types, T cell receptor subtypes, and adhesion molecules of vascular endothelium and studied by immunofluorescence microscopy, and peripheral blood mononuclear cells were phenotyped using flow cytometry. Monocytes/macrophages (lysozyme- or CD 14-reactive cells) were identified among other mononuclear cell types in islet infiltrates. V beta 8-positive T cells were overrepresented, but T cells with other V beta s studied (V beta 5, V beta 5.1, V beta 6, V beta 12) were also found. The vascular endothelium of the islets and many small vessels nearby islets strongly expressed intercellular adhesion molecule-1, whereas vascular cell adhesion molecule-1 and E-selectin were totally absent. We conclude: (a) that increased expression of intercellular adhesion molecule-1 on vascular endothelium may increase endothelial adhesion of mononuclear cells and enhance their accumulation in the pancreas during diabetic insulitis; (b) that T cells with certain T cell receptors can be enriched in infiltrated pancreatic islets; and (c) that macrophages and antigen-specific CD 8-positive T cells are involved in pancreatic beta cell destruction at the onset of IDDM.
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PMID:Macrophages, T cell receptor usage, and endothelial cell activation in the pancreas at the onset of insulin-dependent diabetes mellitus. 138 78

The pathogenetic determinants of sodium retention in IDDM are not fully understood. The aim of this study was to elucidate the action of ANP in 11 IDDM patients with high GFR (greater than or equal to 135 ml.min-1 x 1.73 m-2), referred to here as HF patients; in 10 IDDM patients with normal GFR (greater than 90 and less than 135 ml.min-1 x 1.73 m-2), referred to here as NF patients; and 12 control subjects, here called C subjects, at baseline and during saline infusion administered on the basis of either body weight (2 mmol.kg-1 x 60 min-1; Saline 1) or of ECV (12 mM.ECVL-1 x 90 min-1; Saline 2) during euglycemic insulin-glucose clamp. C subjects and both HF and NF IDDM patients received a second Saline 1 infusion accompanied by ANP infusion (0.02 microgram.kg-1.min-1) at euglycemic levels. HF and NF patients were studied again after 3 mo of treatment with (10 mg/day). Quinapril (CI 906, Malesci, Florence, Italy), an ACE inhibitor without sulfhydryl group. At baseline, both HF and NF IDDM patients had higher plasma ANP concentrations than C subjects (HF, 36 +/- 4, P less than 0.01 and NF, 34 +/- 3, P less than 0.01 vs. C, 19 +/- 3 pg/ml). Plasma ANP and natriuretic response to isotonic volume expansion was impaired both in HF (44 +/- 8 pg/ml, NS vs. base) and NF (40 +/- 7 pg/ml, NS vs. base) compared with C (41 +/- 4 pg/ml, P less than 0.01 vs. base) during Saline 1. On the contrary, plasma ANP response to Saline 2 was similar in HF and NF patients and C subjects, but IDDM patients had still lower urinary sodium excretion rates. The simultaneous administration of ANP and Saline 1 resulted in comparable plasma ANP plateaus in C subjects and HF and NF patients. However, urinary sodium excretion rate was significantly lower in HF and NF patients than in C subjects: HF, 267 +/- 64, P less than 0.01 and NF, 281 +/- 42, P less than 0.01 vs. C, 424 +/- 39 mumol.min-1 x 1.73 m-2. During simultaneous administration of ANP and Saline 1, GFR and FF increased in C subjects, but not in HF and NF patients. HF and NF patients had higher urinary vasodilatory prostanoid excretion rates than C subjects at baseline. Saline infusion did not change urinary excretion rate of prostanoids either in C subjects or IDDM patients (both NF and HF).(ABSTRACT TRUNCATED AT 400 WORDS)
Diabetes 1992 Aug
PMID:Role of atrial natriuretic peptide in the pathogenesis of sodium retention in IDDM with and without glomerular hyperfiltration. 138 91


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