Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011860 (type 2 diabetes)
 57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a family with maturity-onset type of diabetes mellitus inherited as a dominant, autosomal trait (MODY), the HLA genotypes were compared with the glucose tolerance and the plasma insulin response to oral glucose. In the members with impaired glucose tolerance, the plasma insulin response was of the insulino-tardic type, while those with normal or borderline glucose tolerance had a normal plasma insulin response. HLA tissue typing for A, B, C and D series antigens carried out in 19 of the members showed no association between specific HLA antigens and imparied glucose tolerance. Moreover, when analysing the segregation of the disease and the HLA characters, several recombinants between MODY and HLA would have to be postulated if the gene(s) for this form of diabetes mellitus should be closely linked to the HLA locus.
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PMID:HLA antigens in a family with maturity-onset type diabetes mellitus. 58 Aug 33

The frequency of HLA BW54 and B5 in Japanese patients with JOD is increased and decreased, respectively. In JOD patients without a family history of MOD, the frequency of BW54 is significantly increased, whereas in JOD patients with a positive family history the frequency was not increased in a statistically significant manner.
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PMID:HLA BW54 and B5 in Japanese diabetics with juvenile-onset and insulin-dependency (with special reference to the family history). 65 66

We investigated the HLA status of patients with diabetes associated with limited joint mobility and microvascular complications. An increased frequency of HLA-B8, DR3 and DR4 in patients with insulin dependent diabetes mellitus (IDDM) compared to controls and patients with noninsulin dependent diabetes mellitus (NIDDM) was confirmed. HLA antigen DQw1 was detected less frequently in patients with IDDM and was negatively associated with limited joint mobility and retinopathy. Limited joint mobility was significantly correlated with disease duration in IDDM, and was associated with neuropathy in both IDDM and NIDDM and with retinopathy in IDDM. No correlation was found between DR3, DR4 and limited joint mobility or diabetic complications. We also investigated the usefulness of nailfold capillary microscopy in a large group of patients with IDDM and NIDDM. Although capillary enlargement and avascular areas were noted in a few patients, nailfold capillary microscopy was not felt to be a useful tool in the evaluation of diabetes.
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PMID:HLA antigens and nailfold capillary microscopy studies in patients with insulin dependent and noninsulin dependent diabetes mellitus and limited joint mobility. 225 97

HLA antigens (A, B, DR) of the tissues of 171 patients with different types of diabetes mellitus were investigated. Controls were 1867 healthy Leningrad residents (control I), not investigated with the GTT, and 38 pregnant women with the unchanged GTT during pregnancy (control II). Some features of the frequency of occurrence of individual antigens and their interlocular (HLA A, B) combinations in type I and type II diabetes mellitus and diabetes of pregnant women were established. The risk of diabetes mellitus, type I, development was shown to be on the increase in the presence of HLA DR4 in the phenotype and considerably on the decrease in the presence of HLA B17. The results point out to the genetic heterogeneity of different types of diabetes mellitus. The authors think it possible to use HLA typing for the diagnosis of type I diabetes mellitus.
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PMID:[Antigens of the HLA system in different types of diabetes mellitus]. 233 Mar 58

Noninsulin dependent diabetes mellitus (NIDDM) is associated with an entirely different set of genetic alterations from insulin-dependent diabetes mellitus (IDDM). Over 90% of IDDM carry HLA type DR3, DR4 or both. Several theories have been proposed to explain how the genetic alterations are translated into a beta cell destructive process. All involve the elaboration of a beta cell autoantigen. A major current research focus is on the development of pharmacologic approaches to the control of the beta cell destructive process (cyclosporine A). This has led to a shift in interest to the early identification of individuals at risk for IDDM. Many questions remain to be answered. In our paper emphasis is placed on epidemiological research. In Allegheny County, Pennsylvania, we have found an incidence of 1.73 cases/1000 (incidence rate of 15/100,000/year). There were marked geographical variations (incidence rate of 1/100,000/year in Asian countries, of 40/100,000/year in Finland). This suggests that there are major environmental determinants leading to expression of disease in genetically susceptible individuals. There are no geographical differences in the main age of onset, the sex ratio and the clinical patterns in the initial course of newly detected IDDM. In all parts of the world islet cell antibodies are positive in 60-80% of newly diagnosed IDDM. Migration of children from their native homeland with a low incidence rate to a country with high incidence rate was accompanied by an increase of incidence. The following potential environmental factors have been considered: viral infections, environmental toxins, nutrients, and stress. In our view IDDM occurs in genetically susceptible individuals.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:What do epidemiologic observations tell us about the etiology of insulin dependent diabetes mellitus? 240 77

Diabetes mellitus is the second most prevalent chronic disease in children in the U.S. It is associated with severe manifestations which include blindness and circulation deficiencies as well as markedly increased risk of death. The etiology of diabetes mellitus remains a mystery although both genetic and environmental factors have been implicated. The geneticist is confronted with a number of obstacles in his attempts to unravel this problem, including differences in the definition of affected individuals. This matter was certainly clarified by the separation of noninsulin-dependent diabetes (NIDDM) and insulin-dependent diabetes mellitus (IDDM) into two separate disease entities. Twin studies, however, show that IDDM cannot be entirely due to genetic causes as concordance is no more than about 50%. Although the disease is then clearly not inherited per se, the "susceptibility" to diabetes seems almost surely inherited and, provided this susceptibility, the disease can be brought on by environmental factors. Until the underlying mechanism causing IDDM is completely ascertained, we have to rely on genetic markers to approach the study of the inheritance thereof. Since, in the early 1970s, research by Nerup's and Cudworth's groups revealed associations between the HLA-B locus and IDDM, the HLA markers are considered the classical genetic markers for IDDM susceptibility. In this paper, we review the nature of the genetic susceptibility to IDDM and the possible environmental factors which can bring on the disease.
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PMID:Immunogenetics of insulin-dependent diabetes mellitus in humans. 257 May 96

Susceptibility to both insulin-dependent and non-insulin dependent diabetes mellitus is determined to a substantial extent by genetic factors. These probably interact with an environmental trigger to induce expression of the disease state. Significant progress has been made in defining these genetic factors in IDDM. The major contribution comes from a gene or genes within the HLA region, on the short arm of chromosome 6, at least one of which lies close to or within the DQ subregion. Other loci also contribute, most notably the insulin gene, or another closely linked gene on the short arm of chromosome 11, and possibly the T-cell receptor and immunoglobulin genes. In contrast very little is known for NIDDM and such associations as have been described remain controversial.
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PMID:Genes and diabetes mellitus. 257 89

Hyperglycemia and other metabolic derangements resulting from absolute or functional deficiency of insulin are accompanied by typical signs and symptoms of diabetes. The clinical signs and the findings of hyperglycemia over 200 mg/dl should establish a diagnosis of diabetes mellitus. An oral glucose tolerance test (O-GTT) is rarely necessary for diagnosis of diabetes in a child. A small proportion of children, however, present less severe symptoms, and may require an O-GTT. Approximately 14% of IDDM children were in coma at diagnosis in Tokyo, and 11 onset deaths (0.94%) were observed among the 1172 newly diagnosed IDDM cases in Japan. A significant decline in the onset mortality, however, has been observed in the past 20 years in Japan in association with the improvement of early management of childhood diabetes. The clinical distinction of IDDM from NIDDM is often difficult in diabetic children of Oriental origin without obesity. Japanese IDDM can be divided into two forms, abrupt and slow onset forms, but they may be essentially the same disease. There was no difference in the frequency of being tested positive for circulating ICA between the two groups of the patients. But a difference in the frequency of HLA DR4 and DRW9 was noticed between the two groups. Clinical features of 107 children with NIDDM were studied and about 75% of these cases were obese. All of them can be detected by routine urinalysis for glucose. Diet and exercise therapy in most of the newly diagnosed patients resulted in remission but some of them may require insulin or an oral hypoglycemic agent to get better glycemic control.
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PMID:Initial signs and diagnosis of diabetes--special considerations of Oriental patients. 263 91

We report the clinical records of 45 children with abnormalities regarding glycemic regulation characterized by a non-insulin deficient hyperglycemia (NIDH), known under the different names of chemical diabetes, sub-clinical diabetes and more recently MODY. These 45 children belong to 31 families with 532 relatives comprising 137 cases of NIDH which could have been studied. The symptoms of this biochemical abnormality, the pathophysiology of which is not yet clearly understood, are the following: lack of clinical manifestations, except for a variable and intermittent glycosuria; constant abnormal glucose tolerance tests, above 97 percentiles of the reference value with some variations over time; normal immunoreactive insulin levels; percentage of glycosylated hemoglobin at the upper range of normal; dominant autosomal genetic transmission and no association with HLA markers like in insulin-dependent diabetes; lack of degenerative complications of the micro-angiopathic type, at least on these cases even after more than 30 years of follow-up; finally, no tendency towards insulin-dependent diabetes. The NIDH should not be confused with the slow and progressive beginning of insulin-dependent diabetes for which prolonged delay is needed to affirm the diagnosis. The frequency of the biochemical phenomena is about 1.8% of the cases of authentic diabetes mellitus occurring before the age of 15.
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PMID:[Chronic non-insulin deficient hyperglycemia in children]. 265 58

The frequency of secondary failure to oral hypoglycaemic agents (OHA) in patients with non-insulin dependent diabetes (NIDDM) is still unknown, despite more than 30 years of use of OHA. The term secondary failure should be limited to patients who, despite maximal dosages of OHA and despite full compliance with diet and therapy, are no longer controlled and require insulin to obtain an acceptable glucose metabolism. We evaluated 248 out-patients, either on OHA, or on insulin because of poor metabolic control with OHA, in order to assess duration of treatment with OHA since diagnosis, by means of actuarial curves (Mantel-Cox test). Patients with low relative body weight (RBW less than or equal to 100) experienced secondary failure earlier and more often than obese patients (RBW greater than 120) or overweight (RBW 101-120) patients. In 66 of the above out-patients, 33 OHA-treated and 33 insulin-treated, matched for age at onset and duration of disease, islet-cell-antibodies (ICA) and C-peptide release at fasting, 6 min after i.v. glucagon and post prandially were evaluated. Only among lean and overweight patients, was C-peptide release significantly lower in insulin-treated than in OHA-treated patients; differences disappeared in obese patients. ICA were found in only 7 patients (10.6%). HLA phenotype was different from that of healthy blood donors for the loci HLA B5, B13, CW4, with no differences between OHA-treated and insulin-treated patients. These data indicate that secondary failure is more frequent in lean patients with NIDDM, and is related to reduced insulin release.
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PMID:Secondary failure to oral hypoglycaemic agents in non-obese patients with non-insulin-dependent diabetes is related to reduced insulin release. 266 Dec 81


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