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)

Recently, linkage between the ADA gene locus and MODY, a subtype of NIDDM, has been reported. The possibility that the region of chromosome 20q containing the ADA locus also may play a role in susceptibility to NIDDM needs to be investigated. Therefore, we examined the linkage between the ADA locus and NIDDM in affected siblings of 50 European white diabetic pedigrees--21 Italian and 29 British. Departure from independent segregation of the disease and an Alu VpA polymorphism within the 5' flanking region of the ADA locus was tested in the affected sib-pairs with the APM statistical method. After DNA amplification by the PCR and PAGE, five alleles were identified in the ALU VpA tract at the ADA locus in the two populations. Allele frequencies did not differ significantly between the two populations (chi 2 = 2.426, P > 0.05 [NS]). Analysis of the 50 diabetic sib sets, and independently of the Italian and British groups of affected sib pairs, revealed no segregation distortion between the marker locus and NIDDM. We conclude that mutations within or around the ADA locus are unlikely to play a major role in the etiology of NIDDM.
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PMID:Sib-pair analysis of adenosine deaminase locus in NIDDM. 144 5

MODY is a form of NIDDM inherited as an autosomal dominant condition. We studied the linkage of MODY to two loci: ADA and GLUT2 in two large pedigrees with nonradioactive microsatellite polymorphic systems. A positive linkage of ADA to MODY was recently demonstrated in the large RW pedigree. Formal linkage analysis excluded a tight linkage between ADA and MODY with a LOD score of -5.82 and -2.24 at a recombination fraction of 0.01 in the two families. This result suggests genetic heterogeneity in the molecular basis of MODY. GLUT2 is a candidate gene that is expressed in the liver and beta-cells of pancreatic islets. In the two families studied, the disease did not cosegregate with GLUT2 alleles. The LOD scores for GLUT2 were -7.79 and -1.9 at a recombination fraction of 0.001 in the two families, thus providing evidence against the involvement of GLUT2 in MODY.
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PMID:Linkage analysis of maturity-onset diabetes of the young with microsatellite polymorphisms. No linkage to ADA or GLUT2 genes in two families. 162 71

Asbestos liners for investment metal casting has frequently been used in dental laboratory work. In recent years, the dangerous properties of asbestos to the human body were reported in Europe and the United States, and casting liners without asbestos were developed and marketed by many manufacturers. These are so-called non-asbestos liners. This study evaluated the adaptability of MOD inlay castings to dies using 8 kinds of commercial non-asbestos liners of ADA standard No. 2 specifications. The results were as follows; Single and double layers of Casting ribbon, New Asbestos Ribon, Shofu experimental, and KAOLIN showed good adaptation. Shofu experimental with a single layer showed the best marginal adaptation (10 microns). OVAL LINERS and CASTING LINERS with single layer showed good adaptation, but with double layers the adaptation was poor. In FLASK LINER, the double layer showed better adaptation than that with a single layer. Most non-asbestos liners used in this study are adequate in useful to MOD inlay castings.
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PMID:[A study for non-asbestos casting liners. An experimental study of the adaptability of MOD casting to die]. 213 Dec 96

Eight subjects (Ss) with non-insulin-dependent diabetes (NIDDM) monitored their stress, blood glucose (BG), food intake, activity (via pedometer), mood, and coping responses for 8 days. They alternated 2 daily, self-selected ADA food-exchange diets to control for the effects of stress on adherence to diet. BG was significantly higher on high-stress compared to low-stress days. This effect was at least partially mediated by the effect of stress on activity; Ss were significantly less active on high-stress days. Further analyses suggested idiosyncratic relationships between mood and BG, and some evidence was found to suggest a relation between stress, coping, and BG.
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PMID:The effects of stress, mood, and coping on blood glucose in NIDDM: a prospective pilot evaluation. 804 61

Abnormalities of plasma lipids are highly prevalent in both types of diabetes, but there are important quantitative and qualitative differences that this paper reviews. The importance of abnormalities in lipoprotein metabolism as determinant of vascular risk in general population is similar in diabetes, where there is chronic hyperglycemia associated, but it is considered as an independent vascular risk factor. People with IDDM in adequate glycemic control generally have plasma lipid concentrations in normal levels, but in NIDDM, even in good glycemic control, there are another factors associated and usually there are hypertriglyceridemia and total hypercholesterolemia with reduced HDL fraction. Carbohydrate-rich diet increase plasma triglyceride levels and low HDL-cholesterol levels in the majority of studies. Substitute monounsaturated fats in the diet to replace saturated fats lowers total cholesterol and LDL fraction and increase HDL, in addition it acts over others vascular risk factors. These findings were taken into account by ADA and recently revises their 1986 dietary recommendations with the same goals of medical nutrition therapy but with individualized approach appropriate for the personal life style to facilitate adherence to achieve the glycemic, lipid body weight and blood pressure aims with a good quality of live.
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PMID:[Lipid metabolism and new dietetic recommendations in diabetes mellitus]. 867 45

Maturity-onset diabetes of the young (MODY) is a monogenic subgroup of non-insulin dependent diabetes mellitus (NIDDM) characterised bylan early age of onset (< 25 years) and an autosomal dominant mode of inheritance. MODY is genetically heterogeneous with three different genes identified to date; hepatocyte nuclear factor 4 alpha (HNF-4 alpha) [MODY1], glucokinase [MODY2] and hepatocyte nuclear factor 1 alpha (HNF-1 alpha) [MODY3]. A nonsense mutation in the HNF-4 alpha gene has recently been shown to cause MODY in a single large North American pedigree (RW). We screened a large UK Caucasian MODY family which showed weak evidence of linkage to the MODY1 locus on chromosome 20q (lod score for ADA 0.68 at theta = 0) for mutations in the coding region of the HNF-4 alpha gene by direct sequencing. A missense mutation resulting in the substitution of glutamine for glutamic acid was identified in exon 7 (E276Q). The mutation was present in all of the diabetic members of the pedigree plus two unaffected subjects and was not detected in 75 normal control subjects or 95 UK Caucasian subjects with late-onset NIDDM. This is the first missense mutation to be described in the HNF-4 alpha gene.
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PMID:A missense mutation in the hepatocyte nuclear factor 4 alpha gene in a UK pedigree with maturity-onset diabetes of the young. 924 9

Japan Diabetes Society organized a committee for the revision of diagnostic criteria of diabetes mellitus in 1995. Like ADA and WHO reports, this committee adopts a classification based on etiologies, and presents a two-dimensional figure with etiologies and the state of insulin deficiency on different axis. The words IDDM and NIDDM will be retained as terms representing the different degree of insulin deficiency. On the basis of glycemia, diabetic type is defined when fasting plasma glucose exceeded 126 mg/dl and/or 2-hour plasma glucose by 75 g GTT exceeded 200 mg/dl. The diagnosis of diabetes in an individual can be made by confirming sustained diabetic type on repeated tests or co-existance of characteristic clinical features of diabetes. Normal type is defined by FPG < 110 mg/dl and 2hPG < 140 mg/dl. The borderline type, defined as neither normal nor diabetic types, corresponds to IFG plus IGT according to ADA and WHO reports. The application of HbA1c for diagnosis of diabetes and the criteria for gestational diabetes mellitus are also discussed.
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PMID:[Outline of revision of classification and diagnostic criteria of diabetes mellitus in Japan]. 1019 34

Compared with non-diabetic individuals, patients with diabetes have a two- to four-fold greater risk of myocardial infarction, and growing evidence suggests that dyslipidaemia contributes significantly to this excess risk. Based on evidence from the major trials of HMG-CoA reductase inhibitors (statins), the American Diabetes Association have published updated guidelines that outline priorities for the treatment of diabetic dyslipidaemia. These guidelines emphasise that low density lipoprotein (LDL) cholesterol is the first priority for lipid lowering. All diabetic patients with, or at risk of, coronary heart disease (CHD) should be treated to an LDL cholesterol goal of < or = 2.6 mmol/L (100 mg/dL). The recent Joint European Task Force on Coronary Prevention recommend similar goals: total cholesterol <5.0 mmol/L (190 mg/dL) and LDL cholesterol <3.0 mmol/L (115 mg/dL). Both the ADA and Joint European Task Force recommend statins as first choice hypolipidaemic therapy for patients with diabetic dyslipidaemia. Ongoing trials will provide further evidence of the benefits of lipid-lowering therapy with statins in reducing CHD risk in patients with type 2 diabetes. Results from these studies will likely add further support to the recommendations to use statins in the overall management of diabetic patients.
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PMID:The current management of diabetic dyslipidaemia. 1182 49

In order to demonstrate the effect of family history (FH) coexisting with obesity in insulin resistance (IR) and secretion in subjects at risk for type 2 diabetes, fasting and 2 h post-glucose load serum glucose and insulin concentrations were measured in 143 individuals, 66 men and 77 women, ages ranging from 18 to 68 years, who were considered at risk but were normoglycemic following ADA criteria. Insulin resistance was estimated using HOMA(IR), basal hyperinsulinemia and I(0)/G(0) ratio. Insulin secretion was estimated by means of HOMA(beta-cell), DeltaI(30-0)/DeltaG(30-0) ratio and the insulin concentration at 30 min post-glucose load (I(30)). Disposition index (DI) was calculated to verify if insulin secretion compensate IR. Obesity in males produced an increase in all the parameters indicative of IR in both groups of individuals, with (FH(+)) or without (FH(-)) family history of diabetes, increase that was more pronounced in those FH(-). This effect was not observed in women. The parameters indicative of insulin secretion showed that only in males the presence of FH(+) was responsible for a significant decrease in insulin secretion, mainly expressed as lower values of HOMA(beta-cell) in obese as well as in non-obese. The I(30) and the ratio DeltaI(30-0)/DeltaG(30-0), although lower, did not reach statistical significance. The DI showed that only when obesity and FH were associated the decrease in insulin secretion was not a compensatory response to the IR present in those individuals. In conclusion, normoglycemic obese and non-obese male subjects of Hispanic (Latinos) origin with a family history of type 2 diabetes present not only IR but impaired insulin secretion, having the obese FH(+) and additional risk like low DI.
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PMID:Presence of impaired insulin secretion and insulin resistance in normoglycemic male subjects with family history of type 2 diabetes. 1270 17

Type 2 diabetes is a multifactorial disease caused by both oligo- and polygenic genetic factors as well as non-genetic factors that result from a lack of balance between the energy intake and output and other life style related factors. ADA and WHO have recently reclassified diabetes on both clinical stages and aetiological grounds. There is a lot of data related to the genetics of type 2 diabetes. However, many genes and gene products as well as their interactions with the environment at the molecular, cellular, tissue, and the whole organism levels are still unknown. Changes in the frequency of diabetes occurrence in various urban and rural populations and ethnic groups prove the relationship with the transition to the 'western' life style. Understanding of diabetes pathogenesis is essential to the development of new methods of treatment and strategies of effective prevention of this disease.
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PMID:Type 2 diabetes mellitus--a multifactorial disease. 1289 73


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