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Results for “Prediabetic State”

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At least 325 records · Page 18Linked to original sources
PubMed1998

Several different enterovirus serotypes can be associated with prediabetic autoimmune episodes and onset of overt IDDM. Childhood Diabetes in Finland (DiMe) Study Group.

In a prospective multicentre study described previously on prediabetic events in siblings of index cases with insulin-dependent diabetes mellitus, 31 children developed clinical diabetes during the observation period and 51 children seroconverted for islet cell antibodies or insulin autoantibodies. By using nonserotype specific EIA and RIA, it has shown recently that enterovirus infections in both groups were frequently associated with increases of islet cell antibody and/or insulin autoantibody titres. Serum specimens sequentially collected from 12 children during the prediabetic period were still available and were then tested for serotype-specific neutralizing antibodies. Plaque-neutralization assays were carried out for coxsackievirus A9, coxsackievirus B types 1 to 6, and echovirus types 1 and 11. An unequivocal monotypic increase in neutralizing antibodies was observed on seven occasions in six children, on one occasion with coxsackievirus A9, one with coxsackievirus B1, two with coxsackievirus B2, two with coxsackievirus B3, and one with coxsackievirus B5. In four patients, the infection was associated temporally with increases in the levels of islet cell antibodies, insulin autoantibodies and/or antibodies to glutamic acid decarboxylase, and in three other patients, it coincided with the clinical onset of insulin-dependent diabetes mellitus. These results suggest that the association of enterovirus infections with insulin-dependent diabetes mellitus is not restricted to serotype 4 of coxsackie B viruses suspected previously, but that several different serotypes might play a role in the pathogenesis of the disease.

Adolescent↗
PubMed1997

Association between neonatal blood pressure and umbilical cord insulin concentration.

The aetiology of the metabolic syndrome remains unknown. This study investigated whether two components of this syndrome, higher blood pressure and higher plasma insulin concentrations, are related at birth. Neonates in the study were from 23 European, 25 Maori, 22 South Asian, and 25 Pacific Islands women having normal singleton pregnancies as well as 6 Maori, 5 Indian, and 19 Pacific Islands women with gestational diabetes (diagnosed by a 3 h 100 g oral glucose tolerance test at 28-32 weeks). Additional fasting glucose and fructosamine concentrations were measured at 36-38 weeks. Umbilical cord blood was taken for insulin, C-peptide, fructosamine and insulin-like growth factor I. Neonatal anthropometry and blood pressure were measured 24 h after delivery. Compared with those with a lower systolic blood pressure (SBP), neonates with a higher SBP had higher umbilical cord insulin (45.6 (39.6-52.8) vs 63.0 (54.6-72.6) pM, p < 0.01), C-peptide (0.22 (0.20-0.25) vs 0.28 (0.26-0.30) nmol l-1, p < 0.001) and fructosamine concentrations, higher maternal fructosamine concentrations and heavier placentas. These data suggest that neonatal hyperinsulinaemia, possibly driven by minor elevations in maternal glycaemia, may be linked to a higher neonatal SBP.

Asia↗
PubMed1998

Contribution of T cells to the development of autoimmune diabetes in the NOD mouse model.

The nonobese diabetic (NOD) mouse spontaneously develops an autoimmune diabetes that shares many immunogenetic features with human insulin-dependent diabetes mellitus (IDDM), type 1 diabetes. The mononuclear cell infiltrates in the islet, which results in the development of insulitis (a prerequisite step for the development of diabetes) are primarily composed of T cells. It is now well accepted that these T cells play important roles in initiating and propagating an autoimmune process, which in turn destroys insulin-producing islet beta cells in the pancreas. T cells are subdivided into CD4+ helper T cells and CD8+ cytotoxic T cells. CD4+ T cells are further subdivided into Th1 and Th2 cells based on profiles of cytokine production, and these two T-cell populations counterregulate each other. Because many autoimmune diseases are Th1 T-cell mediated, current studies have focused on manipulating the Th1/Th2 imbalance to suppress the autoimmune process in the NOD model. Furthermore, the incidence of disease is much higher in females than that in males, suggesting an involvement of sex-steroid hormones in the development of diabetes. Understanding insights of the mechanism of immune-mediated islet cell destruction and the interaction between the immune and the neuroendocrine system may, therefore, provide new therapeutic means of preventing this chronic debilitating disease.

Animals↗
PubMed2006

Alpha-glucosidase inhibitors for people with impaired glucose tolerance or impaired fasting blood glucose.

BACKGROUND: Alpha-glucosidase inhibitors (AGIs) reduce blood glucose levels and may thus prevent type 2 diabetes and cardiovascular disease in patients with impaired glucose tolerance. These possible effects, and the effects on quality of life, plasma lipids and body weight, have never been investigated in a systematic literature review and meta-analysis. OBJECTIVES: To assess the effects of alpha-glucosidase inhibitors in patients with impaired glucose tolerance (IGT) or impaired fasting blood glucose (IFBG), or both. SEARCH STRATEGY: We searched The Cochrane Library (Clinical Trials database, formerly known as CENTRAL), PUBMED, EMBASE, Web of Science, LILACS, databases of ongoing trials, reference lists of relevant reviews, and we contacted experts and manufacturers. Date of last search was February 2006. SELECTION CRITERIA: Randomised controlled trials of at least one-year duration in patients with IGT or IFBG, or both, comparing AGI monotherapy with any other intervention. DATA COLLECTION AND ANALYSIS: Two reviewers read all abstracts, assessed quality and extracted data independently. Discrepancies were resolved by consensus or by the judgement of a third reviewer. MAIN RESULTS: We included five trials (2360 participants), all investigating acarbose, that included patients with IGT or patients 'at increased risk for diabetes' (n = 1). Study duration was one, three (n = 2), five and six years. One study was at low risk of bias and four studies at high risk of bias. Except for the outcome incidence of type 2 diabetes in acarbose versus no treatment (two studies), meta-analyses were not possible. Data from the study at low risk of bias suggests that acarbose decreases the occurrence of type 2 diabetes (NNT = 10), cardiovascular events (NNT = 50, based on 47 events, study not initially powered for this outcome), post-load blood glucose (-0.6 mmol/L, 95% CI -1.0 to -0.3) and body mass index (0.3 kg/m(2), 95% CI -0.1 to -0.5). No statistically significant effects were observed on mortality, other morbidity, glycated haemoglobin, fasting blood glucose, lipids and blood pressure. The effects on the incidence of type 2 diabetes were confirmed in two studies at high risk of bias (OR 0.2, 95% CI 0.1 to 0.6). Adverse effects were mostly of gastro-intestinal origin (OR 3.5, 95% CI 2.7 to 4.4). AUTHORS' CONCLUSIONS: There is evidence that acarbose reduces the incidence of type 2 diabetes in patients with IGT. However, it is unclear whether this should be seen as prevention, delay or masking of diabetes. Acarbose may prevent the occurrence of cardiovascular events, but this finding needs to be confirmed in more studies.

Acarbose↗
PubMed2005

Long-term non-pharmacological weight loss interventions for adults with prediabetes.

BACKGROUND: Most persons with prediabetes (impaired glucose tolerance or impaired fasting glucose) are overweight, and obesity worsens the metabolic and physiologic abnormalities associated with this condition. Prediabetes is an important risk factor for the development of type 2 diabetes. OBJECTIVES: The objective of this review was to assess the effectiveness of dietary, physical activity, and behavioral weight loss, and weight control interventions for adults with prediabetes. SEARCH STRATEGY: Studies were obtained from computerized searches of multiple electronic bibliographic databases, supplemented by hand searches of selected journals, and consultation with experts in obesity research. The last search was conducted May, 2004. SELECTION CRITERIA: Studies were included if they were published or unpublished randomized controlled trials in any language and examined weight loss or weight control strategies using one or more dietary, physical activity, or behavioral interventions, with a follow-up interval of at least 12 months. DATA COLLECTION AND ANALYSIS: Effects were combined using a random-effects model. MAIN RESULTS: Nine studies were identified, with a total of 5,168 participants. Follow-up ranged from 1 to 10 years. Quantitative synthesis was limited by the heterogeneity of populations, settings, and interventions and by the small number of studies that examined outcomes other than weight. Overall, in comparisons with usual care, four studies with a follow-up of one year reduced weight by 2.8 kg (95 % confidence interval (CI) 1.0 to 4.7) (3.3% of baseline body weight) and decreased body mass index by 1.3 kg/m(2) (95% CI 0.8 to 1.9). Weight loss at two years was 2.6 kg (95% CI 1.9 to 3.3) (three studies). Modest improvements were noted in the few studies that examined glycemic control, blood pressure, or lipid concentrations (P > 0.05). No data on quality of life or mortality were found. The incidence of diabetes was significantly lower in the intervention groups versus the controls in three of five studies examining this outcome at 3 to 6 years follow-up. AUTHORS' CONCLUSIONS: Overall, weight loss strategies using dietary, physical activity, or behavioral interventions produced significant improvements in weight among persons with prediabetes and a significant decrease in diabetes incidence. Further work is needed on the long-term effects of these interventions on morbidity and mortality and on how to implement these interventions in diverse community settings.

Adult↗
PubMedDate not supplied

Proliferative responses to selected peptides of IA-2 in identical twins discordant for Type 1 diabetes.

BACKGROUND: The aim of the study was to define T lymphocyte reactivity to selected peptides of an islet antigen IA-2, associated with Type 1 diabetes. METHODS: We used 10 peptides selected from the IA-2 molecule due to their predicted ability to bind to HLA-DRB1*0401, a Type 1 diabetes-associated allele. We tested 21 identical twin pairs discordant for the disease and 15 control subjects and then followed them prospectively; seven non-diabetic twins developed diabetes. RESULTS: Twins of identical pairs tended to respond to different peptides suggesting that the T cell response is, to a degree, shaped by non-genetically determined factors (p<0. 0001). However, there was no difference in the T cell responses between diabetic twins and either their non-diabetic identical twins or control subjects and the response was heterogenous. T cell responses did not differ in those seven non-diabetic twins who developed diabetes from those twins who did not. T cell responses to peptide 11 (amino acids 502-514) was immunodominant in diabetic twins as well as their non-diabetic twins and controls; responses were not correlated with HLA, IA-2 antibodies, age or duration of disease. CONCLUSION: We conclude that T cell responses to selected IA-2 peptides are not genetically determined, heterogeneous, not strictly HLA controlled and did not distinguish diabetic or prediabetic twins from non-diabetic twins or controls. The identification of an immunodominant T cell response to IA-2 peptide 502-514 raises the possibility that this, or similar, epitopes may be of therapeutic value in disease prevention.

Adolescent↗
PubMedDate not supplied

The molecular specificity of insulin autoantibodies.

Insulin autoantibodies (IAA) are one of several markers for Type I (autoimmune) diabetes, but alone deserve special attention. Unlike the other markers, their ligand is unique to the beta cell. IAA are the first markers to appear during the symptomless period which precedes diabetes and they are present in the vast majority of young children destined to develop diabetes. The primary and tertiary structures of insulin have been known for decades. Binding studies with insulin variants have shown epitope restriction that can distinguish Type 1 diabetes-predictive from non-predictive IAA-positive sera, thereby improving specificity for the test. With two major international Type 1 diabetes prevention trials underway, there is a pressing need to refine markers that reliably indicate the presence of, and remission from, autoimmune insulitis. The binding regions of antibodies are assembled from three multi-gene families, and some of their diversity derives from random mutation during their antigen-driven maturation. There is evidence that mature IAA derive from germline-encoded 'natural' antibodies, and that the gene segments utilised by IAA may be influenced by clinical context. Monoclonal anti-idiotypic (anti-Id) antibodies can serve as probes for antibody variable region determinants, and antibodies to the different epitopes of beef and porcine insulins have already been analysed with monoclonal reagents. Used as antibodies in a radioimmunoassay format, monoclonal anti-Ids will identify and measure autoantibody idiotopes as if they were ligands. The challenge now is to replace the conventional radiobinding assays for IAA, which only detect and titrate, with radioimmunoassays that can be standardised in absolute units. There is sufficient evidence for the existence of Type 1 diabetes-predictive IAA idiotopes to justify the development of idiotope-specific radioimmunoassays which ignore Type 1 diabetes-unrelated IAA.

Amino Acid Sequence↗
PubMedDate not supplied

Congenital anomalies and the diabetic and prediabetic pregnancy.

Congenital anomalies are two to four times more frequent in the offspring of diabetic mothers than in those of non-diabetic mothers, and represent an increasingly important cause of perinatal mortality. These anomalies involve multiple organ systems more often than those found in the children of non-diabetic mothers. The excess of anomalies associated with maternal diabetes occurs in many organ systems. Anomalies are no more frequent in the offspring of diabetic fathers and pre-diabetic mothers than among those of non-diabetics, suggesting that non-genetic factors are the important determinants. Anomalies are most frequent in the offspring of mothers who have developed diabetes at an early age, many of whom have diabetes of long duration, are insulin-treated, and may have vascular complications. The relative importance of each of these factors in the pathogenesis of anomalies is unknown, but present evidence is consistent with a hypothesis that anomalies are the result of metabolic disturbances in the intrauterine environment during the first trimester of pregnancy. Whether or not their incidence can be reduced by optimum metabolic control of maternal diabetes during this period is unknown.

Congenital Abnormalities↗