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At least 235 records · Page 13Linked to original sources
PubMed2002

In vivo evidence for increased oxidation of circulating LDL in impaired glucose tolerance.

Oxidized LDL (oxLDL) is a key mediator in atherogenesis and a marker of coronary artery disease (CAD). Type 2 diabetes is associated with excessive cardiovascular morbidity and mortality. Because atherogenesis starts before diabetes is diagnosed, we investigated whether circulating oxLDL levels are increased in impaired glucose tolerance (IGT). OxLDL levels were measured in 376 subjects with normal glucose tolerance (NGT), 113 patients with IGT, and 54 patients with newly diagnosed type 2 diabetes. After correction for age and BMI, serum levels of oxLDL were significantly increased in IGT versus NGT subjects (P = 0.002). OxLDL levels were not associated with the following parameters of the oxidative/antioxidative balance in the blood: total antioxidant capacity, urate-to-allantoin ratio, and circulating phagocyte oxygenation activity. In stepwise multivariate analysis, LDL cholesterol (P < 0.0005) and triglycerides (P < 0.0005) were the strongest predictors of circulating oxLDL levels, followed by HDL cholesterol (P = 0.003), 2-h postchallenge C-peptide (P = 0.011), fasting free fatty acids (P = 0.013), and serum paraoxonase activity (P = 0.035). The strong correlation of oxLDL with LDL cholesterol and triglycerides indicates that LDL oxidation in IGT is preferentially associated with dyslipidemia. OxLDL increase may explain the high atherogenic potency of dyslipidemia in the prediabetic state.

Adult↗
PubMed2001

Muscle fiber composition and capillary density in Turner syndrome: evidence of increased muscle fiber size related to insulin resistance.

OBJECTIVE: To assess muscle fiber composition and capillary density in Turner syndrome, a condition linked with insulin resistance and increased frequency of type 2 diabetes, and link these findings with insulin sensitivity and physical fitness. RESEARCH DESIGN AND METHODS: A total of 10 patients with Turner syndrome who were off hormone replacement therapy (aged 32.7 +/- 8.9 years) and a control group of 14 normal women (aged 35.6 +/- 9.3 years) were studied. None of the participants had diabetes or any family history of type 2 diabetes. An oral glucose tolerance test was performed, and insulin sensitivity was assessed by homeostasis model assessment (HOMA) and a composite whole-body insulin sensitivity index (ISI(comp)). Physical fitness was assessed, and a muscle biopsy was obtained. RESULTS: Women with Turner syndrome were insulin resistant, as seen by a lower ISI(comp) (P = 0.003) and increased glucose (P < 0.0005) and insulin (P = 0.01) levels at 120 min. Impaired glucose tolerance was present in most Turner syndrome patients (6 of 10), but not in the control subjects. Women with Turner syndrome had an increased size of type IIa fibers (P = 0.01), whereas the size of their type I and IIa fibers were comparable with the control group. The groups did not differ in percentage of type I, Iia, or IIx fibers, and there was no difference in the capillary density. Significant correlations were found among ISI(comp), the HOMA index (R(HOMA)), and the mean area of type IIa fibers (ISI(comp): r = -0.632, P = 0.002; R(HOMA): r = 0.570, P = 0.006). Furthermore, capillaries/type IIa fibers correlated significantly with ISI(comp) (r = -0.618, P = 0.01). There were no significant correlations between VO(2max) and muscle fiber composition. CONCLUSIONS: Healthy women with Turner syndrome are characterized by impaired glucose tolerance, insulin resistance, low physical capacity, and enlarged type IIa muscle fibers, indicating diminished oxygen and substrate supply for metabolic processes. These findings could be indicative of a prediabetic state.

Adult↗
PubMed2003

Blood pressure in young adulthood and the risk of type 2 diabetes in middle age.

OBJECTIVE: Hypertension is known to accompany type 2 diabetes in middle age, but it is unknown how early in life blood pressure (BP) begins to rise among individuals who later develop diabetes. The objective of this study was to evaluate elevated BP as a long-term predictor of type 2 diabetes. RESEARCH DESIGN AND METHODS: We conducted a prospective cohort study of 1,152 white male medical students in The Johns Hopkins Precursors Study to longitudinally assess systolic BP (SBP) and diastolic BP (DBP) from young adulthood through middle age in men who went on to develop diabetes. Incident diabetes was identified by self-report through mailed questionnaires verified by medical record review. RESULTS: During a median follow-up of 38 years, 77 cases of incident diabetes occurred. The mean age of diabetes diagnosis was 58 years. As early as age 30 years, mean SBP and DBP were significantly higher in men who developed diabetes during follow-up than in those who remained nondiabetic (SBP 122 vs. 119 mmHg, P = 0.009; DBP 78 vs. 75 mmHg, P = 0.0005). The rate of increase in SBP and DBP over time in men who developed diabetes was greater than the rate of increase in men who did not develop diabetes (SBP 0.49 vs. 0.27 mmHg/year, P < 0.00003; DBP 0.24 vs. 0.17 mmHg/year; P = 0.09). After adjustment for BMI and other risk factors for diabetes, SBP and DBP at age 30 years remained significantly higher in individuals who developed diabetes than in their nondiabetic counterparts; however, the difference in the rate of increase in SBP was no longer significant following multivariate adjustment. CONCLUSIONS: BP elevations precede the development of type 2 diabetes in middle age by 20-25 years. Higher BP in the prediabetic state might contribute to the presence of vascular disease at the time of diagnosis of type 2 diabetes.

Adult↗
PubMed2000

A role for NF-kappaB and the proteasome in autoimmunity.

Type 1 diabetes (also known as insulin-dependent diabetes mellitus or juvenile-onset diabetes) is usually caused by T cell-mediated autoimmunity, with a prediabetic state characterized by the production of autoantibodies specific for proteins expressed by pancreatic beta cells. The non-obese diabetic (NOD) mouse is a spontaneous model of type 1 diabetes with a strong genetic component that maps to the major histocompatibility complex (MHC) region of the genome. A specific proteasome defect has been identified in NOD mouse lymphocytes that results from down-regulation of expression of the proteasome subunit LMP2, which is encoded by a gene in the MHC genomic region. This defect both prevents the proteolytic processing required for the production and activation of the transcription factor nuclear factor kappaB (NF-kappaB), which plays important roles in immune and inflammatory responses, as well as increases the susceptibility of the affected cells to apoptosis induced by tumor necrosis factor alpha (TNF-alpha). The proteasome dysfunction is both tissue and developmental stage specific and likely contributes to disease pathogenesis and tissue targeting.

Animals↗
PubMedDate not supplied

[Blood sugar and plasma immunoreactive insulin levels in healthy pregnant women undergoing the glucose tolerance test].

The level of blood sugar and of blood plasma immunoreactive insulin (IRI) on fasting stomach and during the glucose (per os) tolerance test (GTT) were studied in apparently healthy 8 nonpregnant and 20 pregnant women (11 of them were examined once and 9 repeatedly in the course of pregnancy). GTT proved to be normal in all the women; there sere no signs pointing to the possibility of prediabetic state. Blood sugar on fasting stomach was somewhat lower in pregnant women than in the nonpregnant ones. Therefore, despite the absence of significant differences between the mean blood sugar values during the GTT in the pregnant and onopregnant women the mean sugar elevation during the whole GTT period was significantly higher in women of the III trimester of pregnancy than in the nonpregnant women. Blood plasma IRI content on fasting stomach during the II trimester of pregnancy had a tendency to elevation, and during the III trimester was significantly greater than in the nonpregnant women and in the I and II trimesters of pregnancy. The maximal blood plasma IRI elevation after taking glucose occurred later in the pregnant women was significantly higher during the II and the III trimesters than in the nonpregnant women. During the III trimester of pregnancy there was a singnificantly greater mean IRI elevation in the whole course of the GGT than in the nonpregnant women. IRI index showed no significant change in the pregnant women. The revealed character of the sugar and IRI ratio in the blood on fasting stomach and during the GTTpermits to suggest that hyperinsulinemia during pregnancy bore the character of a compensatory process. The absence of any changes in the IRI index pointed to the functional preservation of the insular apparatus in healthy pregnant women despite the fact that it was subject to a constant and increasing tension with the progress of pregnancy.

Adult↗
PubMed2001

High prevalence of stress hyperglycaemia in children with febrile seizures and traumatic injuries.

UNLABELLED: Although hyperglycaemia is relatively frequent in the course of severe illnesses and may be looked upon as the possible result of an uncoordinated insulin response to the increased glucose that the body may need during periods of stress, it is generally agreed that it does not constitute a prediabetic condition. Numerous studies have aimed to explain the pathophysiology of this occurrence but none has looked at which conditions are more prone to develop stress hyperglycaemia (SH). Therefore, the aim of this study was to evaluate the main clinical conditions that may be associated with SH in children. A total of 1199 children was studied: 833 children (439 M, 394 F, mean age 5.2 +/- 4.5 y) admitted for an acute illness or injury constituted the stress-exposed group, while 366 children (222 M, 144 F, mean age 6.2 +/- 4.6 y) admitted for elective minor surgery represented the stress-unexposed group and were considered as the control group. SH was defined as plasma glucose concentrations > or = 8.3 mmol l(-1) during an acute illness. Stress-exposed patients had significantly higher glycaemic levels than controls (5.6 +/- 1.4 vs 4.7 +/- 0.7 mmol l(-1); p < 0.0001). SH was found in 41 (4.9%) stress-exposed patients and in none of the controls. SH was significantly more prevalent in children affected by febrile seizures (12.9%) or traumatic injuries (11.7%; p < 0.008 and p < 0.02, respectively, vs other diagnoses). A significant correlation was found between glycaemia and systolic pressure (r = 0.1; p < 0.01), white cell count (r = 0.12; p < 0.0003) and body temperature (r = 0.16; p < 0.0001). SH was more frequent in patients with body temperature > 39 degrees C (14%) than in those with a temperature < or = 39 degrees C (4%; p < 0.0008). SH was more prevalent in clinical conditions of fever associated with seizures or pain (12.9% and 12.5%, respectively) than fever alone (4.4%). After a mean period of 3.5 +/- 0.6 y of follow-up none of the hyperglycaemic patients had developed diabetes mellitus. CONCLUSION: Traumatic injuries, febrile seizures or conditions in which an elevated body temperature may be found are frequently associated with SH in children. In the presence of these conditions specific studies directed towards unmasking a prediabetic state may be unnecessary.

Adolescent↗
PubMed2002

[Stress hyperglycemia in a child with severe acute gastroenteritis].

A case of a two years and ten months old girl with severe acute gastroenteritis, dehydration, and hyperglycaemia is described. Transient hyperglycaemia is a common clinical finding in children under stress. We discuss the distinction between hyperglycaemia as a prediabetic state and that as a physiological response to stress during acute illness.

Acute Disease↗
PubMed2003

Stress induced disturbances of the HPA axis: a pathway to Type 2 diabetes?

Type 2 diabetes is the most common form of hyperglycemia. The disease exists in all populations, but in developed societies, the prevalence has risen as the population ages and above all becomes more obese. In the prediabetic state, type 2 diabetes involves two defects, peripheral insulin resistance and hyperinsulinemia, which is followed by the failure of insulin secretion to compensate for the insulin resistance. As with nearly any disease, it is likely that multiple environmental and genetic factors are involved in the development of insulin resistance. An acquired pathogenic factor is obesity, particularly visceral obesity. Compelling evidence suggests that progressive dysfunction of the hypothalamic-pituitary-adrenal (HPA) axis, with elevated levels of circulating cortisol, is implicated in the development of visceral obesity. The HPA axis perturbations associated with visceral obesity can be accounted for, in part, by increased environmental stress that destabilizes the hypothalamic-pituitary system in individuals with genetic susceptibility.

Diabetes Mellitus↗
PubMed2002

Voluntary discontinuance of seven years successful insulin prophylaxis produced shortly overt diabetes in a first-degree relative of a diabetic child at high risk for type 1 diabetes.

This is the story of a nondiabetic first-degree relative of a child with Type 1 Diabetes who was screened for Type 1 diabetes and was found to be at high risk being positive for genetic, immunologic and metabolic markers. He accepted to be treated with low-dose subcutaneous insulin and for 7 years he has been living in subclinical prediabetes state. At the beginning of eighth year, he voluntary discontinued the preventive insulin therapy and after 18 months clinically overt diabetes appeared.

Adolescent↗
PubMed2002

Postprandial dysmetabolism and large-vessel disease.

The increased cardiovascular disease morbidity and mortality in people with Type 2 diabetes mellitus (T2DM) is not explained by the prevalence of cardiovascular disease risk factors and is often attributed to poor glycaemic control. Epidemiological studies have shown fasting and especially postprandial or post-challenge hyperglycaemia to be strong predictors of cardiovascular disease morbidity and mortality in people with either T2DM or prediabetic states. Post-challenge hyperglycaemia in people with impaired glucose tolerance has been associated with increased cardiovascular disease mortality, regardless of the fasting blood glucose (FBG) concentration, but the relationship between FBG and cardiovascular disease was dependent on post-challenge glycaemia. Improving blood glucose and HbA1c concentrations by intensive insulin treatment reduced the risk of cardiovascular disease in a small group of Japanese patients with T2DM and, in another study, improved the outcome in patients with T2DM who had suffered a myocardial infarction. However, on the basis of currently available data, there is no evidence that improved glycaemic control results in a significant reduction of cardiovascular disease risk in people with T2DM. The aim in the present article is to review existing information on the relationship between glycaemia, particularly postprandial glucose concentrations, and cardiovascular disease in people with T2DM or impaired glucose tolerance, and to point at possible mechanisms by which postprandial hyperglycaemia could lead to cardiovascular disease.

Blood Glucose↗
PubMed1992

Etiology and pathogenesis of type 1 diabetes.

An increasing bulk of evidence suggests that type 1 (insulin-dependent) diabetes mellitus is an autoimmune disease with a strong immunogenetic background. 1st-degree relatives of type 1 diabetic patients, especially HLA-identical individuals, bear an increased risk to develop the disease. The autoimmune reactions are pronounced at the onset of disease where an infiltration of islets with T and B lymphocytes, plasma cells and macrophages can be observed. Autoreactive T lymphocytes play a crucial role among effector mechanisms which finally lead to a selective destruction of pancreatic beta cells. Disease-specific autoantibodies (Ab) include cytoplasmic islet cell Ab (ICA), islet cell surface Ab (ICSA), Ab to the 64KD islet cell protein and Ab to insulin (IAA). As ICA can be detected months or years before the onset of clinical disease, testing of individuals at risk or population screening programs can help to recognize subclinical insulitis. High titers of ICA and high levels of IAA, as measured by radioimmunoassay, indicate a high risk for progression to type 1 diabetes. A blunted first phase insulin response in the i.v. glucose tolerance test is the most sensitive sign of an irreversible metabolic deterioration. It is likely that immunotherapy at a prediabetic state will be more efficacious than its initiation after the clinical manifestation of diabetes. However, the appropriate immunotherapeutical strategies are yet to be worked out.

Antibody Formation↗
PubMed2003

[Diabetes mellitus and the cerebrovascular disease].

Diabetes mellitus is, so called, the disease of the blood vessel. Indeed in many cases, atherosclerosis is already developed from the prediabetic state because of an existence of insulin resistance. Therefore, it is very important to elucidate the pathophysiological relationship between diabetes and cerebrovascular disease accompanied with intravascular calcium precipitation. Here we introduce the recent topics about the underlying relation between diabetes and cerebrovascular disease with atherosclerotic disorders.

English Abstract↗
PubMed2005

DiaPep277 (DeveloGen).

DiaPep277, a 24-amino acid peptide based on residues 437 to 460 of heat shock protein 60, is undergoing phase II clinical trials by DeveloGen for the potential treatment and prevention of established and newly diagnosed type 1 diabetes symptoms of the prediabetic state and of latent autoimmune diabetes of the adult.

Animals↗
PubMed2006

[The guidelines for the diagnosis prevention and treatment of type 2 diabetes mellitus--2005].

The incidence and prevalence of diabetes have reached epidemic proportions worldwide. The reasons for the pandemic are the sharp rise in obesity, decline in physical activity and the increase in life expectancy. There are some 400,000 people with diagnosed diabetes in Israel and they are at a markedly increased risk for cardiovascular disease, blindness, end-stage renal disease and lower limb amputation. To effectively lower this significantly increased burden of disease, a comprehensive multidisciplinary approach to chronic disease management is required. To facilitate such an approach, the Israel Diabetes Association published a guideline for the diagnosis, prevention and treatment of diabetes. The guideline, based on the ADA (American Diabetes Association) and IDF (International Diabetes Federation) guidelines, was approved by other national professional societies including hypertension, family practice, obesity, nephrology, atherosclerosis and internal medicine. The guidelines highlight the metabolic syndrome and prediabetic states, interventions for the prevention of diabetes, the new definitions of diabetes and impaired glucose metabolism and the newly defined targets for glucose, lipid, cholesterol and blood pressure control. In addition, the recommendations for periodic review and screening for complications are summarized. The need for patient education and empowerment are emphasized as is the need for the development and implementation of unique tools including computerized treatment flow-charts, prompts and quality measures, for the long term management of a complex metabolic disease.

Blood Glucose↗
PubMed1990

Clinical studies with CE-inhibitors in diabetes.

Early antihypertensive intervention in diabetes often means intervention in a cluster of cardiovascular risk factors including glucose intolerance per se, hyperlipidemia, obesity and hypertension, which are not just coexistent but may be causally linked together by the resistance of peripheral tissues to the action of insulin. Blood pressure lowering treatment should therefore be metabolically neutral in order to avoid aggravation of this risk factor syndrome. Clinical studies applying CE-inhibitors in type II diabetes are critically reviewed under this aspect. The majority of the available studies in type II diabetes report a reduction of insulin resistance and a marginal improvement of metabolic control. The order of magnitude in HbA1 reduction is nearly 10% of the glycosylated haemoglobin, reduction of fasting and postprandial blood glucose approximates 1 mmol/l. From a more extended view, considering essential hypertension as insulin resistant and thus possibly "prediabetic" state, this marginal metabolic effect gets further support from recent studies in essential hypertension consistently reporting an improvement of metabolic parameters of similar magnitude. This might become a central argument in the discussion about individualized and metabolically neutral antihypertensive treatment in essential hypertension.

Angiotensin-Converting Enzyme Inhibitors↗
PubMedDate not supplied

[Characteristics of the hormonal regulation of glycemia in rats with varying alcoholic motivation].

Rats preferring ethanol differ from those preferring water in a lowered blood serum IRI level in the presence of the same level of glycemia. Ethanol preferring animals are characterized by raised function of the adrenal cortex revealed in an elevated II-oxycordicosteroid content in these glands and a lowered cholesterol level. The glucose tolerance test (4 g/kg by intragastric administration) shows a faster depletion of beta-cells of langerhans islets in ethanol preferring animals which is suggestive of a prediabetic state. A different sensitivity of the insular apparatus to glucose is noted in the study group, too. As for glycemia, rats preferring ethanol demonstrate greater resistance to 48-hour starvation as compared to rats preferring water.

11-Hydroxycorticosteroids↗
PubMed1992

A comparative study of antigen expression by skin and pancreas in the prediabetic and diabetic state of the BB rat.

Type 1, insulin-dependent diabetes mellitus is an autoimmune disease with destruction of beta-cells in islets of Langerhans by activated (antigen-positive) infiltrating mononuclear cells accompanied by serological immune phenomena. The pathological mechanism has not yet been clarified in detail, and some inversion in the proportion of epidermal antigen expression has recently been described in spontaneous diabetes. The BB rat is one of the animal models most closely resembling human type 1 diabetes of autoimmune origin. We compared the class I and class II antigen expression in the islets of Langerhans and in the skin of spontaneously diabetic (BBD) and normoglycaemic (BBND) BB rats in the prediabetic, diabetic and non-diabetic states. Class I and class II antigen expression increased significantly in the islets of BBD rats from prediabetes to diabetes and compared with non-diabetic controls. In the same period, the dermal antigen expression (class I and class II) did not decrease and was not lower in BBD than in BBND animals. These results do not support a loss of activated (antigen-positive) dermal cells at the onset of diabetes in the BB rat and do not show a clear correlation with the antigen expression in infiltrated islets of Langerhans.

Aging↗