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PubMedDate not supplied

[Prediabetic states and the prevention of diabetes mellitus].

Diabetes mellitus predisposition is observed in the increased insulin activity of the pancreatic islet, followed by its exhaustion, and in its congenital or postnatal decreased activity. The former is seen in obese subjects, in large-born children and their mothers or in the children, whose mothers suffered from diabetes mellitus during pregnancy. The latter is discovered in hereditary diabetes mellitus, in hypertension and angiosclerosis. To avert diabetes mellitus in predisposed subjects a fixed-calory diet should be recommended for the pancreatic islet protection. Systematic blood and urine examinations are to be performed for revealing the initial pancreatic islet damage. Prophylactic treatment of these patients is realized by endocrinologists and the selection for therapy is carried out by special physicians.

Diabetes Mellitus↗
PubMed1989

[The value of studying the ocular conjunctiva in case-finding in prediabetic states].

Capillaroscopy, the only method available for the study of the microcirculation, without modifying its hydraulics, often provides a wealth of information in certain systemic diseases in which the microcirculatory involvement precedes clinical manifestations and of course, macrovascular complications. The prospective study of a healthy population is particularly demonstrative and the authors proposed scores on which diabetic microangiopathy could be suspected. The latter was confirmed by detailed laboratory investigations on one hand, and by the course of the disease on the other. For this reason, any subject at risk of diabetes should undergo at least one annual capillaroscopic examination of the ocular conjunctiva or if not, of the peri-ungual region. Furthermore, the study of microvessels in subjects with controlled and treated disease showed a regression of the anomalies which depended on proper control of diabetes, and this particularly nontraumatic test procedure which can be repeated and provides a wealth of information, can give a good reflection of proper therapeutic control, especially if it is performed by a trained and experienced investigator.

Capillaries↗
PubMed1998

Assessing the potential for alpha-glucosidase inhibitors in prediabetic states.

Type 2 diabetes often has an insidious onset with hyperglycaemia being present for many years before diagnosis is made. It is a progressive disease, due in part to loss of beta-cell function, with the reduction in function probably commencing 10-12 years prior to diagnosis and being aggravated by increasing fasting plasma glucose levels. Earlier intervention in those at risk from type 2 diabetes, aimed at minimizing hyperglycaemia, may prevent or delay overt diabetes and the associated development of micro- and macrovascular disease. Six-year follow-up data from the UK Prospective Diabetes Study, confirm that sulphonylurea, metformin and insulin therapy can reduce hyperglycaemia in individuals with type 2 diabetes. Although none of these agents prevent the subsequent progressive increase in fasting glucose levels, preliminary results with acarbose show that fasting plasma glucose levels can be maintained over 1 year of therapy. Three large-scale studies are currently investigating whether treatment with acarbose at an earlier stage of the disease process, in subjects with varying degrees of glucose intolerance, may be beneficial in helping to prevent or delay the onset of diabetes.

Acarbose↗
PubMed1998

Type 1 diabetes and prediabetic state in a monozygotic triplet.

Type 1 diabetes mellitus (IDDM) results from a chronic process of autoimmune destruction of beta cells of the Langerhans islets. The presence of autoantibodies (ICA, GADA, anti-IA2, IAA) in serum precedes the clinical onset of the disease. Genetic predisposition for IDDM is connected with HLA, CTLA-4 and insulin gene region. The aim of the study was the genetic and immunological analysis of a triplet. One of them developed Type 1 diabetes mellitus. We analysed HLA class II, CTLA-4 and insulin gene polymorphisms in the whole family. Besides, we investigated immunological status of three brothers. All patients present identical genotype for VNTR loci: D1S80, D17S5 and Apo B, as well as for HLA-DRB1, -DQA1, -DQB1, CTLA-4 gene and all studied insulin gene polymorphisms. That proves their monozigosity. The triplet presents strong genetic predisposition for IDDM. The two patients without overt diabetes have increased levels of ICA, GADA, IA2 and IAA.

Abatacept↗
PubMed2005

Pathophysiology of prediabetes.

Type 2 diabetic patients pass through a phase of impaired glucose tolerence and/or impaired fasting glucose known as 'prediabetic state'. Prediabetic state form a part of syndrome X, other components being obesity, hypertension, dyslipidaemia, hyperinsulinaemia and insulin resistance. The pathophysiology of prediabetes is similar to type 2 diabetes mellitus, two basic defects are insulin resistance and early beta cell failure. In prediabetes, the rapid oscillations of insulin secretion are lost and amplitude of large pulses are decreased. When insulin is delivered in a pulsatile fashion that mimics the normal rapid oscillation, its hypoglycaemic effects are greater. In prediabetes, the glycaemic excursions after each meal are high and early insulin responses to meals tend to be lower than normal but the second phase of insulin secretion is delayed and prolonged.

Blood Glucose↗
PubMed2002

The relationship between insulin secretion, the insulin-like growth factor axis and growth in children with cystic fibrosis.

OBJECTIVE: Cystic fibrosis-related diabetes mellitus (CFRD) is an increasingly common complication of cystic fibrosis. CFRD is preceded by a progressive decline in insulin secretion but there is no accepted definition of the prediabetic state in CFRD. This prediabetic state appears to have adverse effects on clinical status, nutrition and lung function, but there is no direct evidence that the impaired glucose homeostasis is the cause of these deteriorations. This study examined the prevalence of glucose intolerance and impaired insulin secretion in a population of children with CF without CFRD. Severe CF lung disease is often associated with poor weight gain and slower growth but the mechanism for this is still unclear. The relationships between the current state of glucose homeostasis, insulin secretion and the insulin-like growth factor axis, height velocity, nutrition status and lung function were therefore studied. DESIGN AND PATIENTS: Eighteen children with cystic fibrosis aged 9.5-15 years had oral glucose tolerance tests and 14 of these also had intravenous glucose tolerance tests (four refused). Blood samples were collected for insulin, C-peptide, glucose, HbA1c, insulin-like growth factor (IGF)-I, IGF-II, IGF-binding protein (IGFBP)-1 and IGFBP-3. Data on height, weight, puberty status, clinical score (Shwachman score) and lung function were recorded. Height velocity, height and weight standard deviation scores (SDS) were calculated using WHO/CDC data. RESULTS: The mean height SDS (-0.52 +/- 0.17) was less than the normal population (P = 0.007) and the mean height velocity was 4.6 +/- 0.5 cm/year, 39% with a height velocity less than the third percentile for age. The weight SDS and body mass index (BMI) were similar to the normal population. Four children had impaired glucose tolerance. The first-phase insulin response (FPIR) was below the first percentile of normal population values in nine (65%). Impaired FPIR or impaired glucose tolerance did not correlate with the Shwachman score, nutritional status or pulmonary function. There was a significant positive correlation between insulin secretion (area under the curve) and height velocity (P = 0.001) and serum IGFBP-3 levels (P = 0.001). CONCLUSIONS: Impaired glucose tolerance was present in 20% of children with cystic fibrosis. Impaired insulin secretion was common (65%) even in children with normal glucose tolerance. The mean height SDS for the group was low and the height velocity was abnormally slow in 39%, yet nutritional status as measured by BMI was appropriate for age. Relative insulin deficiency rather than nutritional deprivation or poor clinical status thus appears to be implicated in the poor linear growth of these children with relatively stable lung disease. This was a small study and firm conclusions on this chronic suppurative disease as to the cause of poor growth are not possible. The causes of poor growth are likely to be complex; nevertheless, the apparent decrease in insulin secretion combined with the expected increased demands on insulin production during pubertal growth raises the question as to whether insulin therapy should be considered in children with cystic fibrosis before the onset of cystic fibrosis-related diabetes mellitus.

Adolescent↗
PubMed2003

Insulin resistance modifies plasma fatty acid distribution and decreases cardiac tolerance to in vivo ischaemia/reperfusion in rats.

1. The early stage of insulin resistance, also termed the 'prediabetic state', is characterized by the development of hyperinsulinaemia, which maintains normoglycaemia under fasting conditions. The metabolic disorders induced in myocardial cells during this stage of the disease may constitute a basis for an alteration of the tolerance of the heart to ischaemia and reperfusion. 2. To test this hypothesis, male Wistar rats were fed a 66% fructose diet for 4 weeks, inducing a prediabetic state. Rats were then subjected to in vivo left coronary artery ligation followed by reperfusion. Blood samples were collected for plasma lipid profile determination. 3. The prediabetic state significantly increased the severity of ischaemia-induced arrhythmias (arrhythmia score 1.4 +/- 0.2 vs 2.0 +/- 0.0 in control and fructose-fed rats, respectively; P < 0.05) and the size of infarction (infarct size 41.2 +/- 3.0 vs 56.0 +/- 2.0% in control and fructose-fed rats, respectively; P < 0.01). This alteration of the tolerance to in vivo ischaemia/reperfusion may be the consequence of an increase in mono-unsaturated fatty acids and a decrease in omega3 polyunsaturated fatty acids in fructose-fed-rats. 4. In conclusion, because it is known that the prediabetic state increases the incidence of cardiovascular diseases by promoting coronaropathy, our study suggests that this metabolic disorder may also affect the prognosis of heart disease by decreasing the tolerance of cardiomyocytes to ischaemic insults.

Animals↗
PubMed2005

Nutrition in prediabetes.

Impaired glucose tolerance (IGT) and impaired fasting glucose (IFG) are forerunners of type 2 diabetes mellitus (DM) and are now recognised as prediabetes states. Cardiovascular disease (CVD) is associated with these conditions and there are many studies such as the Da Quin IGT and DM study; Finnish Diabetes Prevention Study(DPS); The Diabetes Prevention Program(DPP) which have clearly shown the efficacy and supremacy of diet intervention in controlling progression of the prediabetes state to type 2 DM. Weight reduction, increasing physical activity and restricting not only total calories but also deriving them from more healthy sources by reducing the total intake of fat, changing n-6 PUFA to n-3 PUFA, increasing the intake of fibre rich carbohydrates and the use of antioxidants have not only long-term health benefits but also can be a very useful cost-effective tool to overcome the burden of type 2 DM in our country. Prevention of type 2 DM is not a dream but a reality and this can be achieved from a path through our kitchen. Faulty nutrition seems to be the main culprit in this wide-spread epidemic of diabetes and nutritional therapy in prediabetes state appears to be the only option in our hands.

Diabetes Mellitus, Type 2↗
PubMed1981

[Fasting glycosylated hemoglobin A1c and behavior of blood sugar and blood insulin after oral glucose tolerance test in subjects with a family history of diabetes].

In a group of subjects with a known family history of diabetes (subjects with high risk of diabetes) and in two control groups, one of normal subjects and the other of poorly controlled insulin-dependent diabetic patients, all with normal blood levels of cholesterol and triglyceride, the fasting HbA1c concentration and the glycemic and insulin response to OGTT (1 g/kg of body weight) were studied. A prompt increase in serum insulin was observed both in normals and in subjects with a known family history of diabetes (poor in diabetics, of course), but insulin peak was significantly higher in the second ones. As in diabetes patients as in subjects with a known family history of diabetes, the HbA1c levels were significantly higher than in normal subjects, but significantly less high in subjects with a known family history of diabetes than in diabetics. These data might suggest that the prediabetic states generally joint with hyperinsulinemia and the HbA1c determination could contribute to the selection of those prediabetic states.

Adult↗
PubMed1996

In vivo glucose metabolism, insulin secretion and, insulin action in Europids with non-insulin-dependent diabetes mellitus (NIDDM) and their first-degree relatives.

In this review we will mainly concentrate on the most common form of NIDDM in Europe, namely the form linked to overweight, arterial hypertension, dyslipoproteinaemia and coronary heart disease (CHD)-the Insulin Resistance Syndrome (IRS). This form of NIDDM seems to be growing epidemically world wide following the industrial growth or the 'cocacolanization', as it has been mentioned. Around 2-3% of the population in Europe suffers from this disease, but for subjects beyond 60 years of age the prevalence is 5-20%. Thus, we face an enormous economical, social, and humanitarian challenge. Therefore it is important to continue the research on aetiology and pathophysiology of this syndrome. The results of treatment of NIDDM patients (often started at 60 years of age) have been rather disappointing; even properly treated NIDDM patients develop substantial complications, especially macroangiopathy. Coronary heart disease is the main cause of death in these patients and the overall mortality rate in NIDDM patients is 3-4 times higher than in comparable non diabetic-subjects. Furthermore, several complications may already be present at the diagnosis of the disease, which indicate that macroangiopathy may not be secondary to the diabetic state itself, but rather a part of the NIDDM phenotype. Based on these findings it seems obvious that the IRS must be diagnosed in the prediabetic states before macroangiopathy has started or reached a clinically manifest level. In this review, therefore, we will discuss the metabolic background of NIDDM and especially focus on the pathophysiological mechanisms leading to hyperglycaemia, i.e. alterations in glucose effectiveness, insulin action and insulin secretion in prediabetic states.

Adult↗
PubMed2005

Role of PPAR- gamma agonist thiazolidinediones in treatment of pre-diabetic and diabetic individuals: a cardiovascular perspective.

The peroxisome proliferator-activated receptors (PPARs) are nuclear fatty acid receptors, which contain a type II zinc finger DNA binding motif and a hydrophobic ligand binding pocket. These receptors are thought to play an important role in metabolic diseases such as obesity, insulin resistance, and coronary artery disease. Three subtypes of PPAR receptors have been described: PPARalpha, PPARdelta/beta, and PPARgamma. PPARalpha is found in the liver, muscle, kidney, and heart. In the liver, its role is to up-regulate genes involved in fatty acid uptake (beta-oxidation and omega-oxidation). PPARdelta/beta is involved in fatty acid oxidation in muscle. PPARgamma has high expression in fat, low expression in the liver, and very low expression in the muscle. The thiazolidinediones (TZD) are synthetic ligands of PPARgamma. By activating a number of genes in tissues, PPARgamma increases glucose and lipid uptake, increases glucose oxidation, decreases free fatty acid concentration, and decreases insulin resistance. There is a sound rationale for the use of TZDs in patients with type 2 diabetes mellitus and promising preliminary data in patients with patients with pre-diabetes. In patients with type 2 diabetes, thiazolidinediones had been shown to decrease mean HbA(1c)by 1.5% and lower HbA(1c) to less than 7% in 30% of patients. Decreased muscle insulin resistance primarily mediates the glucose lowering effect. In addition, there are several nonhypoglycemic effects of TZDs which may be beneficial to both diabetics and patients with pre-diabetes. These include effects on lipid metabolism, blood pressure, endothelial function, atherosclerotic plaque, coagulation, and albuminuria. In a pilot study, we recently demonstrated that insulin sensitizers such as thiazolidinediones appear to be associated with better clinical outcomes compared to insulin providers in diabetic patients presenting with acute coronary syndromes. In another study, we showed that the prediabetic state is a marker for worse prognosis in patients with acute coronary syndromes. In this article, we review the existing literature on the effectiveness of PPAR-gamma agonists in patients with either overt diabetes or a prediabetic state.

Diabetes Mellitus, Type 2↗
PubMed2000

Plasma lipid and blood glucose levels in patients with destructive periodontal disease.

Hyperlipidaemia and hyperglycaemia are major risk factors for cardiovascular disease. In recent years, some evidence has been presented that periodontal disease is associated with an increased risk of cardiovascular disease. To further elucidate this association, we have studied standard blood chemistry variables known as risk markers for cardiovascular disease in periodontally diseased and healthy subjects. We have measured levels of plasma lipids and fasting blood glucose in 39 subjects with moderate periodontal disease (age 50-60 years) and compared the results with those obtained in 40 age- and sex-matched controls. Both groups were systemically healthy according to their medical history. Total cholesterol, low density lipoprotein cholesterol and triglycerides were significantly higher in periodontally diseased subjects by about 8% (p<0.03), 13% (p<0.003) and 39% (p<0.001), respectively, when compared to controls. Although subjects with diabetes were excluded from the study, we found significantly higher blood glucose levels in the patient than in the control group (85 +/- 25 versus 73 +/- 17 mg/dl; p<0.02). There was also a significantly higher frequency of pathological plasma lipid profiles in the patient than in the control group. The results indicate that hyperlipaemia and pre-diabetes may be associated with periodontal disease in systemically healthy subjects. These data do not allow us to decide, whether periodontal disease causes an increase in hyperlipaemia and in a prediabetic state or whether periodontal disease and cardiovascular disease share hyperlipidaemia and the prediabetic state as common risk factors.

Aged↗
PubMed1993

Insulin receptor isotype expression correlates with risk of non-insulin-dependent diabetes.

Skeletal muscle insulin resistance plays a pivotal role in the pathogenesis of non-insulin-dependent diabetes mellitus (NIDDM), as individuals with this defect are at increased risk of developing the disease later in life. To assess whether the abnormal expression of the structurally distinct human insulin receptor isoforms, HIR-A and HIR-B, which has been found in skeletal muscle of NIDDM patients, is a feature of a prediabetic state, skeletal muscle biopsies from nondiabetic individuals ranging from high insulin sensitivity to insulin resistance were examined. Polymerase chain reaction analysis of mRNA from muscle biopsies detected exclusive or predominant expression of HIR-A in 13 patients with normal insulin sensitivity. In contrast, 7 subjects with various degrees of insulin resistance exhibited abnormally increased HIR-B RNA expression. This association suggests the abnormal expression of receptor isoforms as a characteristic of the prediabetic state and supports the notion of a connection of this aberration with the pathogenesis of NIDDM. Changes in HIR-A/B expression in the skeletal muscle may thus provide a prognostic criterion for the development of NIDDM.

Adult↗