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 17,070 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It is now well recognized that insulin resistance and/or hyperinsulinemia are characteristic of a number of common human disease states including obesity, non-insulin dependent diabetes mellitus (NIDDM), essential hypertension, and atherosclerotic cardiovascular disease. More recent evidence suggests that impaired insulin action and elevated levels of circulating insulin may also be present in a substantial proportion of apparently healthy nonobese individuals. Considerable attention is now being focused on the potential long term adverse consequences of elevated circulating insulin levels. In particular, the frequent concurrence of these clinical disorders of carbohydrate metabolism, lipid metabolism, and vascular disease has led to the hypothesis that insulin resistance and the ensuing hyperinsulinemia may be a common pathophysiologic factor in the etiology of these disease states. In this review, we will examine the evidence for this hypothesis with particular attention to the adverse effects of chronic hyperinsulinemia.
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PMID:Hyperinsulinemia and its sequelae. 220 24

Mortality among 4740 diabetic men and women aged 35-55 years participating in the WHO Multinational Study of Vascular Disease in Diabetics has been studied. Ten of the original centres (Warsaw, Berlin, Havana, Arizona, Oklahoma, Hong Kong, Switzerland, London, Tokyo, Zagreb) were able to identify the life/death status of their study participants on 1 January 1983, giving an average follow-up period of six to seven years. All-cause mortality rates in males varied about threefold among the ten participating centres with the highest rates in Warsaw, Berlin and Havana and the lowest rates in Tokyo and Zagreb. All-cause mortality rates for females varied about fourfold with the highest rates in Warsaw and Oklahoma and the lowest rates in Tokyo. The proportion of deaths ascribed to circulatory disease varied among the centres ranging from 32% for males and 0% for females in Tokyo to 67% for males and 47% for females in London. There was an excess all-cause mortality in males compared to females for all centres except Zagreb. This excess also applied to circulatory diseases in general, ischaemic heart disease in particular and occurred in both insulin-dependent and non-insulin-dependent diabetic patients. Death rates for insulin-dependent diabetic patients were generally higher than those for non-insulin-dependent patients.
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PMID:International variations in mortality among diabetic patients: the WHO Multinational Study of Vascular Disease in Diabetics. 221 Jan 20

Doppler flow velocity waveform analysis (FVWFA), recorded from the dorsalis pedis artery (DPA) and the radial artery (RA), was performed on 36 women in attempting to detect an initial diabetic microangiopathy (DM). The study comprised two groups of women affected by non-insulin-dependent diabetes mellitus, 6 patients (pts) of reproductive age (1), 12 pts in menopause (II), and two groups of age-matched healthy controls (C) (III and IV). Clinical signs of initial DM were present in group I. All the examined pts were nonsmokers and normotensive and without cardiopathy, signs of diabetic macroangiopathy, collagen vascular disease and/or Raynaud's phenomenon, and renal failure. Four waveform dimensions capable of separating different degrees of peripheral obstructive arteriolar disease were determined on velocity tracing and the results used in a single best discriminant equation. The resultant discriminant score (DS), derived by FVWFA on DPA, showed a highly accurate rate of separating the young pts with DM from both C and the pts in menopause without DM. Furthermore, the resultant DS was statistically not different in groups II, III, and IV. In conclusion, FVWFA on DPA, in this experience, has proved to be an accurate and sensitive method in the detection of initial DM.
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PMID:Use of Doppler flow velocity waveform analysis in detection of initial diabetic microangiopathy. 222 66

The elderly patient with type II diabetes should be treated in much the same fashion as a younger person with the same disease, although emphasis needs to be placed on minimizing side effects, drug interactions, and hypoglycemia. Chlorpropamide should not be used in these patients, unless there is no other choice. The remaining agents--tolbutamide, acetohexamide, tolazamide, glyburide, and glipizide--should be started at low doses and gradually increased until optimal diabetic control is reached. The initial treatment goal is a FPG level of less than 180 mg/dl and a final goal is a 1- to 2-hour PPG concentration between 140 and 180 mg/dl. The glycosylated hemoglobin value should be no greater than 1.5% above the upper limit of normal, and should be lower, if possible. It must be kept in mind, however, that the closer diabetic patients are to achieving euglycemia, the more likely is hypoglycemia. Treatment goals therefore may have to be relaxed in someone at increased risk of hypoglycemia (e.g., patients with irregular eating habits or renal insufficiency) or when hypoglycemia may pose a greater hazard (e.g., patients with coronary artery or cerebral vascular disease). Patients on sulfonylurea agents should have blood glucose values measured once a month and glycosylated hemoglobin levels determined once every 3 months to alert the clinician to the possible need to adjust therapy. In this way, potential hypoglycemia can be avoided if blood glucose levels are drifting too low and chronic hyperglycemia can be identified and treated within a short period of time. When a patient's status changes--e.g., he is placed on new medication, becomes depressed and anorexic, or develops another medical problem--care must be taken to re-evaluate his diabetes management. Drugs such as sulfonamide antibiotics can potentiate the action of the sulfonylureas and cause hypoglycemia, renal insufficiency may necessitate changing the type of sulfonylurea agent or decreasing the dose, and malnutrition may obviate any need for therapy with an oral hypoglycemic agent. If these guidelines are kept in mind, the older diabetic patient can be managed on a sulfonylurea agent in conjunction with the appropriate diet. Should these measures prove to be ineffective, then insulin therapy should be instituted. Controlling chronic hyperglycemia will help improve the quality of life for patients with diabetes and decrease the probability of developing some of the devastating complications associated with this disease.
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PMID:Use of sulfonylurea agents in older diabetic patients. 222 54

The 497 members of the London Cohort of the WHO Multinational Study of Vascular Disease in Diabetics have been followed for mortality from 1975 to 1987. During this period 92 patients died. The most common cause of death was myocardial infarction: 36 (39.1%) deaths, heart disease was responsible for 51.1% of deaths and all cardiovascular disease for 55.4%. Neoplastic disease accounted for 25% of the deaths and diabetic nephropathy for 5.4%. Age-standardised mortality rates were higher in men than in women in both Type 1 (insulin-dependent) diabetes and Type 2 (non-insulin-dependent) diabetes. Standardised mortality ratios for the first and second five year follow-up periods were higher for men than for women in Type 2 diabetes but were higher for women than men in Type 1. The results suggest that the female survival advantage seen in the general population may persist in Type 2 but not in Type 1 diabetes.
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PMID:A prospective study of mortality among middle-aged diabetic patients (the London Cohort of the WHO Multinational Study of Vascular Disease in Diabetics) I: Causes and death rates. 225 30

Potential risk factors have been examined for association with mortality over a 10-12 year follow-up of the patients of the London Cohort of the WHO Multinational Study of Vascular Disease in Diabetics (aged 35-54 years at entry to the study). Proteinuria has the strongest association with all-cause mortality in univariate analysis being significant in patients of both sexes with Type 2 (non-insulin-dependent) diabetes mellitus and in women with Type 1 (insulin-dependent) diabetes mellitus; both systolic blood pressure (men) and hypertension (both sexes) (as a categorical variable) are significant in Type 1 diabetes. Hypertension is also significantly associated with all-cause mortality in multivariate analysis in both sexes with Type 1 diabetes as proteinuria is in women with Type 2 diabetes. There is an unexpected negative association between plasma creatinine and all-cause mortality in men with Type 2 diabetes. Systolic blood pressure and hypertension are also significantly linked with cardiovascular mortality in Type 1 diabetes, hypertension having an estimated relative risk of 4.6 [corrected] in multivariate analysis. Serum cholesterol and proteinuria showed the strongest associations with cardiovascular mortality in Type 2 diabetes. Proteinuria is associated with non-cardiovascular mortality in both types of diabetes in univariate but not multivariate analysis. In multivariate analysis hypertension (Type 1 diabetes) and diabetes duration (Type 2 diabetes) are associated with non-cardiovascular mortality. Hypertension and proteinuria have the most consistent associations with mortality in the different analyses with the effect of hypertension appearing stronger in Type 1 diabetes and proteinuria in Type 2 diabetes.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A prospective study of mortality among middle-aged diabetic patients (the London Cohort of the WHO Multinational Study of Vascular Disease in Diabetics) II: Associated risk factors. 225 31

Glucose tolerance and insulin secretion were studied in 56 women 6-12 years following a pregnancy complicated by gestational diabetes, and in 23 matched controls. At recall 14 women were known to have diabetes and five were again pregnant with recurrent gestational diabetes. The early development of diabetes was associated with a fasting plasma glucose greater than 6 mmol/l during pregnancy and with a high plasma glucose response to oral glucose which persisted after delivery. Obesity was predictive of non-insulin-dependent diabetes whereas those that later required insulin were not obese. At recall, seven of the remaining 37 women were found to have unrecognized diabetes, 13 had impaired glucose tolerance (IGT) and 17 were normal by WHO criteria using a 75 g oral glucose tolerance test. In these 37 women, fasting plasma glucose and the glucose response to oral glucose in pregnancy were not predictive of subsequent diabetes or impaired glucose tolerance. Obesity in pregnancy and subsequent weight gain were associated with non-insulin-dependent diabetes and impaired glucose tolerance at recall. Insulin deficiency was observed during the oral glucose tolerance test in the diabetics (the mean +/- SEM ratio insulin area:glucose area 4.1 +/- 1.3 diabetics, 10.7 +/- 1.8 controls, p less than 0.05), whereas in the group with impaired glucose tolerance insulin levels were high and in proportion to their hyperglycaemia (insulin area:glucose area 10.9 +/- 1.4 IGT, 9.4 +/- 1.4 controls). Women with normal glucose tolerance and previous gestational diabetes had significantly lower insulin responses than their controls, despite mild hyperglycaemia (insulin area:glucose area 4.0 +/- 0.7 normal glucose tolerance, 7.6 +/- 1.1 controls, p less than 0.02). Abnormalities of glucose tolerance and insulin secretion are present following a gestational diabetic pregnancy. Gestational diabetes identifies women at risk for developing diabetes and impaired glucose tolerance, both of which are risk factors for premature vascular disease.
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PMID:Abnormalities of glucose tolerance following gestational diabetes. 229 Sep 18

Seven hundred and sixty seven Doppler umbilical artery velocity waveform analyses were performed in 108 pregnant insulin-dependent diabetes mellitus (IDDM) women. No significant correlation between mean third trimester systolic to diastolic (S/D) ratio and either mean blood glucose (r = 0.19) or glycosylated hemoglobin levels (r = 0.28) was found. Mean second and third trimester S/D ratios differed significantly in patients with or without vascular disease (P less than 0.05). Furthermore, women without vasculopathy who demonstrated an elevated S/D developed preeclampsia and delivered appropriate for gestational age infants while patients with vascular disease or chronic hypertension and elevated third trimester S/D (greater than 3) delivered intra uterine growth retarded (IUGR) infants. Moreover, in most of the latter group elevated S/D ratios were recorded in the second trimester prior to ultrasound documentation of IUGR. Our data suggest that in the absence of vasculopathy normal fetal placental resistance can be expected in most pregnancies complicated by diabetes. Patients with vasculopathy are at higher risk for fetal IUGR, which may be identified by early umbilical artery velocimetry.
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PMID:Umbilical artery velocimetry in insulin dependent diabetes mellitus (IDDM) pregnancies. 229 61

Platelet and plasma vasoactive amine concentrations were measured in healthy controls and in type 1 (insulin-dependent) diabetic patients with or without vascular disease. Platelet concentrations of serotonin and noradrenaline were similar in all groups and were unrelated to age or gender, or to duration of diabetes, blood pressure, glycaemia or renal function in the diabetic subjects. Plasma concentrations of serotonin in the diabetic groups were comparable (118 +/- 16 (mean +/- SEM) and 127 +/- 21 pmol/mL), and were significantly higher in comparison to the healthy controls (66 +/- 12 pmol/mL, P = 0.002).
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PMID:Platelet and plasma vasoactive amines in type 1 (insulin-dependent) diabetes mellitus with and without vascular disease. 238 58

This review summarizes aspects of the phenotypic expression, natural history, recognition, pathogenesis, and heterogeneous nature of maturity-onset diabetes of the young (MODY), which is inherited in an autosomal-dominant pattern. There are differences in metabolic, hormonal, and vascular abnormalities in different ethnic groups and even among White pedigrees. In MODY patients with low insulin responses, there are delayed and decreased insulin and C-peptide secretory responses to glucose from childhood or adolescence even before glucose intolerance appears, which may represent the basic genetic defect. When followed for decades, nondiabetic siblings have normal insulin responses. The fasting hyperglycemia of some MODY patients has been treated successfully with sulfonylureas for up to 30 yr. In a few patients, after years or decades of diabetes, the insulin and C-peptide responses to glucose are so low that they resemble those of early insulin-dependent diabetes mellitus. The progression of the insulin secretory defect over time distinguishes between these two types of diabetes. In contrast are patients from families who have very high insulin responses to glucose, despite glucose intolerance and fasting hyperglycemia similar to that seen in patients with low insulin responses. In many of these patients, there is in vivo and in vitro evidence of insulin resistance. Whatever its mechanism, the compensatory insulin responses to nutrients must be insufficient to maintain normal carbohydrate tolerance. This suggests that diabetes occurs only in those patients who have an additional islet cell defect, i.e., insufficient beta-cell reserve and secretory capacity. In a few MODY pedigrees with high insulin responses to glucose and lack of evidence of insulin resistance, a structurally abnormal mutant insulin molecule that is biologically ineffective is secreted. No associations have been found between specific HLA antigens and MODY in White, Black, and Asian pedigrees. Linkage studies of the insulin gene, insulin-receptor gene, erythrocyte/HepG2 glucose-transporter locus, and apolipoprotein B locus have shown no association with MODY. Vascular disease may be as prevalent as in conventional non-insulin-dependent diabetes mellitus. Because of autosomal-dominant transmission and penetrance at a young age, MODY is a good model for further investigations of etiologic and pathogenetic factors in non-insulin-dependent diabetes mellitus, including the use of genetic linkage strategies to identify diabetogenic genes.
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PMID:Scope and heterogeneous nature of MODY. 240 17


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