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Query: UMLS:C0011860 (type 2 diabetes)
 57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Obesity and pattern of fat distribution are both important factors related to poor health outcomes. Many measures of obesity and fat distribution pattern have been employed by different authors and to facilitate interpopulation comparisons and interpretation of secular trends it is necessary that standardized methods for measurement and classification are set in place. The use of BMI as a measure of fatness for epidemiological studies is widely accepted, easily measured and BMI predicts morbidity and mortality in many populations. The most appropriate level at which to define obesity is a matter of debate but systems which use BMI > or = 25 and < or = 30 kg/m2 as overweight, and BMI > 30 kg/m2 as obese for all adults are simple, easily remembered, already widely used and BMIs above 30 kg/m2 are clearly associated with increased risk of morbidity and mortality. In some populations there may be a case for using a lower cut-off but not unless there is specific evidence to support this. For the present WHR is probably the best method for assessing fat distribution, although waist circumference on its own may be more useful in determining risk levels. Standard sites for measurement of both waist and hip girths have been described. There is a large variation in the prevalence of obesity across the populations for which data is available, with high prevalences of obesity and dramatic secular trends especially apparent in modernizing Pacific Island populations. The 'thrifty genotype' hypothesis has been invoked to try and explain this situation. The clustering of obesity, NIDDM and CVD risk factors has been recognized and various 'syndromes' have been described which group different factors together, with hyperinsulinaemia and insulin resistance proposed as the underlying problem.
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PMID:The epidemiology of obesity. 798 Mar 48

Diabetes is associated with increased morbidity and mortality from cardiovascular disease in the absence of the major risk factors--cigarette smoking, hypertension and serum cholesterol concentration. When these risk factors are present, the attributable risk to each factor alone and to the combination of risk factors is higher in diabetic than in nondiabetic subjects. Thus, stringent measures to correct risk factors for cardiovascular disease have been advocated in diabetic patients. In addition to hypercholesterolaemia, other lipid and lipoprotein abnormalities collectively referred to as diabetic dyslipidaemia probably contribute to vascular risk. Hypertriglyceridaemia, often associated with low high-density-lipoprotein cholesterol, is common in NIDDM patients and is associated with insulin resistance. Recent information in diabetic patients, pointing to the association of hypertriglyceridaemia with accumulation of remnant particles and alterations in low-density-lipoprotein subfractions, helps to explain the strong relationship between hypertriglyceridaemia and vascular risk in these individuals. Although there are as yet no intervention trials with lipid-lowering diets or drugs in diabetic patients to judge the impact on vascular disease, national and international bodies have furnished guidelines for the identification and treatment of lipid disorders in diabetes in the hope of reducing the huge toll of vascular disease in these patients.
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PMID:Diabetic dyslipidaemia: treatment implications. 798 8

In 370 non-insulin-dependent diabetic (NIDDM) patients less than 66 years of age, we found the prevalence of albuminuria (> 300 mg 24 h-1) to be 13.8%. Males had a higher prevalence than females (19 vs. 5%). A kidney biopsy was performed in 35 patients. The biopsy revealed diabetic glomerulosclerosis in 77% of the cases and a variety of non-diabetic glomerulopathies in the remaining 23%. Fifty-six per cent of the patients with diabetic glomerulosclerosis had diabetic retinopathy, whereas none of the patients with non-diabetic glomerulopathies had signs of retinopathy. The presence of diabetic retinopathy strongly suggests that diabetic glomerulosclerosis is the cause of albuminuria. During a 5-year (range 1-7 years) prospective study, the course of kidney function was followed in 26 NIDDM patients with diabetic glomerulosclerosis. The glomerular filtration rate declined, and elevated systolic blood pressure was positively correlated to the rate of decline. The frequency of diabetic complications increased with increasing levels of urinary albumin excretion. In a cross-sectional study of 549 NIDDM patients, the prevalence of proliferative retinopathy was 2, 5 and 12%, the prevalence of hypertension 46, 68 and 85%, and the prevalence of ischaemic heart disease 22, 26 and 46% in normo-, micro-, and macroalbuminuria, respectively. The mortality from cardiovascular disease is increased ninefold in NIDDM patients with macroalbuminuria compared to the non-diabetic background population. The presence of the well-established risk factors cannot account for this finding alone.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Dyslipidaemia and cardiovascular disease in non-insulin-dependent diabetic patient with and without diabetic nephropathy. 798 14

In mid-1990 we evaluated blood pressure and its associations in 366 nondiabetic adult Navajos and 400 Navajos with type 2 diabetes attending Indian Health Service outpatient clinics in Tuba City, Arizona. In nondiabetics, systolic blood pressure (SBP) rose with increasing age while diastolic blood pressure (DBP) fell; 13.4% had hypertension by diagnosis or treatment. Female nondiabetics had lower blood pressures than males. SBP and DBP correlated with age, body mass index (BMI), and urinary albumin excretion (UAE). Hypertension was associated with a sixfold increase in nephropathy, a threefold increase in renal insufficiency, and an almost sixfold increase in cardiovascular disease. Diabetics had higher blood pressures than age- and sex-matched nondiabetics; 58.4% had hypertension by diagnosis or treatment, and, in spite of widespread antihypertensive treatment, blood pressures in almost 50% were suboptimal from the perspectives of cardiovascular and renal protection. Blood pressures of female diabetics were similar to those of males. Blood pressures correlated with age, BMI, and increasing UAE. Rates of nephropathy and cardiovascular disease were much higher in diabetics than nondiabetics, and within the diabetic population hypertension was associated with a greater than threefold increase in nephropathy, an eightfold increase in renal insufficiency, a five-fold increase in peripheral and cerebrovascular disease, and more than doubling of the rate of heart disease. The relationship of blood pressure to renal and cardiovascular disease suggest similar mechanisms in nondiabetics and diabetics, with diabetes contributing an accentuated susceptibility. Albuminuria and cardiac disease are generated at "subhypertensive" blood pressures, while established hypertension appears to drive overt renal, cerebrovascular, and peripheral vascular disease, and to further increase heart disease risk.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Blood pressure in Navajo Indians and its association with type 2 diabetes and renal and cardiovascular disease. 803 47

The term reduced glucose tolerance is often used to describe an intermediate phase between normal glucose metabolism and diabetes, and WHO discriminates between type 2 diabetes and reduced glucose tolerance. However, biologically there is no clear distinction between the two groups. As a biological phenomenon reduced glucose tolerance is important because it is a risk factor for cardiovascular disease. The article describes reduced glucose tolerance as a part of the metabolic cardiovascular syndrome, and several models which might help to explain some of the mechanisms. The distribution of musculoskeletal fibres, the impact of physical activity, and the relation between insulin and blood pressure, lipids and the disposition for thrombosis, are discussed. Genetic disposition is also an important factor. The research in this field is rapidly increasing, and a survey can only be a snapshot. However, greater understanding of the mechanisms linking reduced glucose tolerance and the metabolic cardiovascular syndrome is a strong argument to focussing the total risk profile, and not only, single risk factors, in preventive cardiovascular medicine.
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PMID:[Reduced glucose tolerance as a risk factor of cardiovascular diseases]. 807 81

Prospective studies showed that hypersecretion of albumin in the urine of patients with type 2 diabetes mellitus is associated with high morbidity and mortality from cardiovascular disease and nephropathy. 65 type 2 diabetes from 6 family medicine practices were studied. Microalbuminuria was found in 37% and was significantly more common in men than in women (53% and 23%, respectively; p < 0.02). Uncontrolled blood glucose levels were also more common in men (p < 0.03). Using logistic regression with microalbuminuria as the dependent variable, a significant correlation was found with male gender, fasting blood glucose 155 mg/dl or more, and systolic blood pressure 159 mm Hg or higher. Among those with microalbuminuria, ischemic heart disease was significantly more common in those 65 years or older than in those younger (p = 0.02). This study strengthens the assumption that type 2 diabetics with microalbuminuria might be at greater risk for developing ischemic heart disease. Strict detection and control are recommended.
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PMID:[Microalbuminuria and ischemic heart disease in noninsulin-dependent diabetes]. 820 May 83

In cross-sectional studies of asymptomatic diabetic patients, multiple abnormalities in left ventricular (LV) function have been found. Long-term significance of these abnormalities is unknown because follow-up studies have not been previously performed. LV ejection fraction (EF) by radionuclide angiocardiography was examined in middle-aged control subjects (n = 44), in patients with insulin-dependent (IDDM) (n = 32) and non-insulin-dependent (NIDDM) (n = 32) diabetes mellitus at baseline and after 4-year follow-up. At baseline, all study subjects were free from cardiovascular disease. LVEF at rest did not differ between the groups at baseline. The decrease in LVEF at rest during follow-up was 1.1 +/- 1.1% (mean +/- SEM) in control subjects, 3.1 +/- 1.3% (p = NS, compared with control subjects) in patients with IDDM, and 7.2 +/- 1.4% (p < 0.01) in patients with NIDDM. At follow-up examination, abnormally low LVEF at rest (< 50%) was found in 7% of control subjects, 13% of patients with IDDM (p = NS), and in 31% of patients with NIDDM (p < 0.05). Compared with control subjects, the prevalence of an abnormal LVEF response to exercise (an increase by < 5%, or a decrease) was higher in diabetic groups at both examinations. This prevalence increased in control subjects from 10% at baseline to 26% at follow-up examination.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Left ventricular systolic function in middle-aged patients with diabetes mellitus. 820 39

Because of the frequent occurrence of premature cardiovascular disease in patients with non-insulin-dependent, type II diabetes mellitus (NIDDM), the attenuated fibrinolytic activity of plasma from type II diabetic patients with increased concentrations of plasminogen activator inhibitor type-1 (PAI-1), and the fact that insulin stimulates synthesis of PAI-1 by human hepatic cells in vitro, we and others have hypothesized that accelerated vascular disease in type II diabetes may result in part from impaired fibrinolysis secondary to excessive elaboration of PAI-1 stimulated by insulin. Alternatively, the hyperglycemia associated with type II diabetes could influence the synthesis and secretion of PAI-1 directly. The present study was performed to determine whether PAI-1 secretion is or is not sensitive to the prevailing concentration of glucose in the conditioned medium of endothelial and liver cells, which are thought to be the major sources of circulating PAI-1 in vivo. Confluent cells were exposed to 0, 2.8, 5.6, 11.1, or 22.2 mmol/L (0, 50, 100, 200, or 400 mg/dL) glucose in medium without serum and subsequently to media with or without insulin (7.3 nmol/L). Secretion of PAI-1 by highly differentiated human hepatoma (Hep G2) cells did not increase as a function of increasing concentrations of glucose, whether or not insulin was present. In contrast, with pig aortic endothelial cells, the secretion of PAI-1 increased significantly with extracellular glucose with or without insulin. The increases in PAI-1 were specific (as shown by metabolic labeling experiments) and not attributable to osmotic effects (as shown by replacement of glucose by sorbitol).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Augmentation of synthesis of plasminogen activator inhibitor type-1 in arterial endothelial cells by glucose and its implications for local fibrinolysis. 824 Nov 3

In IDDM or NIDDM, the total plasma cholesterol and triglycerides are usually within normal limits when the blood glucose is controlled. Marked hypertriglyceridemia can develop with loss of glycemic control and is often due to superimposed genetic abnormalities in lipoprotein metabolism. Tight control in IDDM usually reduces LDL and VLDL to normal levels and may raise HDL above the normal range. Low HDL cholesterol and mild to moderate elevations of VLDL triglyceride are common in NIDDM if obesity or proteinuria is also present. Both HDL and LDL may be smaller and more dense and may be enriched with triglyceride as compared with cholesterol. These abnormalities may require weight loss for control. The increased incidence of cardiovascular disease in diabetes is unexplained but is amplified by the well-defined cardiovascular risk factors. The new American Diabetes Association guidelines call for treatment of high triglycerides and LDL cholesterol to be aggressively reduced. Triglycerides should be under 200 mg/dL, are considered borderline high between 200 and 400 mg/dL, and high when above 400 mg/dL. Low HDL is defined as less than 35 mg/dL. Control of obesity with diet and exercise and reduced intake of saturated fat and cholesterol are important first steps. If needed, drug therapy is appropriate to reduce LDL to levels below 130 mg/dL in all adult diabetics and below 100 mg/dL in those with cardiovascular disease.
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PMID:Lipoprotein disorders in diabetes mellitus. 828 28

Hyperinsulinemia is very much in the spotlight. Debate rages as to its significance and role in the etiology not only of NIDDM, but also other morphological and metabolic risk factors for atherosclerotic cardiovascular disease, including upper-body obesity, dyslipidemia, hypertension, and hyperuricemia. Epidemiological data support a key role for hyperinsulinemia in these disorders but it is far from conclusive except for the fact that hyperinsulinemia and insulin resistance may be present many years before the onset of impaired glucose tolerance and NIDDM, and clearly play a role in their etiology. The thrifty genotype hypothesis provides a plausible basis for a better understanding of how hyperinsulinemia and insulin resistance could lead to glucose intolerance and atherosclerotic cardiovascular disease, but the detailed biochemical mechanisms remain elusive. A role for increased sympathetic nervous system activity, resulting from hypothalamic stimulation as a primary event causing hyperinsulinemia, cannot be excluded as a cause of hyperinsulinemia. The current focus on hyperinsulinemia also has resulted in closer examination of the therapy of diabetes and hypertension, emphasizing the need to avoid hyperinsulinemia in both IDDM and NIDDM individuals because of the putative risk of atherosclerotic cardiovascular disease and hypertension. There is still a paucity of epidemiological data to support a role for hyperinsulinemia in the etiology of hypertension. However, clinical practice already is being influenced by the fact that ACE inhibitors have been shown to reduce insulin resistance in clinical research studies. The research reviewed here, particularly that relating to hyperinsulinemia, insulin resistance, and cardiovascular disease risk factors, has opened new vistas for the treatment and prevention of NIDDM and atherosclerotic cardiovascular disease. Appropriate exercise clearly is associated with improved insulin sensitivity, modification of CVD risk factors, and lower prevalence of NIDDM. Upper-body obesity, the latest culprit in the field, can also be reduced by exercise. Hyperinsulinemia and insulin resistance can be detected in children, adolescents, and young adults. NIDDM can be prevented, but clearly, intervention needs to commence in childhood, and intensive risk factor intervention in subjects with NIDDM can reduce the risk of atherosclerotic cardiovascular disease. It seems paradoxical that prevention of NIDDM and atherosclerotic cardiovascular disease are now possible even though the biochemical and molecular basis of these disorders is not fully understood.
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PMID:Hyperinsulinemia--how innocent a bystander? 829 79


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