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

Long-term vascular complications still represent the main cause of morbidity and mortality in diabetic patients. Although randomized long-term clinical studies comparing the effects of conventional and intensive therapy have demonstrated a clear link between hyperglycemia and the development of complications of diabetes, they have not defined the mechanism through which excess glucose results in tissue damage. Evidence has accumulated indicating that oxidative stress may play a key role in the etiology of diabetic complications. Isoprostanes are emerging as a new class of biologically active products of arachidonic acid metabolism of potential relevance to human vascular disease. Their formation in vivo seems to reflect primarily, if not exclusively, a nonenzymatic process of lipid peroxidation. Enhanced urinary excretion of 8-iso-PGF(2alpha) has been described in association with both type 1 and type 2 diabetes mellitus, and correlates with impaired glycemic control. Besides providing a likely noninvasive index of lipid peroxidation in this setting, measurements of specific F(2) isoprostanes in urine may provide a sensitive biochemical end point for dose-finding studies of natural and synthetic inhibitors of lipid peroxidation. Although the biological effects of 8-iso-PGF(2alpha) in vitro suggest that it and other isoeicosanoids may modulate the functional consequences of lipid peroxidation in diabetes, evidence that this is likely in vivo remains inadequate at this time.
Cardiovasc Res 2000 Aug 18
PMID:Oxidative stress and cardiovascular complications in diabetes: isoprostanes as new markers on an old paradigm. 1096 21

Insulin resistance is a common metabolic abnormality that is associated with an increased risk of both atherosclerosis and type 2 diabetes. The phenotype of insulin resistance includes a dyslipidemia characterized by an elevation of very low-density lipoprotein triglyceride, a reduction in high-density lipoprotein cholesterol, and the presence of small, triglyceride-enriched low-density lipoproteins. The underlying metabolic abnormality driving this dylipidemia is an increased assembly and secretion of very low-density lipoprotein particles, leading to an increased plasma level of triglyceride. Hypertriglyceridemia, in turn, results in a reduction in the high-density lipoprotein level and the generation of small, dense low-density lipoproteins; these events are mediated by cholesteryl ester transfer protein. In addition, hypertension, obesity, and a prothrombotic state are also integral components of the insulin resistance syndrome. In this review, we will provide a pathophysiologic basis, based on studies on humans and in tissue culture, for the dyslipidemia of insulin resistance. We will also review the effects of insulin resistance on the coagulation and fibrinolytic pathways. It is hoped that this review will allow health professionals better to evaluate and treat their patients with insulin resistance, thereby reducing the very much increased risk of atherosclerotic cardiovascular disease carried by these individuals.
J Cardiovasc Risk 2000 Oct
PMID:The insulin resistance syndrome: impact on lipoprotein metabolism and atherothrombosis. 1114 62

Dyslipidemia is very common in diabetics and substantially increases the risk of fatal and non-fatal cardiovascular disease. Pharmacological therapy with 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors ('statins') is effective for dyslipidemia, but the cost and efficacy of individual therapies vary. Therefore, the interest in cost-effective pharmacologic interventions for the prevention of cardiovascular disease events in diabetics has increased. In this article, the literature pertaining to the epidemiology, cost and efficacy of statins in preventing cardiovascular disease in patients with type 2 diabetes mellitus, in both the primary and secondary prevention settings, is reviewed. Cost-effectiveness studies of statins in the diabetic population are detailed, along with recommendations for further research.
J Cardiovasc Risk 2001 Jun
PMID:Pharmaco-economic impact of HMG-CoA reductase inhibitors in type 2 diabetes. 1145 43

It is clear that the PPAR receptors are exciting targets for therapeutic compounds likely to impact on insulin sensitivity, lipid and glucose homeostasis and vascular disease. The PPARgamma receptor agonists rosiglitazone and pioglitazone are very useful additions to the treatment options for type 2 diabetes. Currently they have limited licences, particularly in Europe, and hopefully as further clinical trial data becomes available these will be extended. Clinical outcome studies are important to ensure that the surrogate effects on glucose and other parameters translate into improved outcomes. There is exciting potential for these agents with the possibility of a combination of effects not only on glucose and lipid homeostasis but also on coagulation and thrombosis, blood pressure and microalbuminuria, which are likely to impact on vascular disease. If the current lack of evidence of serious hepatic toxicity persists they have an advantage over metformin in terms of tolerability and can be used in patients with impaired renal function. In addition to potential effects on diabetic outcome it will be of tremendous interest to determine whether these compounds, which improve insulin sensitivity and beta-cell function, will impact on the natural history of the disease. From what is known of the PPAR receptor systems it is likely that compounds acting as agonists or partial agonists for these receptors will have differing effects and it is possible to envisage the tailoring of compounds to enhance wanted effects and diminish unwanted effects, particularly fluid retention and weight gain. The future certainly looks exciting in this area.
J Cardiovasc Risk 2001 Aug
PMID:PPARS, insulin resistance and type 2 diabetes. 1155 Sep 95

An important complication of insulin-resistant states, such as obesity and type 2 diabetes, is an atherogenic dyslipidemia profile characterized by hypertriglyceridemia, low plasma high-density lipoproteins (HDL) cholesterol and a small, dense low-density lipoprotein (LDL) particle profile. The physiological basis of this metabolic dyslipidemia appears to be hepatic overproduction of apoB-containing very low-density lipoprotein (VLDL) particles. This has focused attention on the mechanisms that regulate VLDL secretion in insulin-resistant states. Recent studies in animal models of insulin resistance, particularly the fructose-fed hamster, have enhanced our understanding of these mechanisms, and certain key factors have recently been identified that play important roles in hepatic insulin resistance and dysregulation of the VLDL secretory process. This review focuses on these recent developments as well as on the hypothesis that an interaction between enhanced flux of free fatty acids from peripheral tissues to liver, chronic up-regulation of de novo lipogenesis by hyperinsulinemia and attenuated insulin signaling in the liver may be critical to the VLDL overproduction state observed in insulin resistance. It should be noted that the focus of this review is on molecular mechanisms of the hypertriglyceridemic state associated with insulin resistance and not that observed in association with insulin deficiency (e.g., in streptozotocin-treated animals), which appears to have a different etiology and is related to a catabolic defect rather than secretory overproduction of triglyceride-rich lipoproteins.
Trends Cardiovasc Med 2001 Jul
PMID:Mechanisms of hepatic very low-density lipoprotein overproduction in insulin resistance. 1159 27

The leading cause of death among patients with type 2 diabetes mellitus (DM) is cardiovascular disease, with 75% of these deaths attributed to coronary heart disease. Over the previous two decades the pathophysiological basis of type 2 DM has been extensively investigated. Although many of the underlying molecular mechanisms involved in the development of this disorder remain to be explained, it is clear that type 2 DM is a complex medical disorder characterized by insulin resistance and defects in insulin secretion. The process through which the metabolic derangements of type 2 DM accelerate the development of cardiovascular disease in type 2 DM has yet to be determined and remains an area of intense investigation, focusing on hyperglycemia and insulin resistance as major underlying contributors. This article explores current information related to the pathophysiology of type 2 DM alone and its relationship to the development to cardiovascular disease.
J Cardiovasc Nurs 2002 Jan
PMID:Mechanisms in the development of type 2 diabetes mellitus. 1180 64

Genetic, environmental, and metabolic risk factors are interrelated and contribute to the development of type 2 diabetes mellitus. A strong family history of diabetes mellitus, age, obesity, and physical inactivity identify those individuals at highest risk. Minority populations are also at higher risk, not only because of family history and genetics, but also because of adaptation to American environmental influences of poor dietary and exercise habits. Women with a history of gestational diabetes as well as their children are at greater risk for progressing to type 2 diabetes mellitus. Insulin resistance increases a person's risk for developing impaired glucose tolerance and type 2 diabetes. Individuals who have insulin resistance share many of the same risk factors as those with type 2 diabetes. These include hyperinsulinemia, atherogenic dyslipidemia, glucose intolerance, hypertension, prothrombic state, hyperuricemia, and polycystic ovary syndrome. Current interventions for the prevention and retardation of type 2 diabetes mellitus are those targeted towards modifying environmental risk factors such as reducing obesity and promoting physical activity. Awareness of risk factors for developing type 2 diabetes will promote screening, early detection, and treatment in high-risk populations with the goal of decreasing both microvascular and macrovascular complications.
J Cardiovasc Nurs 2002 Jan
PMID:Risk factors for type 2 diabetes mellitus. 1180 65

Major clinical trials have shown that excellent glycemic control, sustained over time, can prevent or delay the microvascular complications of diabetes, including retinopathy, nephropathy, and neuropathy. No prospective trial has clearly shown that glycemic intervention can prevent the macrovascular complications of diabetes, such as myocardial infarction, cerebrovascular accident, and amputation. However, a number of landmark clinical trials have shown the efficacy of control of blood pressure and lipids and use of antiplatelet agents (mainly aspirin) in protecting the macrovasculature of individuals with diabetes. In this article, glycemic, blood pressure, lipid, and antiplatelet trials relevant to the treatment of people with type 2 diabetes are reviewed.
J Cardiovasc Nurs 2002 Jan
PMID:Clinical trial evidence for cardiovascular risk reduction in type 2 diabetes. 1180 66

The phenomenal growth in the rate of type 2 diabetes presents an enormous burden to society. Diabetes and its complications cost billions and significantly impact quality of life in individuals with diabetes. Diabetes management has transitioned from focusing exclusively on glycemic control to an approach that addresses both glucose abnormalities and the chronic complications of the disease. Increased understanding of the underlying mechanisms of disease and the multifactorial basis of diabetes complications suggest the importance of early diagnosis and treatment of all diabetes complications. Preventive approaches emphasizing risk factor reduction strategies are essential. The American Diabetes Association Standards of Medical Care for People with Diabetes assist both the health care provider and the individual with diabetes to appreciate the comprehensive treatment goals in diabetes and provide specific guidelines for achieving these goals. This article presents these guidelines in an easy-to-remember ABC format.
J Cardiovasc Nurs 2002 Jan
PMID:Glycemic control and beyond: the ABCs of standards of care for type 2 diabetes and cardiovascular disease. 1180 67

Since 1995 there have been several new medications approved for the treatment of type 2 diabetes. The availability of these new medications has made the treatment regiment for type 2 diabetes complex. There are currently five classes of oral antidiabetic agents available in the United States. These classes include: sulfonylureas, meglitinides, alpha-glucosidase inhibitors, thiazolidinediones, and biguanides. Additionally there are several types of insulin and insulin analogs available for the treatment of hyperglycemia: regular, lispro, aspart, NPH, lente, ultralente, glargine, 70/30, 50/50, and 75/25. In this article, the mechanism, site of action, and adverse effects of these classes will be reviewed. The efficacy and important management issues of these glucose-lowering drugs used in monotherapy and in combination will be discussed.
J Cardiovasc Nurs 2002 Jan
PMID:Treatment of type 2 diabetes mellitus: pharmacologic intervention. 1180 68


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