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

Only recently are we beginning to understand the complex interplay of factors involved in vascular disease and diabetes. Insulin resistance provides a starting point to explain the many factors that lead to the more severe vascular disease characteristic of diabetes. Insulin resistance syndrome comprises insulin resistance and compensatory hyperinsulinaemia as well as hypertension, dyslipidaemia, macrovascular disease, and increased plasminogen activator inhibitor-1 activity. The development of type 2 diabetes may be viewed as the inability of the pancreas to continue to overcome insulin resistance, even with excessive insulin production.
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PMID:Pathogenesis of vascular disease. 1121 Feb 41

In all industrialized countries, life expectancy has risen in the past 100 years. The incidence of elderly patients reaching end-stage renal disease (ESRD) and requiring renal replacement therapy has also increased. During the past few decades, the pattern of ESRD has changed significantly with the emerging predominance of elderly patients. The causes of this phenomenon are manifold and include an increasing number of chronic diseases typical of the 'third age', such as type 2 diabetes mellitus and vascular disease. In many species, a consequence of aging includes deterioration of renal function, partly due to structural alterations, and partly as the result of a diminishing blood flow. In humans, the aging kidney is characterized by modifications resulting from organic and functional disturbances. In particular, type 2 diabetes mellitus has emerged as an important condition, the microvascular and macrovascular complications of which are a common cause of morbidity and mortality in older patients. In part I of this review, the morphological and functional changes of the aging kidney will be reviewed, as well as the pathological conditions leading to the loss of renal function in the elderly.
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PMID:Renal function and renal disease in the elderly: Part I. 1129 10

Certain dietary risk factors for physical ill health are also risk factors for depression and cognitive impairment. Although cholesterol lowering has been suggested to increase vulnerability to depression, there is better support for an alternative hypothesis that intake of n-3 long-chain polyunsaturated fatty acids can affect mood (and aggression). Possible mechanisms for such effects include modification of neuronal cell membrane fluidity and consequent impact on neurotransmitter function. Stronger evidence exists concerning a role for diet in influencing cognitive impairment and cognitive decline in older age, in particular through its impact on vascular disease. For example, cognitive impairment is associated with atherosclerosis, type 2 diabetes and hypertension, and findings from a broad range of studies show significant relationships between cognitive function and intakes of various nutrients, including long-chain polyunsaturated fatty acids, antioxidant vitamins, and folate and vitamin B12. Further support is provided by data on nutrient status and cognitive function. Almost all this evidence, however, comes from epidemiological and correlational studies. Given the problem of separating cause and effect from such evidence, and the fact that cognitive impairment and cognitive decline (and depression) are very likely to be significant factors contributing to the consumption of a poor diet, greater emphasis should now be placed on conducting intervention studies. An efficient approach to this problem could be to include assessments of mood and cognitive function as outcome measures in studies designed primarily to investigate the impact of dietary interventions on markers of physical health.
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PMID:A healthy body, a healthy mind: long-term impact of diet on mood and cognitive function. 1131 Apr 19

In all industrialized countries, life expectancy has risen in the past 100 years. The incidence of elderly patients reaching end-stage renal disease (ESRD) and requiring renal replacement therapy has also increased. During the past few decades, the pattern of ESRD has changed significantly with the emerging predominance of elderly patients. The causes of this phenomenon are manifold and include an increasing number of chronic diseases typical of the 'third age', such as type 2 diabetes mellitus and vascular disease. In many species, a consequence of aging includes deterioration of renal function, partly due to structural alterations, and partly as the result of a diminishing blood flow. In humans, the aging kidney is characterized by modifications resulting from organic and functional disturbances. In particular, type 2 diabetes mellitus has emerged as an important condition, the microvascular and macrovascular complications of which are a common cause of morbidity and mortality in older patients. In Part II of this review, the specific aspects of renal replacement therapy in the elderly will be discussed.
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PMID:Renal function and renal disease in the elderly: Part II. 1139 95

In developed countries diabetics patients are the most numerous group with renal replacement therapy (USA 34%). The main and diagnostically irreplaceable criterion of incipient diabetic nephropathy is microalbuminuria which is usually associated with hypertension and poor glycaemic compensation. With advancing microalbuminuria progresses diabetic retinopathy and neuropathy. The increased transcapillary albumin escape rate and changes of some haemocoagulation factors in diabetics patients with microalbuminuria indicate that endothelial dysfunction is involved. In type 1 diabetes microalbuminuria is an indicator of increased mortality in which participate in particular cardiovascular diseases and to a minor extent renal failure. In type 2 diabetes microalbuminuria is an independent risk of generalized vascular disease. Microalbuminuria is also in non-diabetic subjects with hypertension associated with abnormalities such as impaired glucose tolerance and insulin resistance, an unflavourable lipidogram and altered diurnal blood pressure rhythm. The results of a coronarographic investigation revealed that the risk of severe coronary artery disease is more than double in subjects with microalbuminuria. Hypertension and hypercholesterolaemia are causal risk factors of cardiovascular diseases and concurrent microalbuminuria implies a higher expression of already existing microvascular damage in hormonal and metabolic disorders with an atherogenic potential.
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PMID:[Microalbuminuria--a risk factor for diabetic nephropathy and cardiovascular disease]. 1139 74

Aging in Westernized industrialized societies is associated with an increasing prevalence of hypertension, type II diabetes mellitus, renal disease, and atherosclerotic vascular disease. This increase in the chronic disease processes in industrialized societies is related, in part, to increasing obesity, reduced physical activity, medications such as nonsteroidal anti-inflammatory agents, and other environmental influences. Hypertension in the elderly is characterized by high peripheral vascular resistance, reduced baroreflex sensitivity, a low renin state with reduced cardiac output/increased hypertrophy, reduced intravascular volume, and an increased propensity to salt-sensitivity. Initial antihypertensive therapy in the elderly patient should be based on attempts to affect hygienic measures such as weight reduction, decreased salt and fat intake, and a careful aerobic exercise program. The initial antihypertensive drugs of choice are low doses of diuretics, which have been shown to reduce cardiovascular mortality in the elderly. Low doses of diuretics do not substantively affect carbohydrate and lipid metabolism. Lipid abnormalities in the elderly should generally be treated in a similar fashion to those in the middle-aged individual. Compliance with medical therapy in the elderly patient has been demonstrated to be relatively good.
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PMID:Treatment of Elderly Hypertensive Patients With Diabetes, Renal Disease, and Coronary Heart Disease. 1141 94

Polycystic ovary syndrome (PCOS) is classically characterised by ovarian dysfunction (oligomenorrhoea, anovulation and infertility), androgen excess (hirsutism and acne), obesity, and morphological abnormalities of the ovaries (cystic enlargement and stromal expansion). More recently, insulin resistance has been found to be common in PCOS, along with an increased prevalence of other features of the "metabolic syndrome", namely glucose intolerance, type 2 diabetes mellitus, and hyperlipidaemia. Hyperinsulinaemia is likely to contribute to the disordered ovarian function and androgen excess of PCOS. Reducing insulin resistance by lifestyle modifications such as diet and exercise improves endocrine and menstrual function in PCOS. These lifestyle modifications are the best initial means of improving insulin resistance. Metformin, an oral hypoglycaemic agent that increases insulin sensitivity, has been shown to reduce serum concentrations of insulin and androgens, to reduce hirsutism, and to improve ovulation rates. The effect of metformin alone on fertility rates is unknown. Some studies suggest that metformin will reduce total body weight to a small extent, but with a predominant effect on visceral adipose reduction. The effects of metformin on lipid abnormalities, hypertension or premature vascular disease are unknown, but the relative safety, moderate cost, and efficacy in reducing insulin resistance suggest that metformin may prove to be of benefit in combating these components of the "metabolic" syndrome in PCOS. Further properly planned randomised controlled trials are required.
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PMID:Metformin and intervention in polycystic ovary syndrome. Endocrine Society of Australia, the Australian Diabetes Society and the Australian Paediatric Endocrine Group. 1145 23

Insulin resistance is a uniform finding in type 2 diabetes, as are abnormalities in the microvascular and macrovascular circulations. These complications are associated with dysfunction of platelets and the neurovascular unit. Platelets are essential for hemostasis, and knowledge of their function is basic to understanding the pathophysiology of vascular disease in diabetes. Intact healthy vascular endothelium is central to the normal functioning of smooth muscle contractility as well as its normal interaction with platelets. What is not clear is the role of hyperglycemia in the functional and organic microvascular deficiencies and platelet hyperactivity in individuals with diabetes. The entire coagulation cascade is dysfunctional in diabetes. Increased levels of fibrinogen and plasminogen activator inhibitor 1 favor both thrombosis and defective dissolution of clots once formed. Platelets in type 2 diabetic individuals adhere to vascular endothelium and aggregate more readily than those in healthy people. Loss of sensitivity to the normal restraints exercised by prostacyclin (PGI(2)) and nitric oxide (NO) generated by the vascular endothelium presents as the major defect in platelet function. Insulin is a natural antagonist of platelet hyperactivity. It sensitizes the platelet to PGI(2) and enhances endothelial generation of PGI(2) and NO. Thus, the defects in insulin action in diabetes create a milieu of disordered platelet activity conducive to macrovascular and microvascular events.
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PMID:Platelet dysfunction in type 2 diabetes. 1147 89

The close association between diabetes and cardiovascular disease suggests that current predictions of a massive increase in the prevalence of type 2 diabetes foreshadow an equally daunting rise in the incidence of vascular disease. The limited cardiovascular benefits obtained by glucose-lowering treatments, although perhaps not surprising, indicate that other cardiovascular risk factors must be given serious consideration as therapeutic targets. The impressive reductions in the number of vascular events observed in diabetic patients, albeit in small patient populations, participating in various drug trials amply justify such an approach. A necessary prerequisite, however, is a clear understanding of the clinical importance of individual risk factors to the occurrence of vascular disease in type 2 diabetic patients. This would appear essential for defining treatment strategies in the face of a bewildering array of potential therapeutic targets. The present review considers recent studies that have assessed the predictive value of risk factors against a diabetic background.
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PMID:Diabetes and other coronary heart disease risk equivalents. 1150 28

Insulin resistance and its dreaded consequence, type 2 diabetes, are major causes of atherosclerosis. Adiponectin is an adipose-specific plasma protein that possesses anti-atherogenic properties, such as the suppression of adhesion molecule expression in vascular endothelial cells and cytokine production from macrophages. Plasma adiponectin concentrations are decreased in obese and type 2 diabetic subjects with insulin resistance. A regimen that normalizes or increases the plasma adiponectin might prevent atherosclerosis in patients with insulin resistance. In this study, we demonstrate the inducing effects of thiazolidinediones (TZDs), which are synthetic PPARgamma ligands, on the expression and secretion of adiponectin in humans and rodents in vivo and in vitro. The administration of TZDs significantly increased the plasma adiponectin concentrations in insulin resistant humans and rodents without affecting their body weight. Adiponectin mRNA expression was normalized or increased by TZDs in the adipose tissues of obese mice. In cultured 3T3-L1 adipocytes, TZD derivatives enhanced the mRNA expression and secretion of adiponectin in a dose- and time-dependent manner. Furthermore, these effects were mediated through the activation of the promoter by the TZDs. On the other hand, TNF-alpha, which is produced more in an insulin-resistant condition, dose-dependently reduced the expression of adiponectin in adipocytes by suppressing its promoter activity. TZDs restored this inhibitory effect by TNF-alpha. TZDs might prevent atherosclerotic vascular disease in insulin-resistant patients by inducing the production of adiponectin through direct effect on its promoter and antagonizing the effect of TNF-alpha on the adiponectin promoter.
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PMID:PPARgamma ligands increase expression and plasma concentrations of adiponectin, an adipose-derived protein. 1152 76


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