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

The obvious syntropy of obesity and type II (non-insulin dependent) diabetes mellitus has always suggested a causal inter-relationship between the two diseases. However, the actual pathophysiological connection still remains to be elucidated. Recent findings have suggested that insulin resistance and hyperinsulinaemia might link glucose intolerance/type II diabetes mellitus, hypertension and hyperlipoproteinaemia in the context of a hypothetical 'syndrome X' characterized by an excessive risk constellation for the development of atherosclerosis. However, as to the practical consequences of the ('diabesity') syndrome of type II diabetes mellitus and structured programmes for effective therapy, very little new information has been gathered during the past 100 years.
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PMID:Risk of obesity in type II diabetes mellitus. 133 84

Non-insulin-dependent diabetes (NIDDM) has long been recognized as being associated with a cluster of disorders including obesity, hypertension, dyslipidemia, and atherosclerotic heart disease. It was only recently, however, that Reaven, DeFronzo, and Ferrannini with techniques to quantitate insulin resistance suggested that this represents a common factor in this group of disorders and that hyperinsulinemia resulting from insulin resistance could be the cause of the hypertension, dyslipidemia, and atherosclerosis. The names syndrome X or the insulin-resistance syndrome have been used to identify this pathological entity, and considerable investigations have been done and are in progress to establish whether or not these coexisting disorders represent an as yet unexplained association of cardiovascular risk factors or if, indeed, insulin resistance and hyperinsulinism represent the primary cause for most of the other disorders. To paraphrase a philosophical comment, if syndrome X did not exist, we probably would have had to invent it. In addition to the intellectual satisfaction of being able to "lump" these diverse ills under a single etiology, the main value of grouping these disorders as a syndrome is to continually remind physicians that the therapeutic goals are not only to correct hyperglycemia in NIDDM but also to manage the elevated blood pressure and dyslipidemia that cause cerebrovascular and cardiac morbidity as well as mortality in these patients. Having a syndrome X reduces the fragmentation of medical care among subspecialties and decreases the likelihood of prescribing drugs that correct hypertension but raise lipids or drugs that lower lipids but raise blood glucose. Finally, it encourages the selection of drugs that reduce hyperglycemia without increasing insulin secretion and to the development of new drugs for this purpose. Unfortunately, the concept of insulin resistance with hyperinsulinism being a cause of the other associated disorders is still unproved but continues to be open to experimental investigation. The remainder of this article reviewed the use of sulfonylureas in the management of NIDDM, discussed new molecular and cellular mechanisms by which they promote insulin secretion, and reviewed the controversy as to whether an extrapancreatic action contributes to their glucose-lowering effects in NIDDM. A closing section listed some other oral drugs that can lower blood glucose without stimulating the pancreatic beta cell. Their insulin-sparing hypoglycemic effect makes them potentially useful in NIDDM therapy, particularly if the fundamental premise of syndrome X is substantiated, which implicates hyperinsulinemia as contributing to the morbidity and mortality from atherosclerotic vascular disease.
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PMID:Type II diabetes and syndrome X. Pathogenesis and glycemic management. 161 69

Non-insulin dependent diabetes mellitus (NIDDM) is an important cause of morbidity and mortality, both in developed as well as in developing countries. The eyes, kidneys, and cardiovascular and neurological systems are predominantly affected by this chronic disease, leading to loss of employment and sometimes life. The most common setting is uncontrolled glycaemia after dietary restriction, exercise and oral hypoglycaemic drug therapy. Insulin may be needed for treating NIDDM some time during the course of the disease. Insulin therapy results in improved beta-cell function, a decrease in the hepatic glucose output and an improvement of the lipoprotein profile. Some of these beneficial effects are due to nullification of 'glucose toxicity'. Objective evidence of a link between tight metabolic control and chronic complications of NIDDM is still not established, despite the results of recent trials. Many insulin regimes have been tried. Recently, attention has been focused on combination therapy with sulphonylureas and insulin, using long-acting insulin at bedtime only. This regime improves the glycaemic profile (due to a reduction of hepatic glucose output), using lower doses of insulin and sulphonylureas. However, experience with this regime suggests that it is only suitable for a subset of NIDDM patients. Adverse effects of insulin therapy include weight gain and hypoglycaemia, which can usually be easily managed. It is hyperinsulinaemia, with its complex array of adverse metabolic effects, that has recently concerned physicians. Acceleration of atherosclerosis, hypertension and worsening of the lipoprotein profile have been cited as possible adverse effects. The presence of such dysregulation is included in the recently described syndrome X.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Insulin treatment in non-insulin dependent diabetes mellitus. 763 12

The author summarizes mechanisms by which insulin resistance and compensatory hyperinsulinism are manifested in the clinical picture. He divides the mechanisms into prereceptor, receptor and postreceptor mechanisms. The latter dominate in the population quantitatively and thus also by their impact because they create the so-called 5H syndrome (association of hyperinsulinism with hyperglycaemia (NIDDM), hyperlipoproteinaemia, hypertension, hirsutism and the polycystic ovary syndrome) or the so-called hormonal metabolic syndrome X, lethal tetrad, metabolic syndrome, syndrome of insulin resistance). The term syndrome X does not appear suitable as it is frequently mistaken for coronary X syndrome which probably is also conditioned by hyperinsulinism, for the hormonal metabolic X syndrome and probably also fot the "fragile X syndrome" in genetics. The 5H syndrome is caused by a postreceptor disorder of insulin efficiency for which so far the molecular basis and dominating organ site have not yet been defined adequately. Hyperinsulinism is conceived as an insulin resistance compensating phenomenon. In its development participates, however, in addition to compensatory hypersecretion also impaired insulin utilization (liver, muscles) and an impaired primary secretory response caused probably by a disorder of blood sugar control (glucokinase, GLUT 2). This is suggested by the frequently inadequate response of the blood sugar level, IRI and C-peptide during the oral glucose tolerance test (OGGT). A hyperinsulinaemic response may be encountered when the blood sugar curve is normal, flat, in impaired glucose tolerance and in diabetes. Thus OGGT alone is not suited for the early detection of the 5H syndrome unless concurrently the IRI and C-peptide response is recorded.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Clinical manifestations of the insulin resistance syndrome. The hormonal-metabolic syndrome X, the 5H syndrome and their etiopathogenesis]. 772 46

The general practitioner man be confronted with the X syndrome, which includes central obesity, impaired glucose tolerance or type II diabetes mellitus, dyslipidemia and eventually hypertension. Insulinoresistance and hyperinsulinaemia contribute to the pathogenesis of these disorders. The syndrome X, which leads to important cardiovascular morbidity, needs appropriate treatment, which has to take into account the actions of drugs on glucose and lipid profiles. Syndrome X is rarely treated as a whole, but to treat separately each of its manifestations would be a mistake. The necessity of a global approach, a complete understanding of the familial environment and also the duration of the development of syndrome X justify the prominent part of the family doctor in the follow-up.
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PMID:[Syndrome X and general medicine]. 778 42

NIDDM has been postulated to be a component of a more generalized metabolic syndrome, Syndrome X, caused by insulin resistance. Although the components of the syndrome include glucose intolerance, hypertension, increased TG, and decreased HDL cholesterol, their relationship to insulin resistance and/or hyperinsulinemia is controversial. Recent investigations have shown racial differences in the relationship between insulin resistance and BP in nondiabetic populations. We assessed the relationship between insulin resistance and the other components of the syndrome in 37 black men and 53 black women with NIDDM. Insulin sensitivity was determined by measuring glucose disposal with the euglycemic insulin clamp technique with a 1 mU.kg-1.min-1 insulin infusion. We also determined fasting lipid profiles and BP. In this group of black men and women with NIDDM, 30% were insulin sensitive, and 70% were insulin resistant. No correlation existed between insulin sensitivity and sBP or dBP in either sex. Fasting serum TGs were inversely correlated with insulin sensitivity for both men (r = -0.401, P = 0.02) and women (r = -0.366, P = 0.008). Serum HDL cholesterol was highly correlated with insulin sensitivity for men (r = 0.421, P = 0.01) but not for women (r = 0.071, P = 0.62). Fasting serum TG levels and serum HDL-cholesterol levels were highly correlated in an inverse relationship in men (r = -0.368, P = 0.03), but not women (r = -0.199, P = 0.17). In summary, BP does not correlate with insulin resistance in blacks with NIDDM. Normal insulin sensitivity occurs in 33% of black men and 25% of black women with NIDDM.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Do blacks with NIDDM have an insulin-resistance syndrome? 843 15

Studies of macrovascular disease in non-insulin-dependent diabetes (NIDDM) have shown a significant increase in peripheral vascular, coronary, and carotid artery disease in diabetics compared to non-diabetics. This prevalence appears to be related to insulin levels and to the degree of hyperinsulinemia as measured in the blood of these patients. Indeed, a cluster of markers, including hyperinsulinemia, insulin resistance, hypertension, dyslipoproteinemia, and a high waist-hip ratio, has been associated with NIDDM and increased risk for macrovascular disease. Variously described as Metabolic Syndrome or Syndrome X, this syndrome may be operative for many years before NIDDM is diagnosed. Given the complexity of Metabolic Syndrome, a single-factor intervention for preventing macrovascular disease in NIDDM is unlikely. However, it seems advisable to screen, on a regular basis, all patients presenting a pre-NIDDM state, as well as those with overt NIDDM, for pertinent cardiovascular risk parameters and for emerging macrovascular disease. It is suggested that any attempt to prevent macrovascular disease in subjects with glucose intolerance should aim at decreasing insulin resistance and hyperinsulinemia.
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PMID:Hyperinsulinemia and atherosclerosis. 854 11

The prevalence of hypertension in diabetes is significantly higher than in non-diabetics, perhaps twice as common. The excess is related to diabetic nephropathy, mainly in type 1 diabetes, to obesity, mainly in type 2 diabetes, but also to increased sympathetic activity. Furthermore, the increased prevalence of hypertension may relate to insulin resistance and its sequelae. Insulin resistance leads to hyperinsulinemia, relates to increased LDL and reduced HDL levels, causes the development of impaired glucose tolerance and type 2 diabetes and might also be causally related to the onset of hypertension. Syndrome X has relevant therapeutic implications in the management of hypertension. Hypertension is a major risk factor for large vessel disease in diabetics and also a risk factor for microangiopathy, particularly nephropathy. The incidence of atherosclerotic disease is dramatically increased in both type 1 and type 2 diabetics and is the major cause of morbidity and premature death mainly in patients with raised urinary albumin excretion. Thus, diabetics show a two-fold increased risk of coronary heart disease, 2-6 fold increased risk of stroke and a several-fold increased risk of peripheral vessel disease. Some evidence suggests that hypertension may be a risk factor for retinopathy, particularly its progression, but surely hypertension is a significant risk factor for nephropathy, accelerating its progression and perhaps even causing the onset of the glomerulopathy. The mechanisms by which hypertension might contribute to the evolution of both large vessel as well as small vessel disease is still unknown, although increased capillary leakage and vascular endothelium alterations might be important factors.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Hypertension and diabetes]. 856 58

Diabetic patients typically have a low compliance rate to intervention and lifestyle change. Although diabetes has been studied for years, the disease remains a leading cause of death in the United States and approaches a prevalence of 40% in certain ethnic populations. The mortality rate for NIDDM is two three times higher than the average healthy person, primarily due to cardiovascular complications. More than 10 million people in the United States alone are diagnosed with diabetes. Clearly, with health care resources dwindling, improved treatment outcomes are needed. The physiologic mechanism involved in the development of the preliminary phase of Type II diabetes or syndrome X is particularly amenable to primary and secondary prevention as well as health promotion activities. NPs provide an alternative delivery of care based on health-promotion and disease-prevention principles. NPs working in a primary care delivery model with patients at risk for diabetes have the opportunity to bring about measurable outcome differences.
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PMID:Syndrome X. Primary care provider's role in health promotion and disease prevention. 878 75

Hyperinsulinemia, a manifestation of insulin resistance, precursor of non-insulin dependent diabetes mellitus (NIDDM) and the hallmark of Syndrome X was assessed in 27 obese post-menopausal women. Insulin-like growth factor binding protein-1 (IGFBP-1), which had been shown previously to correlate inversely with insulin in animal and human studies, was evaluated as a diagnostic marker for abnormal glucose stimulated area under the curve (AUC) insulin (defined a priori as > or = 100 microU/ml). We performed analysis of variance and logistic regression to assess IGFBP-1 and other study covariates, including body mass index, blood pressure, lipids and measures of glucose and insulin in hyperinsulinemic vs. normal women and evaluated performance characteristics (sensitivity, specificity, positive and negative predictive values and accuracy rates). The mean IGFBP-1 was 6.1 ng/ml (95% confidence interval (CI) 3.1 to 8.9) for the hyper-insulinemic women compared to 33.5 ng/ml (CI 15.8 to 51.2) for normal women (P = .0027). At a cutoff point of 15ng/ml, which was selected to correspond to the lower 95% confidence limit for the normal study population, IGFBP-1 was abnormal in all 13 women with hyperinsulinemia and 4 women with normal insulin levels (sensitivity 100%, specificity 69%; positive predictive value 76%, negative predictive value 100%, diagnostic accuracy rate 85%). Logistic regression models indicated that, of all study covariates, IGFBP-1 was the best predictor variable for AUC-insulin as a binary dependent variable. These results suggest that IGFBP-1 may be a simple serum marker for hyperinsulinemia in a subpopulation of obese menopausal women.
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PMID:Insulin like growth factor-binding protein-1 as a marker for hyperinsulinemia in obese menopausal women. 895 66


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