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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Findings on left ventricular function in microvascular angina (syndrome X) are somewhat controversial. Recently, an increased prevalence of insulin resistance and hyperlipoproteinemia has been demonstrated as well as arterial hypertension potentially impairing the left ventricular diastolic function. In an attempt to analyze the diastolic function at rest, we investigated by Doppler echocardiography the transmitral blood flow in 16 patients (51 +/- 8 years). The diastolic data were compared with those of 12 healthy people (50 +/- 6 years) who were matched for age. The patients with microvascular angina revealed a slightly higher systolic blood pressure (134 +/- 18 mm Hg vs 125 +/- 9 mm Hg, n.s.), but imposed by higher left ventricular mass index (92 +/- 18 g/m2 vs 65 +/- 13 g/m2, p < 0.001). There was a trend to an elevated A-wave-peak during transmitral blood flow (61 +/- 14 cm/s vs 50 +/- 9 cm/s). The findings suggest impairment of the left ventricular relaxation before manifestation of left ventricular hypertrophy and hypertension takes place.
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PMID:[Diastolic left ventricular dysfunction with microvascular angina (Syndrome X)]. 871 43

In this paper we presented characteristics of insulin resistance syndrome (IRS), also known as metabolic syndrome and syndrome X, with an emphasis on insulin resistance in hyperandrogenemic women. The aim features of IRS are obesity, hypertension, dyslipidemia-hypertriglyceridemia and decreased HDL cholesterol, impaired glucose tolerance with hyperinsulinemia and higher cardiovascular morbidity. It is considered typical that in hyperandrogenemia, especially in PCO syndrome, insulin resistance and hyperinsulinemia without other characteristics of IRS are expressed.
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PMID:[Androgen excess in women and the metabolic syndrome (syndrome X)]. 875 4

The paper reviews epidemiological studies published since 1989, not including ecological studies and addressing the relationship between the fetal environment and component elements of the chronic insulin resistance syndrome (syndrome X). Thirty papers have been recorded. Birth weight associated or not with other perinatal characteristics are studied in 24 articles. A relationship with further occurrence of hypertension (17 papers), dyslipemia (3), non insulin-dependent diabetes or altered glucose tolerance (8), or of a combination of these disorders (2), has been sought for. A negative relationship between birth weight and these disorders is found in adults, inconstantly in children. Some findings support a mechanism implying nutritional condition during pregnancy. Methodology inaccuracies jeopardize the validity of the conclusions drawn. The interpretation of a causal relationship between fetal environment and insulin resistance is compared to alternative assumptions relating to genetic mechanisms or selection biases.
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PMID:[Fetal environment and coronary ischemia risk: review of the literature with particular reference to syndrome X]. 876 85

Syndrome X, or the syndrome of insulin resistance, is a cluster of related metabolic abnormalities of hyperinsulinemia, glucose intolerance, increased very low density lipoprotein (VLDL), decreased high density lipoprotein (HDL), and hypertension in nonobese adults and plays an important role in the genesis of cardiovascular disease. The aim of the present study was to examine the relationships among insulin sensitivity, plasma lipid levels, and body composition in the pediatric age group to determine whether these associations are present in childhood. Twenty healthy Caucasian Tanner stage I (TI) children (age, 10.7 +/- 0.3 yr; body mass index, 18.9 +/- 0.8 kg/m2) and 22 pubertal Tanner stage II-IV (TII-IV) adolescents (age, 14.0 +/- 0.3 yr; body mass index, 20.0 +/- 0.4 kg/m2) were studied. In vivo insulin-mediated glucose disposal (Rd) was evaluated during a 40 mu/m2. min hyperinsulinemic-euglycemic clamp. Body composition was assessed isotopically by the H218O dilution principle. Fasting blood was obtained for cholesterol, triglyceride (TG), VLDL, low density lipoprotein (LDL), and HDL determinations. In both groups, the strongest correlation of Rd was with percent body fat (%BF) (TI: r = -0.82; P < 0.001; TII-IV: r = -0.73; P < 0.001). In addition, in TI, Rd was correlated with TG (r = 0.64; P = 0.001), VLDL (r = 0.64; P = 0.001), and diastolic blood pressure (r = -0.50; P = 0.01). There were no such correlations in TII-IV. In TI, % BF correlated positively with LDL and negatively with TG and VLDL. In TII-IV, % BF correlated positively with cholesterol and LDL. After correcting for %BF, partial correlation analysis revealed no relationship between Rd and lipid levels in either group. This suggests that the relationship of insulin sensitivity to lipid levels was secondary to the effect of body composition on lipid levels. However, regardless of body composition, the basal insulin level was correlated with TG (r = 0.38; P = 0.04) and VLDL (r = 0.40; P = 0.04) in TII-IV subjects. We conclude that 1) the primary correlate of insulin sensitivity is %BF in both prepubertal and pubertal subjects, with no relationship to plasma lipids; 2) in prepubertal children, diastolic blood pressure is negatively correlated with insulin sensitivity and positively with insulin levels, independent of adiposity; and 3) after the onset of puberty, basal insulin levels are positively correlated with VLDL and TG regardless of the degree of adiposity. This observation could be a very early manifestation of the genesis of syndrome X in childhood.
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PMID:Insulin sensitivity, lipids, and body composition in childhood: is "syndrome X" present? 877 76

Fructose (FR) feeding in rats provides a model of dietary-induced insulin resistance that has been used to examine interactions among the cluster of metabolic disorders including insulin resistance, hyperinsulinemia, hypertension, and dyslipidemia known as Syndrome X. In animals with reduced beta-cell mass, however, insulin resistance may not have similar associated disorders. Therefore this study examined the consequences of FR feeding in rats with a reduced beta-cell mass. Formerly diabetic islet-transplanted (TX) or shamoperated (SHAM) male Wistar Furth rats were fed a purified control (CNTL) diet or a diet containing either 40 or 70% (wt/wt) FR for 3-5 wk. FR feeding in SHAM animals resulted in elevated triglyceride levels but did not affect fed or fasting glucose and insulin concentrations, blood pressure, glucose tolerance, and the acute insulin response to a glucose bolus compared with CNTL-fed animals. Among TX animals, hypertriglyceridemia and fasting hyperglycemia were observed only in those fed FR. Thus the effects of diet-induced insulin resistance are limited to dyslipidemia, if insulin secretory capacity is adequate, but are detrimental to both glucose and lipid metabolism in combination with a reduced beta-cell mass.
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PMID:Consequences of high dietary fructose in the islet-transplanted rat with suboptimal beta-cell mass. 877 51

Recent trends in the American lifestyle, such as a high-fat diet and inactivity, have promoted the emergence of a metabolic disorder titled syndrome X. Although originally linked to non-insulin-dependent diabetes mellitus (NIDDM) and characterized by insulin resistance, syndrome X is now better described as a cascade of disorders encompassing not only NIDDM, but also hypertension, atherosclerosis, centrally distributed obesity, and dyslipidemia. Further pathology has been linked to syndrome X, such as polycystic ovary disease, microvascular angin, and the presence of acanthosis nigricans. Recognition and appropriate management of syndrome X will prevent deleterious patient outcomes that might occur without continuity of care in treating associated disorders. Pharmacological management of syndrome X includes the use of insulin-sparing antihyperglycemic agents and/or combination therapy and avoidance of several frequently prescribed medications. Clinicians need to initiate renewed efforts to provide lifestyle counselling to promote ideal body weight, since interpretation of research data concerning syndrome X reinforces that serious health consequences will result from obesity and inactivity.
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PMID:Syndrome X. Recognition and management of this metabolic disorder in primary care. 878 76

Excess activity of the sympathetic nervous system (SNS) is linked to human obese hypertension and to salt-sensitive hypertension. Paradoxically, reduced SNS activity has been implicated as a contributor to obesity, particularly in animal models, and salt loading usually inhibits SNS activity. We have investigated the relationship between SNS activity, diet, and hypertension in the obese spontaneously hypertensive rat (SHROB), a model with a recessive obesity trait superimposed on a hypertensive background with multiple metabolic abnormalities resembling human syndrome X. We examined the role of SNS overactivity in the adverse impact of excess dietary salt and the possible beneficial effects of sympatholytic therapy. Mean blood pressure (MBP) was increased in SHROB and SHR fed a 4% NaCl diet. The pressor effect of dietary salt was abolished by ganglionic blockade, suggesting that increased SNS activity contributed to the pressor effect of the high-salt diet. Moxonidine, a second-generation central antihypertensive, controlled hypertension in both SHROB and SHR. Kidney damage in SHROB was accelerated by dietary salt and was reduced by moxonidine. Moxonidine elicited progressive weight loss in SHROB but not in SHR. Food intake in SHROB was reduced to the level of lean SHR. SHROB and SHR treated with moxonidine showed improved glucose tolerance. Additionally, SHROB showed reduced levels of triglycerides, cholesterol, and insulin following moxonidine therapy. Inhibition of the SNS, as with moxonidine therapy, may ameliorate multiple abnormalities and have therapeutic advantages in obese hypertensive syndromes.
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PMID:Sympathetic nervous system in salt-sensitive and obese hypertension: amelioration of multiple abnormalities by a central sympatholytic agent. 882 50

Aging is associated with an increased incidence of hypertension, noninsulin-dependent diabetes mellitus, and coronary heart disease. Because these conditions often cluster in the same individuals, there has been speculation that a common mechanism is responsible for all of these pathological states. Both epidemiological and clinical research has shown that insulin resistance and/or hyperinsulinemia are associated with glucose intolerance, dyslipidemia (high plasma triglyceride and low high-density lipoprotein-cholesterol levels), and higher systolic and diastolic blood pressures. Therefore, insulin resistance and hyperinsulinemia have been proposed as the causal link among the elements of the cluster mentioned above, now most commonly referred to as the insulin resistance syndrome, syndrome X, or the metabolic syndrome. The elderly are more glucose intolerant and insulin-resistant, but it remains controversial whether this decrease in function is an inevitable consequence of "biological aging" or the result of what might be referred to as environmental or lifestyle variables: increased obesity, a detrimental pattern of fat distribution, or physical inactivity that usually accompany age. All of these modifiable environmental factors have also been shown to result in increases in insulin resistance and hyperinsulinemia and are risk factors for the development of the diseases of the metabolic syndrome. Recent interventional studies that have attempted to reverse these conditions in the elderly have shown improved insulin sensitivity, and glucose tolerance. Insulin secretion, on the other hand, seems to decrease with age even after adjustments for differences in adiposity, fat distribution, and physical activity. This may be responsible for the glucose intolerance in the very old even after improvements have been made in their lifestyle variables.
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PMID:The effect of age on insulin resistance and secretion: a review. 882 67


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