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

Metabolic disturbances such as hyperinsulinaemia, dislipoproteinaemia and glucose intolerance are often associated with essential hypertension and markedly affect cardiovascular morbidity in hypertensive patients. In order to shed some light on the prognostic significance of white coat hypertension (raised clinic and normal ambulatory blood pressure), we compared the metabolic profile in a group of white coat and sustained previously untreated hypertensives. We studied 84 newly detected hypertensive patients (49 men, 35 women, 47 +/- 8 years, range 28-59 years). Subjects with obesity (BMI > 30), NIDDM and target organ damage were excluded. Ambulatory blood pressure monitoring was performed by SpaceLabs 90207-31. Total cholesterol and triglycerides, LDL-cholesterol, HDL-cholesterol (HDL-C) and subclasses HDL2 and HDL3 cholesterol as well as apolipoprotein A1 and B were measured in fasting plasma. Glucose and insulin were determined in fasting and postload (glucose 75 g plasma. Twenty patients (24%, 8 men and 12 women) were classified as white coat hypertensives. No differences in age, BMI and waist to hip ratio were observed between white coat and sustained hypertensive patients. Plasma glucose and lipoprotein levels were similar in the two groups. Fasting and postload insulin levels were significantly lower in white coat hypertensives (fasting insulin 7.1 +/- 2.9 vs. 12 +/- 8.6 microU/ml, P < 0.02; insulin 120 minutes 48 +/- 27 vs. 65 +/- 41 microU/ml, P < 0.05); glucose/insulin rate was higher in white coat than in sustained hypertensive patients (15 +/- 7 vs. 11 +/- 7, P = 0.03).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Metabolic risk factors in white coat hypertensives. 793 8

Several large family studies are reviewed to identify results suggesting single gene traits contributing to the occurrence of hypertension in humans. Segregation analysis in families has suggested major gene effects for several highly heritable traits associated with hypertension. These include recessively segregating high sodium-lithium countertransport (major gene H2 = 34%), additively segregating low urinary kallikrein excretion (major gene H2 = 51%), and recessively segregating hyperinsulinemia (major gene H2 = 33%). In some families, hypertension and metabolic abnormalities (dyslipidemia, hyperinsulinemia, and obesity) seem to be related to several candidate genes studied but not conclusively proven (LPL deficiency mutations, dense LDL subfractions, or NIDDM with hyperinsulinemia). More recently, DNA markers have identified genes promoting hypertension. Glucocorticoid-remediable aldosteronism (GRA) promotes a rare but unusual form of hypertension that is unresponsive to ordinary medications but very responsive to glucocorticoid medications. GRA has been found in hypertensive persons with a specific mutation of the 11 beta-hydroxylase gene on chromosome 8q21. Many persons with essential hypertension carry a common "susceptibility gene" at the angiotensinogen locus (chromosome 1q4) identified using linkage studies in siblings, association studies, and in studies of preeclampsia and hypertension in pregnant women. These first two well-established genetic loci promoting human hypertension represent two ends of a broad spectrum. The rare "determinant" gene for GRA by itself seems to produce severe hypertension and early strokes. The angiotensinogen (AGT) "susceptibility" gene is very common (30% of Utah Caucasians) and seems to predispose to hypertension but probably requires other genetic and environmental influences to be fully expressed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Evidence for single gene contributions to hypertension and lipid disturbances: definition, genetics, and clinical significance. 798 84

The aim of this work is to evaluate whether type 2 diabetes mellitus, obesity and arterial hypertension, three conditions characterized by the presence of insulin resistance, share some common genetic markers. A potential candidate is the Na+/H+ antiporter, the increased activity of which is considered a marker of essential hypertension. This ion exchanger seems to be related to the Na+/Li+ countertransport, that is considered a marker of insulin resistance in essential hypertension and in type 1 diabetes mellitus. In this study we wished to clarify whether the activity of the Na+/H+ antiporter is increased not only in hypertensive subjects, but also in obese and type 2 diabetic patients, both in the presence and in the absence of arterial hypertension. The activity of the ion exchanger was measured in peripheral blood lymphocytes (PBL) by clamping intracellular pH (pHi) at 5.8-6.2 and then detecting the rate of the proton efflux after sodium addition. In the absence of arterial hypertension, no significant difference in this parameter was observed in obese and type 2 diabetic patients in comparison with normal subjects. In the presence of arterial hypertension, there was a significant increase in the Na(+)-induced H+ efflux at the internal pH (pHi) values of 5.8 and 6.2 both in hypertensive controls and in hypertensive obese and type 2 diabetic patients (P = 0.05-0.0001 vs. normotensive subjects and patients).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Na+/H+ antiporter activity in peripheral blood lymphocytes of obese and type 2 diabetic patients is increased only in the presence of arterial hypertension. 803 50

We investigated both sodium-lithium countertransport (Na-Li CT) and ouabain-sensitive sodium transport (Na pump) of erythrocytes in healthy subjects (group A), patients with non-insulin-dependent diabetes (NIDDM) without nephropathy (group B), patients in the proteinuric stage (group C), and those in the renal insufficiency stage (group D). Erythrocytes from all four groups had a similar initial water and ionic content and were loaded with similar degrees of Li and Na for efflux studies. There were no significant differences in erythrocyte Na-Li CT or Na pump among the four groups. However, the maximal rate of Na-Li CT was significantly higher in a group of subjects with essential hypertension when compared with groups A, B and C, consistent with the view that there is a genetic marker for essential hypertension. Ouabain-insensitive Na efflux (Na leak) of erythrocytes was found to be significantly higher in group D than in groups A or B. Also, a significant positive correlation existed between Na leak and urine protein levels of the subjects studied. Our results thus indicate that in contrast with insulin-dependent diabetic patients (IDDM) where an elevated Na-Li CT is observed, with diabetic nephropathy, Na-Li CT in NIDDM is apparently not associated with nephropathy; rather the ouabain-insensitive Na efflux appears to be correlated with the stages of nephropathy in NIDDM. The association suggests that the rate of ouabain-insensitive Na efflux may provide an index for assessing the degree of nephropathy in NIDDM patients.
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PMID:Abnormalities of sodium transport in non-insulin-dependent diabetes: association with renal disease. 810 99

Association between insulin resistance and hypertension: Insulin resistance and reactive hyperinsulinemia occur not only with obesity, impaired glucose tolerance or non-insulin-dependent (type 2) diabetes mellitus, but also in many non-obese, non-diabetic patients with essential hypertension and their currently normotensive, lean young offspring and in some other conditions known to promote hypertension. Insulin resistance impairs glucose tolerance, while insulin resistance and/or hyperinsulinemia promote dyslipidemia, body fat deposition and probably atherogenesis. Therefore, the common coexistence of a genetic predisposition for hypertension with insulin resistance helps to explain the frequent, although temporally often dissociated, occurrence of hypertension as well as dyslipidemia, obesity and type 2 diabetes in a given subject. Pathogenetic mechanisms: In the pathogenesis of hypertension, inappropriate vasoconstriction (due to dysbalance of vasoactive substances and/or raised cytosolic Ca2+) and/or a structural vasculopathy is a very important ultimate causative event. In the presumed mosaic of participating pressor mechanisms, distinct Na+ retention is almost obligatory with diabetes mellitus, while essential and particularly obesity-associated hypertension probably involves a tendency for sympathetic activation. Development of insulin resistance: Insulin resistance may develop as a consequence of an intracellular excess of Ca2+ or decrease in Mg2+, an impaired insulin-mediated rise in skeletal muscle blood flow, increased sympathetic activity or being overweight. Acute hyperinsulinemia on the one hand causes arterial vasodilation and on the other hand enhances renal sodium reabsorption and sympathetic activity. Chronically, hyperinsulinemia may promote cardiovascular muscle cell proliferation and atherogenesis, and it has been proposed that insulin resistance in certain transmembranous cation exchange systems may elevate cytosolic Ca2+. Nevertheless, whether insulin resistance and/or hyperinsulinemia itself contribute to the pathogenesis of hypertension is still unclear.
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PMID:Insulin resistance, hyperinsulinemia and hypertension. 815 79

Subtle abnormalities of carbohydrate metabolism and overt diabetes mellitus are both associated with a substantial increase in the prevalence of hypertension and the accelerated development of atherosclerosis. Hypertension is also a presumed independent risk factor for atherosclerosis, although some of the atherogenic properties of hypertension may be related to the recently recognized subtle metabolic abnormalities commonly found in persons with essential hypertension. The results of epidemiologic studies suggest that the elevated fasting and postprandial insulin levels that often occur in patients with essential hypertension, as well as in patients with type II diabetes mellitus, are an independent risk factor for atherosclerotic cardiovascular disease. Elevated glucose levels in patients with diabetes and hypertension appear to contribute to the acceleration of atherosclerosis, perhaps through toxic effects on the vascular endothelium. Other cardiovascular risk factors that are accentuated in persons with carbohydrate intolerance and hypertension include abnormalities in platelet function, clotting factors, the fibrinolytic system, and dyslipidemia. The goals of both nonpharmacologic and pharmacologic therapy for patients with abnormal carbohydrate metabolism and hypertension are to decrease cardiovascular risk as well as lower blood pressure.
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PMID:Hyperinsulinemia, insulin resistance, and hyperglycemia: contributing factors in the pathogenesis of hypertension and atherosclerosis. 839 10

Great pathophysiological significance has recently been placed on the association of metabolic abnormalities, such as hyperinsulinemia, insulin resistance, obesity, and frank diabetes mellitus, with essential hypertension and coronary artery disease, and the clinical coincidence of these features has been termed "syndrome X." Despite the suggestion that insulin itself mediates this clinical linkage, the specific mechanisms underlying this syndrome remain poorly understood. We have attempted to understand these phenomena at the cellular level, and have investigated the role of cellular mineral ion species such as cytosolic free calcium (Cai), free magnesium (Mgi), and intracellular pH (pHi) in various insulin resistant states, including essential hypertension, obesity, and type II (non-insulin-dependent) diabetes mellitus (NIDDM). Utilizing nuclear magnetic resonance spectroscopic techniques to noninvasively assess intracellular concentrations of these ions, we observed that each of these disease states is characterized, in whole or in part, by common abnormalities of cellular ion metabolism, including elevated Cai levels and suppressed levels of Mgi and pHi. Furthermore, despite the predominant use of red cells as a tissue source, the measured levels of Cai, Mgi, and pHi were closely related to the ambient blood pressure, the degree of cardiac hypertrophy, and to the hyperinsulinemic response to oral glucose challenge. Altogether, these data suggest an integrated "ionic hypothesis" in which the frequent clinical coexistence of hypertension and altered insulin metabolism derives from common abnormalities of cellular ion handling, resulting in excess steady-state levels of Cai, reciprocal depletion of Mgi, and lowered pHi. These cellular ion alterations would be expected to have tissue-specific consequences, appearing in vascular tissue as vasoconstriction and elevated blood pressure, in skeletal muscle and fat as insulin resistance, in pancreatic beta-cells as hyperinsulinemia, and in neural tissue as potentiated neurotransmitter release and increased sympathetic nerve activity. Thus, according to this hypothesis, essential hypertension, insulin resistance, hyperinsulinemia, and NIDDM are in reality different clinical components of what should be better designated as "generalized cardiovascular-metabolic disease" (GCMD).
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PMID:Ionic basis of hypertension, insulin resistance, vascular disease, and related disorders. The mechanism of "syndrome X". 850 40

The effects of nilvadipine on the peripheral circulation in the lower extremities using a duplex system of two-dimensional colour and pulse Doppler ultrasonography were studied in 32 patients with type 2 diabetes mellitus and mild essential hypertension. The patients (19 men and 13 women) were randomly divided into treatment and control groups. The anatomical cross-sectional area and blood flow index of the dorsal pedis artery were determined by colour and pulse Doppler ultrasonography before and 60 min after administration of 4 mg nilvadipine or placebo. Pulse rate and blood pressure were measured simultaneously. There were no significant changes in pulse rate or blood pressure after administration of either drug. Both cross-sectional areas (from 4.3 +/- 0.4 to 5.2 +/- 0.5 mm2, p < 0.05) and blood flow index (from 40.3 +/- 4.3 to 58.8 +/- 9.0, p < 0.05) were significantly increased in the treatment group, whereas there were no significant changes in either measurement in the control group. The findings showed that a single administration of nilvadipine increases blood flow in the dorsal pedis arteries of diabetic patients.
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PMID:The effect of nilvadipine on bloodflow in the dorsal pedis artery in type 2 diabetic patients--a study using duplex Doppler ultrasonography. 854 90

GENETIC PREDISPOSITION: Insulin resistance and reactive hyperinsulinemia occur not only with obesity, impaired glucose tolerance or non-insulin-dependent (type 2) diabetes mellitus, but also in many non-obese, non-diabetic patients with essential hypertension and their currently normotensive, lean, young offspring, as well as in some other conditions known to promote hypertension. Insulin resistance impairs glucose tolerance, while insulin resistance and/or hyperinsulinemia promote dyslipidemia, body fat deposition and probably atherogenesis. Therefore, the common coexistence of a genetic predisposition for hypertension with insulin resistance helps to explain the frequent, although temporally often dissociated, occurrence of hypertension together with dyslipidemia, obesity and type 2 diabetes in a given patient. INSULIN RESISTANCE AND HYPERINSULINEMIA AS SLOW PRESSOR MECHANISMS: In the pathogenesis of hypertension, inappropriate vasoconstriction (due to an imbalance of vasoactive substances and/or raised cytosolic calcium) and/or structural vasculopathy is particularly important. Among the mosaic of assumed pressor mechanisms, distinct Na+ retention is almost invariably involved in diabetes mellitus, while sympathetic activation tends to occur in essential hypertension, particularly in association with obesity. Insulin resistance may develop as a consequence of an intracellular excess of Ca2+ or a decrease in Mg2+, an impaired insulin-mediated rise in skeletal muscle blood flow, increased sympathetic activity or excess body weight. Acute hyperinsulinemia causes arterial vasodilation on one hand and increases sympathetic activity and renal Na+ reabsorption on the other. Chronically, hyperinsulinemia may promote cardiovascular muscle cell proliferation and atherogenesis, while insulin resistance may be associated with certain transmembraneous cation transporters, leading to an increase in cytosolic Ca2+. Hyperinsulinemia and/or insulin resistance may also be associated with an increased blood pressure sensitivity to high salt intake. In the mosaic of many different blood pressure-raising mechanisms, insulin resistance and/or hyperinsulinemia is likely to represent an amplifying slow or very slow pressor factor.
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PMID:Insulin resistance and hyperinsulinemia in hypertension. 857 90

We propose the term Profactor-H for chronic elevated circulating insulin. Profactor-H is common in atherosclerosis, essential hypertension, non-insulin dependent diabetes mellitus, some forms of obesity, some forms of cancer, cardiovascular disease, peripheral vascular disease and some forms of stroke. Profactor-H appears to be the central pathophysiologic consideration in the etiology of many diseases and health risk factors. Profactor-H's impact depends on genetic predisposition, frequency consumption of refined simple and complex carbohydrates, deficiency in dietary chromium, sedentary life style and stresses of modern day living. In many obese individuals, Profactor-H disturbs metabolic balance, favoring anabolic metabolism, and is exacerbated through chronic insulin production and impairment of insulin action. This vicious cycle also appears to be common in many apparently healthy, non-obese individuals destined to develop health risks and diseases in response to long-term adverse consequences of Profactor-H. We believe that a four-pronged program which 1) reduces the daily frequency of carbohydrate consumption, particularly refined foods and simple sugars, 2) supplements the daily dietary intake of chromium, 3) encourages activity, and 4) reduces stress, will minimize the impact of Profactor-H and thereby reduce health risks and result in improved health.
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PMID:Profactor-H (elevated circulating insulin): the link to health risk factors and diseases of civilization. 857 92


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