UMLS:C0028754 - FACTA Search

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Query: UMLS:C0028754 (obesity)
124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Confirmation of the diagnosis of OSA currently requires overnight polysomnography. This study evaluates the usefulness of pulse oximetry together with a clinical score in identifying OSA. Forty patients were assigned a clinical score based on the presence or absence of loud snoring, observations of interrupted breathing during sleep, hypersomnolence, obesity and essential hypertension. Each underwent a night of domiciliary pulse oximetry followed by nocturnal polysomnography. Significant OSA was confirmed in 26. All 15 patients with positive pulse oximetry tracings had significant OSA (apnea index greater than or equal to 10). Five of eight with negative tracings were also shown to have significant OSA along with six of the seven patients with inadequate or indeterminate tracings. Clinical scores were significantly different for those with and without OSA. This study confirms the usefulness of nocturnal pulse oximetry in establishing the diagnosis of OSA and highlights the value of a clinical score in improving its sensitivity as a screening tool.
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PMID:Screening for sleep apnea using pulse oximetry and a clinical score. 188 45

Recently, we reported that the blunted natriuretic ability related to an attenuation of renal dopaminergic activity might play an important role in the hypertensive mechanisms of overweight patients with essential hypertension. On the other hand, the interrelationships between obesity, blood pressure and renal sodium handling in normotensives (NT) have not been clear. The purpose of the present study is to reveal the role of renal dopaminergic activity on renal sodium handling in overweight NT. The study consisted of 52 hospitalized NT receiving a regular diet containing 200mEq of sodium, 75mEq of potassium, 2400kcal/day, who were divided into two groups of 31 non-obese (NNT) and 21 obese (ONT) subjects. NNT was categorized as the body mass index (BMI) less than, and ONT as the BMI equal to or more than, 25kg/m2. In the early morning, after overnight fasting, all subjects remained in a supine state and were examined for renal clearance. During the clearance period, mean arterial pressure (MAP), heart rate (HR), endogenous creatinine clearance (Ccr), urinary excretion of sodium (UNaV), fractional excretion of sodium (FENa) and of inorganic phosphorus (FEP) and urinary excretion of free dopamine (uDA) were determined. There were no significant differences in age, HR, Ccr or UNaV between the two groups. Higher MAP and lower FENa) were observed in ONT than in NNT, but the differences in these parameters were not statistically significant. However, FENa in ONT was significantly lower than in MAP-and Ccr-matched NNT. In addition, FENa correlated negatively with BMI in ONT, unlike in NNT. MAP was correlated positively with FENa, and a similar tendency was found between MAP and FEP in NNT, but not in ONT. On the other hand, there was no significant correlation between BMI and uDA in either NNT or ONT. This result was different from our previous data in patients with essential hypertension (EHT) in which BMI correlated with uDA positively in non-obese EHT and negatively in obese EHT. These findings suggest that blunted natriuretic ability may exist in ONT, and the role of renal dopaminergic activity related to the attenuated natriuretic ability in ONT may be less important than in obese EHT.
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PMID:[Renal sodium handling and renal dopaminergic activity in overweight normotensive subjects]. 188 10

Essential hypertension is frequently associated with several metabolic abnormalities, of which obesity, glucose intolerance, and dyslipidemia are the most common. This report discusses the epidemiologic evidence for the coexistence of these risk factors and questions why hyperinsulinemia and essential hypertension cosegregate. The euglycemic insulin clamp and the insulin suppression test are documented with respect to the physiologic functions of insulin, and the mechanisms of insulin resistance in essential hypertension are discussed. Evidence to suggest that insulin resistance is a marker for an "atherogenic syndrome" is reviewed. It is concluded that all the hemodynamic and metabolic disorders of essential hypertension and insulin resistance are closely related. The clinical approach to the patient with any of the abnormalities in question should take into consideration the whole cluster, with therapy aimed at ameliorating the entire hemodynamic-metabolic profile.
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PMID:Essential hypertension, metabolic disorders, and insulin resistance. 200 56

Hypertension is related to several conditions with abnormalities in carbohydrate and lipid metabolism, such as obesity and impaired glucose tolerance. However, perturbed metabolism is also seen in non-obese hypertensive individuals. In addition, hypertension is linked to impaired fibrinolysis and elevated levels of the plasminogen activator inhibitor of endothelial type (PAI-1). Insulin resistance and hyperinsulinaemia in essential hypertension may be an important cause of these metabolic and fibrinolytic abnormalities. Whether hyperinsulinaemia is the cause of hypertension is currently unknown. However, it is clear that the relationship between hypertension and insulin is complex, and further studies are required to clarify this association. Based on the evidence states, it is suggested that insulin resistance and hyperinsulinaemia play a role in hypertension. However, it is also clear that hyperinsulinaemia occurs in the absence of hypertension, which suggests that other factors, such as genetic susceptibility, may be important.
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PMID:Hypertension as a metabolic disorder--an overview. 204 18

Epidemiological evidence suggests that there is a close association between obesity, non-insulin-dependent diabetes (NIDDM) and hypertension. Obesity and NIDDM are the classical insulin-resistant states. Even in the absence of these conditions, essential hypertension is associated with insulin resistance. In view of the acute effects of insulin on renal sodium reabsorption, the sympathetic nervous system, the renin-angiotensin-aldosterone system, the transmembranous cation transport, the cardiovascular reactivity, the atrial natriuretic peptide and the kallikrein-kinin system, hyperinsulinaemia may contribute to the development of hypertension in these diseases. Preliminary evidence suggests that sensitivity to these possible blood-pressure-elevating action(s) of insulin is still present despite the resistance to the glucose-lowering action of the hormone. However, extrapolation of the epidemiological data and results of acute experiments indicate that the impact on blood pressure is rather small. The pathophysiological mechanisms of hypertension in the above-mentioned conditions are also not always consistent with insulin action(s). Moreover, some data suggest that insulin resistance, and not hyperinsulinaemia per se, underlies the blood pressure elevation, while the possibility cannot be excluded that both hypertension and insulin resistance are co-inherited, but unrelated, abnormalities.
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PMID:Insulin and blood pressure regulation. 204 23

Resistance to the action of insulin on glucose metabolism, with the ensuing compensatory hyperinsulinaemia, is closely linked to essential hypertension. The decreased insulin sensitivity observed in hypertensive patients is independent of obesity. Hyperinsulinaemia is likely to promote the dyslipidaemia that frequently accompanies the hypertensive state, and often presents as increased total and very low density lipoprotein (VLDL)-triglycerides, low high density lipoprotein (HDL)-cholesterol and, in some studies, elevated levels of low density lipoprotein (LDL)-cholesterol. Lipid abnormalities, hypertension and possibly hyperinsulinaemia act together to increase the risk of atherosclerotic disease manifestations in hypertensive patients. Acutely, insulin has been shown to stimulate sympathetic nervous system activity and transmembrane electrolyte transport, to promote sodium retention and to cause vascular wall changes, including increased cholesterol biosynthesis and smooth muscle proliferation. If these mechanisms operate on a chronic basis, the continuous exposure to elevated plasma insulin levels may play a pathogenetic role in the development of high blood pressure, and also of a predisposition toward atherosclerosis in patients with hypertension. Further studies are necessary to establish these hypothetical cause-effect relationship which, if shown to be true, will contribute to a more wide-ranging view of essential hypertension and the optimum strategy for antihypertensive treatment.
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PMID:Insulin resistance in hypertension--a relationship with consequences? 204 24

Diabetes mellitus is commonly associated with systolic/diastolic hypertension, and a wealth of epidemiological data suggest that this association is independent of age and obesity. Much evidence indicates that the link between diabetes and essential hypertension is hyperinsulinemia. Thus, when hypertensive patients, whether obese or of normal body weight, are compared with age- and weight-matched normotensive control subjects, a heightened plasma insulin response to a glucose challenge is consistently found. A state of cellular resistance to insulin action subtends the observed hyperinsulinism. With the insulin/glucose-clamp technique, in combination with tracer glucose infusion and indirect calorimetry, it has been demonstrated that the insulin resistance of essential hypertension is located in peripheral tissues (muscle), is limited to nonoxidative pathways of glucose disposal (glycogen synthesis), and correlates directly with the severity of hypertension. The reasons for the association of insulin resistance and essential hypertension can be sought in at least four general types of mechanisms: Na+ retention, sympathetic nervous system overactivity, disturbed membrane ion transport, and proliferation of vascular smooth muscle cells. Physiological maneuvers, such as calorie restriction (in the overweight patient) and regular physical exercise, can improve tissue sensitivity to insulin; evidence indicates that these maneuvers can also lower blood pressure in both normotensive and hypertensive individuals. Insulin resistance and hyperinsulinemia are also associated with an atherogenic plasma lipid profile. Elevated plasma insulin concentrations enhance very-low-density lipoprotein (VLDL) synthesis, leading to hypertriglyceridemia. Progressive elimination of lipid and apolipoproteins from the VLDL particle leads to an increased formation of intermediate-density and low-density lipoproteins, both of which are atherogenic. Last, insulin, independent of its effects on blood pressure and plasma lipids, is known to be atherogenic. The hormone enhances cholesterol transport into arteriolar smooth muscle cells and increases endogenous lipid synthesis by these cells. Insulin also stimulates the proliferation of arteriolar smooth muscle cells, augments collagen synthesis in the vascular wall, increases the formation of and decreases the regression of lipid plaques, and stimulates the production of various growth factors. In summary, insulin resistance appears to be a syndrome that is associated with a clustering of metabolic disorders, including non-insulin-dependent diabetes mellitus, obesity, hypertension, lipid abnormalities, and atherosclerotic cardiovascular disease.
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PMID:Insulin resistance. A multifaceted syndrome responsible for NIDDM, obesity, hypertension, dyslipidemia, and atherosclerotic cardiovascular disease. 204 34

Seventeen normotensive, premenopausal women were treated with the 5-hydroxytryptamine-reuptake inhibitor dexfenfluramine 30 mg per day, for 4 days in a randomised double-blind, cross-over, placebo controlled trial. Energy intake was held constant during the study as the aim was to study the endocrine and metabolic effects of dexfenfluramine dissociated from its weight-lowering properties. Body weight, blood glucose, plasma insulin, cholesterol triglycerides and C-peptide after an overnight fast and during an oral load of 100 g glucose did not change after dexfenfluramine compared to placebo. Supine and standing systolic and diastolic blood pressures were significantly decreased, while heart rate remained unchanged. Plasma noradrenaline and plasma renin were markedly reduced by dexfenfluramine, and cortisol, beta-endorphin and thyroid hormones were not changed. Thus, dexfenfluramine has a significant hypotensive effect in normotensive, obese women after 4 days of treatment, independent of a negative energy balance. This was associated with decreased circulating plasma noradrenaline, indicating decreased sympathetic nerve activity. Dexfenfluramine may be a candidate drug for longer-term trials in the treatment of primary hypertension associated with obesity.
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PMID:Haemodynamic, metabolic and endocrine effects of short-term dexfenfluramine treatment in young, obese women. 206 May 60

The frequent concurrence of other cardiovascular risk factors in hypertensive patients, such as obesity and diabetes mellitus, suggests that overlapping genetic and environmental factors may contribute to the common metabolic and cardiovascular derangements observed in these populations. Hypertension and hyperglycemia accelerate atherosclerosis in diabetics, and play an important role in associated morbidity and mortality. Several abnormalities in blood pressure regulatory systems such as the renin-angiotensin system, the sympathetic nervous system, and sodium/volume control have been described in diabetes mellitus. Sodium retention and cardiovascular hyperreactivity appear to occur early in the course of diabetes mellitus, even at normal blood pressure levels and before onset of renal failure, and could set the stage for the development of hypertension. The relationship between obesity and hypertension is also well-established, and may reflect metabolic and cardiovascular adaptations in obese subjects which predispose to blood pressure elevations. Obese subjects display changes in sympathetic nervous system activity, sodium metabolism, and vascular hemodynamics. Sodium-sensitive blood pressure responses in the obese may be secondary to increased cardiac output or fluid volume, and are directly related to circulating insulin levels. Certain metabolic and vascular characteristics of obesity and diabetes mellitus are found in patients with essential hypertension. It has been suggested that insulin and insulin resistance may be the common link between these risk factors. Improved understanding of metabolic considerations in the treatment of obese and diabetic hypertensives should lead to more careful selection of medications that avoid metabolic complications. Although diuretics and beta-blockers may be useful in some patients, there are several reasons not to recommend their use as initial therapy in obese and diabetic hypertensives. On the other hand, calcium channel blockers and angiotensin converting enzyme inhibitors are highly effective, with minimal effects on metabolic parameters, and are well-suited as first-line therapy in the treatment of obese and diabetic hypertensives.
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PMID:Metabolic considerations in hypertension. 207 23

Obesity represents an important risk factor for cardiovascular disease and in children it is often associated to the future development of essential hypertension. To evaluate the early hemodynamic alterations in obese normotensive children, ambulatory monitoring was performed in 18 obese children aged 9.6 +/- 2.9 and in 33 controls of equivalent age by ICR 5200 (Spacelabs, USA). Blood pressure daily curves in the two groups were compared by MANOVA. Basal blood pressure did not differ in the two groups (115 +/- 17 mmHg and 79 +/- 7 mmHg respectively systolic and diastolic in controls and 115 +/- 12 mmHg and 79 +/- 6 mmHg in obese children). On the contrary ambulatory monitoring showed higher systolic values in obese children when compared to controls (112 +/- 7 versus 107 +/- 7, p less than 0.04) (MANOVA test, p less than 0.03). The difference was observed both during the day time (115 +/- 6 vs 111 +/- 7, p less than 0.03) and during the night (107 +/- 9 vs 102 +/- 8, p less than 0.5). No differences in diastolic pressure and in heart rate were observed. Those findings indicate that in obese children blood pressure alterations unrecognized at usual blood pressure checks are detectable by ambulatory 24 hour monitoring.
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PMID:[Changes in the ambulatory arterial pressure of normotensive obese children]. 208 24

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