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)

The effects of obesity on target organ injuries and cardiovascular risk factors were examined in hypertensive subjects. The subjects were 22 obese (OB-HT) and 54 nonobese (NO-HT) men with never-treated essential hypertension, and 37 obese (OB-NT) and 50 nonobese (NO-NT) normotensive men. In these 4 groups with the average age of about 50 years, we evaluated serum lipids, glucose tolerance, and hypertensive organ injuries in the heart, kidney, and optic fundus. Although the fasting blood glucose levels were similar in the 4 groups, the area under the blood glucose curve after 75 g glucose ingestion (NO-NT 15.6, OB-NT 17.5, NO-HT 15.8, OB-HT 17.6 x 10(3) mg/dl.min; p < 0.02) and the fast serum insulin level (NO-NT 7.3, OB-NT 10.1, NO-HT 7.7, OB-HT 12.2 mU/l; p < 0.001) were increased in obese men. In OB-HT, serum HDL-cholesterol was decreased (-11%, p < 0.05) and triglycerides were increased (+ 58%, p < 0.01) comparing with NO-NT. The incidence of electrocardiographic left ventricular hypertrophy was not significantly different among the 4 groups, however, urinary albumin excretion was increased in OB-HT (NO-NT 3.0, OB-NT 3.4, NO-HT 3.6, OB-HT 4.3 mg/g creatinine; p < 0.05) and sclerotic lesions of the retinal arteries were observed even in normotensive OB-NT. These data suggest that obesity unfavorably alters lipid and glucose metabolism, and facilitates organ injuries such as arteriosclerosis and renal dysfunction in hypertensive subjects.
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PMID:[Implications of obesity for target organ injuries and cardiovascular risk factors in hypertensive subjects]. 939 43

There has been increasing interest in the question of whether microalbuminuria can be used in the risk stratification of patients with essential hypertension. A cluster of cardiovascular and/or renal risk factors may be associated with microalbuminuria in hypertension. Despite this, prospective data about the potential role of microalbuminuria as a prognostic marker of cardiovascular and/or renal risk have been sparse and inconclusive until now. Blood pressure values have been considered the most important determinant of microalbuminuria in essential hypertension; however, hyperinsulinaemia--a metabolic component-was noted to be present in conjunction with high blood pressure. Furthermore, 2 other factors may be also related to microalbuminuria: salt sensitivity and renal structural changes (nephrosclerosis). We are now aware that the clinical and physiological implications of abnormal urinary albumin excretion (UAE) are much broader than anticipated, possibly involving haemodynamic, metabolic and vascular components overlapping several clinical syndromes. Achievement of short term UAE reduction with antihypertensive treatment depends on structural abnormalities established in the glomerulus, the extent of blood pressure reduction and the antihypertensive drug class used. In terms of UAE reduction, better results are obtained with ACE inhibitors or angiotensin II antagonists such as losartan and valsartan, than with other antihypertensive classes, although their true impact in preserving renal function needs to be assessed. The capacity of new calcium antagonists, such as amlodipine, lacidipine or mibefradil, to reduce UAE also needs to be assessed further. Thus, microalbuminuria may be seen as an integrated marker of risk and should be assessed in recently diagnosed patients with essential hypertension. In microalbuminuric patients, the target should be to decrease blood pressure < 135/85 mm Hg, reduce salt intake to around 100 mmol/day and prescribe a low-calorie diet if obesity is present. ACE inhibitors or angiotensin II antagonists have more potential benefits than the other classes of antihypertensive drugs in reducing UAE. Finally, a yearly assessment of microalbuminuria is recommended during treatment, to monitor the impact of therapy.
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PMID:Treatment of patients with essential hypertension and microalbuminuria. 942 93

People with type II diabetes have a twofold to fourfold increased risk of dying from the complications of cardiovascular disease. Atherosclerosis and vascular thrombosis are major contributors. The increased risk is present before fasting hyperglycemia is seen. These individuals often have a sedentary life-style, poor physical conditioning, insulin resistance, centripetal obesity, hypertension, dyslipidemia, and a prothrombotic state. Chronic hyperglycemia is then added to these risk markers. Microalbuminuria may precede hyperglycemia in type II diabetes, occurs in 30% to 40% of these individuals after diabetes is established, and is a predictor of cardiovascular events. Early intervention in high-risk individuals may delay or prevent fasting hyperglycemia. An all-inclusive approach that focuses on early risk factor (or marker) identification and management to prevent or delay accelerated atherosclerosis and thrombosis in type II diabetes is an attractive strategy. However, the database to support this strategy is limited. In particular, large-scale prospective trial data are not available to support the concept of intensive glycemic regulation to prevent progression of macrovascular disease in type II diabetes. This is in contrast to the situation regarding microvascular disease of the eyes and kidneys. Recently, indirect data of a correlative nature have emerged, and short- and long-term prospective trials at early and late stages of type II diabetes are now being reported. These studies are analyzed and interpreted in this report. In contrast, the database to support an intensive antiplatelet regimen to prevent vascular thrombotic events in people with type II diabetes is large, and these studies are reviewed. They are of a type and magnitude to allow definite recommendations for aspirin therapy in type II diabetes. Aggressive therapy directed at hypertension, hyperlipidemia, and elevated urinary albumin in people with type II diabetes appears to be indicated. Increased attention to the multifactorial aspects of treatment of the type II diabetic patient is needed. Our present challenge is to translate these findings for patients and primary health care providers so that effective actions may be implemented.
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PMID:Multifactorial aspects of the treatment of the type II diabetic patient. 943 50

Microalbuminuria is associated with excess cardiovascular mortality in both diabetic and nondiabetic subjects. Patients with NIDDM and microalbuminuria are more insulin resistant than those without microalbuminuria. However, the relationship between insulin resistance and microalbuminuria in patients with NIDDM could be due to hyperglycemia, which can cause both insulin resistance and an increase in albumin excretion rate. Little is known about microalbuminuria and insulin resistance in nondiabetic subjects. Therefore, we examined, cross-sectionally, the relationship of insulin sensitivity (S(I) x 10(-4) min x microU(-1) x ml(-1)), estimated by a frequently sampled intravenous glucose tolerance test and the minimal model and fasting plasma insulin concentration, to microalbuminuria (albumin-to-creatinine ratio > or = 2 mg/mmol) in 982 nondiabetic subjects aged 40-69 years. Altogether, 15% of the subjects had microalbuminuria, and 32% had hypertension. Subjects with microalbuminuria had a lower degree of insulin sensitivity (means +/- SE, 1.70 +/- 0.11 vs. 2.25 +/- 0.07, P = 0.003) and higher fasting insulin concentrations (17.4 +/- 1.1 vs. 15.7 +/- 0.5 mU/l, P = 0.059) compared with subjects without microalbuminuria. In logistic regression analysis, an increasing degree of insulin sensitivity was related to a decreasing prevalence of microalbuminuria (odds ratio = 0.86, 95% CI: 0.79-0.94, P < 0.001). Although this relationship attenuated after adjustment for age, sex, ethnicity, hypertension, fasting glucose, and BMI, it still remained significant. The association between insulin sensitivity and microalbuminuria was shown not to be different between normotensive and hypertensive subjects. Our results suggest a relationship between insulin resistance and microalbuminuria in nondiabetic subjects that is partially dependent on blood pressure, glucose levels, and obesity.
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PMID:Microalbuminuria is associated with insulin resistance in nondiabetic subjects: the insulin resistance atherosclerosis study. 958 52

Associations between a high daily insulin dose and cardiovascular risk factors, including those of the insulin-resistance syndrome, were studied in 479 Type 1 diabetic children 6 to 18 years of age. Insulin dose increased over the first two years after diagnosis of diabetes (p = 0.0001) and was significantly higher in girls (p = 0.01). For those children with diabetes duration of more than 2 years, the insulin requirement increased up to 13-14 years of age (p < 0.05) and was higher in pubertal than pre-pubertal children (p < 0.05). For girls, the requirement was higher in puberty than in post-puberty (p < 0.05) and increased with diabetes duration (p < 0.05). Triglyceride concentrations were associated positively and significantly with the insulin dose of both boys and girls, after adjustment for age, pubertal stage, diabetes duration, and metabolic control (fructosamine levels). No other consistent associations were found between insulin dose and other cardiovascular risk factors: body mass index, central adiposity, arterial blood pressures, serum total cholesterol, apoA1, apoB, Lp(a), uric acid, or urinary albumin excretion. Parental obesity, hypertension and diabetes were not related to the insulin dose of children. The results did not differ when the population was limited to the 375 children with diabetes duration of more than 2 years. It is concluded that in these Type 1 diabetic children the insulin dose for a given level of metabolic control (our surrogate measure of insulin resistance) was related to a single cardiovascular risk factor: triglyceride concentrations.
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PMID:Insulin dose and cardiovascular risk factors in type 1 diabetic children and adolescents. 959 39

Urinary albumin excretion (UAE) was evaluated in 26 subjects with essential hypertension and no diabetes (5 men, 21 women; 19 whites and 7 blacks), with creatinine clearance (Ccreat) > or = 75 ml/min/1.73 m2, in individualized treatment with various antihypertensive drugs. Clinical and laboratorial data were the following: mean age, 53 +/- 2 years (SEM); duration of hypertension, 14.9 +/- 2.2 years; body mass index (BMI), 26.8 +/- 0.7; arterial blood pressure, 142 +/- 4/89 +/- 3 mmHg; serum creatinine, 0.8 +/- 0.03 mg/dL; Ccreat, 99.3 +/- 3.8 ml/min/1.73 m2 and UAE, 9.3 +/- 1.5 micrograms/min. No significant difference was found when data were evaluated for gender and race. Microalbuminuria, defined as UAE > 13.9 micrograms/min, was found in 19% of the hypertensives (range: 16.3 to 28.1 micrograms/min). UAE correlated positively and significantly with systolic (r = 0.6309; P = 0.0005), diastolic (r = 0.4146; P = 0.0352), and mean blood pressure (r = 0.5000; P = 0.0093). The correlation between UAE and systolic pressure was stronger than with diastolic pressure. There was a positive and significant correlation between BMI and UAE values (r = 0.5623; P = 0.0028), and between BMI values with those of systolic (r = 0.5271; P = 0.0057) and mean blood pressure (r = 0.3930; P = 0.470). No correlation was found between UAE and age, duration of hypertension or Ccreat. Systolic, diastolic and mean blood pressures were significantly higher in microalbuminuric than in non microalbuminuric hypertensives. Obese hypertensives presented higher mean values of UAE, systolic, diastolic and mean pressures than non obese.
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PMID:Microalbuminuria in essential hypertensives in treatment for hypertension. 959 80

Microalbuminuria is associated with increased morbidity and early mortality in non-insulin-dependent diabetes mellitus (NIDDM), mostly due to cardiovascular disease. This association may be due to a higher prevalence of known cardiovascular risk factors in those with microalbuminuria. We examined the relationship of microalbuminuria to components of the metabolic syndrome in 98 NIDDM patients with elevated urinary albumin excretion rate (UAER) (> 10.5 micrograms/min) (high UAER) and 102 normoalbuminuric NIDDM patients. Patients with high UAER were older than normoalbuminuric patients (P < 0.05), but they did not differ with respect to duration of diabetes, total cholesterol, body mass index (BMI) or the prevalence of smoking. A total of 58 (60%) patients with elevated UAER had two or more of hypertension, ischaemic heart disease (IHD), hypertriglyceridaemia and obesity compared with 41 (40%) in the normoalbuminuric group, (P < 0.05). Only nine (9.2%) high UAER patients had none of the above risk factors compared with 26 (25.5%) in the normoalbuminuric group (P < 0.01). The prevalence of hypertension (blood pressure (BP) > 160/95) was significantly higher in high UAER patients; 61/98 (62%) versus 39/102 (38%) in normoalbuminuric group, (P < 0.05). Elevated UAER was also associated with a higher risk of macrovascular disease (P < 0.01). The high UAER group included 50 Caucasian, 30 Asian and 18 Afro-Caribbean. The three groups did not differ with respect to total cholesterol, glycosylated haemoglobin (HbA1c) or prevalence of smoking. Asians had a lower BMI, a lower BP and a lower prevalence of peripheral vascular disease (PVD), but had a higher serum triglyceride (P < 0.01 for all) compared with Caucasian. Patients of Afro-Caribbean origin had a lower prevalence of IHD (0%) compared with both Asians (16%) and Caucasians (22%). Elevated UAER in NIDDM is closely associated with components of the metabolic syndrome and an increased risk of IHD and PVD. There are however, significant ethnic differences in this association.
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PMID:Relationship of elevated urinary albumin excretion to components of the metabolic syndrome in non-insulin-dependent diabetes mellitus. 959 78

The authors examined the nutritional status of 50 patients admitted on account of exacerbation of chronic obstructive lung disease. The mean height of patients was 168 +/- 8.8 cm, the body weight 72.2 +/- 16.2 kg, BMI 25.5 +/- 5.5 kg/m2. The mean albumin concentration was 33.1 +/- 4.6 g/l, transferrin 2.3 +/- 0.6 g/l, the skinfold thickness 17.3 +/- 9.9 mm, arm circumference 28.6 +/- 7.2 cm. The mean energy expenditure at rest (REE) was 122.1 +/- 12.3%. The total number of undernourished patients was 7 (14%), there were 27 obese patients (54%). The authors did not find a relationship between respiratory parameters and values of blood gases on the one hand and body weight, skinfold thickness, BMI, REE, arm circumference, albumin, transferrin and the number of lymphocytes on the other hand. This is obviously due to the fact that the group comprised more obese than undernourished patients. Obese and undernourished patients were found in all three stages of the disease.
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PMID:[Nutritional status in patients with chronic obstructive pulmonary disease]. 960 34

We evaluated the role of obesity in proteinuria by treadmill exercising of simple obese subjects and non-obese subjects with non-insulin dependent diabetes mellitus in whom the albumin excretion rate at rest was within normal range. Non-obese healthy volunteers were studied as the controls. The fractional renal clearances of four endogenous proteins, albumin, IgG, IgG4, and beta2-microglobulin were measured before, during, and after treadmill exercise in 17 simple obese and 15 non-obese diabetic subjects, and in 21 normal subjects. Exercise increased the fractional albumin clearance in all groups. In diabetic subjects, the fractional IgG4 clearance also increased: fractional beta2-microglobulin clearance increased in normal controls and in diabetics. In obese subjects, the fractional clearances of albumin, IgG, and IgG4 were similar to those in normal controls, but fractional beta2-microglobulin clearance was significantly lower. These results suggest that enhanced microalbuminuria in obese subjects is probably of glomerular origin. In normal subjects and diabetics, exercise-induced microproteinuria is probably of both glomerular and tubular origin. Defect in the charge-selective barrier of the glomerular capillary wall has been implicated in diabetics. Thus some additional factors relevant to obesity must be taken into account in the consideration of the mechanism of microalbuminuria in diabetics with obesity.
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PMID:Do obesity and non-insulin dependent diabetes mellitus aggravate exercise-induced microproteinuria? 972 Oct 70

Animal studies suggest that lipids are risk factors for kidney diseases. Some prospective studies and clinical trials have reported predictive effects of lipoproteins on different stages of diabetic nephropathy in humans. We examined lipoprotein abnormalities to determine if they predict abnormal urinary excretion of albumin (> or = 30 mg albumin/g creatinine), using logistic regression. We followed 671 American Indians (211 men, 460 women) with Type II diabetes for a mean of 3.9 years (range 1.7-6.2). Participants were aged 45-74 years. They had normal excretion of albumin and normal serum creatinine at baseline. 67 men and 144 women developed abnormal excretion of albumin. In models controlled for age, treatment with oral hypoglycaemic agents or insulin, HbA1c, study site, degree of Indian heritage, mean arterial blood pressure, albumin excretion at baseline and duration of diabetes, a high HDL cholesterol was a protector for abnormal excretion of albumin in women [odds ratio (OR) comparing the 90th with the 10th percentile = 0.56, 95% confidence interval (CI) = 0.32-0.98], but not in men (OR = 1.5, 95% CI = 0.66-3.4). Further adjustment for obesity, insulin concentration, alcohol consumption or physical activity did not change the results. There was a tendency for high values of VLDL and total triglyceride and small LDL size to predict abnormal excretion of albumin in women only. We conclude that low HDL cholesterol was a risk factor for abnormal excretion of albumin in women, but not in men. Sex hormones may be responsible for sex differences in the association between HDL cholesterol and abnormal excretion of albumin.
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PMID:Plasma lipoproteins and the incidence of abnormal excretion of albumin in diabetic American Indians: the Strong Heart Study. 975 17

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