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

Hypertension is known to be strongly associated with multiple metabolic abnormalities. A recent population survey carried out in Italy (the Gubbio study) involving 5,376 individuals showed that, up to the age of 64 years, hypertensive men were more markedly overweight (body mass index > or = 30) than normotensive men, whereas in women the prevalence of obesity was higher in hypertensive women at all ages. The prevalence of marked hypercholesterolemia (> or = 250 mg/dL) was uniformly higher in hypertensive compared with normotensive men except in the oldest age group; it was also higher in hypertensive women in the age 45-74 years group. Postabsorptive hyperglycemia and hyperuricemia were also more prevalent in hypertensive men and women, especially in the older age groups. Furthermore, the Tecumseh Blood Pressure Study indicated that not only patients with "sustained" hypertension but also those with so-called "white-coat" hypertension are, as a group, overweight and have elevated levels of cholesterol, insulin, and triglycerides and decreased levels of high-density lipoprotein. The multiple metabolic abnormalities clustered in hypertensives are important in relation to prognosis and therapy. The most recent World Health Organization/International Society of Hypertension guidelines for management of mild hypertension give considerable attention to the global assessment of cardiovascular risk in patients with hypertension and stress that, among individuals with mild hypertension, the risk of serious cardiovascular disease is also determined by a variety of risk factors other than blood pressure. The higher the absolute risk, the greater is the absolute benefit brought about by lowering blood pressure and correcting other risk factors, such as dyslipidemia.
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PMID:Hyperlipidemia in the hypertensive patient. 801 63

The objectives of this research were to determine the prevalence of essential and borderline hypertension in a population of blood donors and their families and to determine if there is a correlation between blood pressure and lifestyle and/or other cardiovascular risk factors. The study was comprised of 1976 individuals, of whom 1290 were men and 686 were women, aged 18-65 years. The prevalence of essential hypertension was 15.1% for males and 12.5% for females: the prevalence of borderline hypertension was 22.3% for males and 15.7% for females. The population was divided into two groups: the first group included only subjects (1170 men, 543 women) who did not regularly use drugs that could modify the blood pressure and the heart rate, the second group included the entire population. In the first group, the multiple regression analysis indicated, in order of importance: age, BMI (body mass index), and heart rate. These variables were important in determining the systolic blood pressure in both sexes, uricemia for males and glycemia for females. The diastolic blood pressure was dependent on BMI, heart rate, and alcohol in both sexes, and glycemia, LDL cholesterol, and uricemia in the men. In the second group, primary and borderline hypertension are significantly correlated with age, BMI, and uricemia in both sexes and glycemia in females. A program of health and nutritional education could modify some factors related to blood pressure, such as obesity and alcohol consumption. The result would be a reduction of the prevalence not only of essential and borderline hypertension, but also of metabolic diseases such as dyslipidaemias, diabetes and hyperuricemia, with a global reduction of the cardiovascular risk.
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PMID:[Arterial hypertension in relation to life style and other cardiovascular risk factors. Epidemiologic study of a population of blood donors. Project AVIS]. 802 51

Serum uric acid concentration and fractional excretion were evaluated in lean (n = 67) and obese (n = 56) girls before and during pubertal development. In both lean and obese girls, uricemia gradually increased as puberty advanced. Obese girls were hyperuricemic compared with lean controls (prepubertal: 184 +/- 83 v 130 +/- 29 mumol/L, P = .007; Tanner stage II-III: 190 +/- 53 v 178 +/- 47 mumol/L, NS; Tanner stage IV-V: 232 +/- 53 v 191 +/- 53 mumol/L, P = .02). Fractional excretion of urate decreased with puberty in lean girls (6.46% +/- 2.29%, 4.61% +/- 2.48%, and 3.54% +/- 1.84%), but not in obese subjects (3.74% +/- 2.27%, 4.01% +/- 1.90%, and 4.26% +/- 2.26%). Urate homeostasis was similar in prepubertal obese girls and in adolescent lean controls. We conclude that an increased serum urate concentration occurring at puberty may be due to decreased renal clearance of urate in lean girls, and at least in part to urate overproduction in obese subjects. Obesity may prematurely evoke changes in urate metabolism usually observed at puberty.
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PMID:Uric acid homeostasis in lean and obese girls during pubertal development. 802 3

In this review the independent risk factors of hypertension, diabetes mellitus type II and large vessel disease are discussed. Hyperinsulinemia as the most important factor is associated with obesity, dyslipoproteinemia, alcohol drinking, physical inactivity, hyperfibrinogenemia, smoking (among men), microalbuminuria and hyperuricemia, which are sometimes partially related. If one factor occurs, the other associated factors have to be searched for in order to initiate an adequate treatment. To improve the acceptance of adequate advice, the knowledge of risk reduction should influence the health education.
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PMID:[Hypertension, Type II diabetes mellitus and macroangiopathy: risk factors and their association]. 812 58

Metabolic disorders including diabetes mellitus, glucose intolerance, dyslipidemias, hyperuricemia, and hypervitaminosis A have often been mentioned in association with diffuse idiopathic skeletal hyperostosis (DISH). Production of bone under the influence of insulin or retinol has been suggested as a possible mechanism for this disease. We prospectively studied metabolic disorders in 25 patients with DISH and 25 controls matched for age, sex, and body mass index. Correlations between simultaneously evaluated parameters were looked for. Obesity was prevalent in both groups. Serum levels of glucose, insulin, glycated hemoglobin, total cholesterol, HDL cholesterol, triglycerides, uric acid, retinol, and retinol binding protein were similar in the two groups. A positive correlation was found between body mass index and serum insulin. We found no correlation between serum levels of insulin and retinol. None of the metabolic parameters studied showed alterations likely to explain the development of hyperostosis. Other growth factors such as retinoic acid or insulin-like growth factor 1, perhaps produced on a paracrine basis, may be the cause of increased bone at enthesis production.
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PMID:[Forestier disease and metabolism disorders. A prospective controlled study of 25 cases]. 816 24

The associates of gout-obesity, hypertriglyceridemia, glucose intolerance, and hypertension, strikingly resemble those of insulin resistance. In the present study we determined whether hyperuricemia is associated with insulin resistance and, if so, whether this association can be explained by other components of the syndrome. For this purpose we quantitated insulin sensitivity (euglycemic clamp) in 37 nondiabetic subjects (aged 30-68 yr) exhibiting varying degrees of the metabolic syndrome (body mass index, 21.5-35.7 kg/m2; serum triglycerides, 0.4-22.0 mmol/L; high density lipoprotein cholesterol 0.38-1.86 mmol/L; blood pressure, 190-100/116-60 mm Hg). In simple linear regression analysis, the serum uric acid concentration (range, 182-568 mumol/L) was inversely correlated with insulin sensitivity (rate of glucose utilization; r = -0.61; P < 0.001) and positively with serum triglycerides (r = 0.68; P < 0.001), but not with body mass index, age, or the plasma glucose concentration. In multiple linear regression analysis, both insulin sensitivity (P < 0.05) and serum triglycerides (P < 0.005) were independently associated with the serum uric acid concentration, and together explained 50% of its variation. Addition of body mass index or age to the model did not improve the degree of explanation. Acute elevation of serum triglycerides about 3-fold, of plasma FFA about 9-fold, or of serum insulin about 28-fold had no effect on the serum uric acid concentration in healthy volunteers. The data indicate that hyperuricemia is indeed an inherent component of the metabolic syndrome and could also be used as a simple marker of insulin resistance.
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PMID:Hyperuricemia and insulin resistance. 828 9

Hyperinsulinemia is very much in the spotlight. Debate rages as to its significance and role in the etiology not only of NIDDM, but also other morphological and metabolic risk factors for atherosclerotic cardiovascular disease, including upper-body obesity, dyslipidemia, hypertension, and hyperuricemia. Epidemiological data support a key role for hyperinsulinemia in these disorders but it is far from conclusive except for the fact that hyperinsulinemia and insulin resistance may be present many years before the onset of impaired glucose tolerance and NIDDM, and clearly play a role in their etiology. The thrifty genotype hypothesis provides a plausible basis for a better understanding of how hyperinsulinemia and insulin resistance could lead to glucose intolerance and atherosclerotic cardiovascular disease, but the detailed biochemical mechanisms remain elusive. A role for increased sympathetic nervous system activity, resulting from hypothalamic stimulation as a primary event causing hyperinsulinemia, cannot be excluded as a cause of hyperinsulinemia. The current focus on hyperinsulinemia also has resulted in closer examination of the therapy of diabetes and hypertension, emphasizing the need to avoid hyperinsulinemia in both IDDM and NIDDM individuals because of the putative risk of atherosclerotic cardiovascular disease and hypertension. There is still a paucity of epidemiological data to support a role for hyperinsulinemia in the etiology of hypertension. However, clinical practice already is being influenced by the fact that ACE inhibitors have been shown to reduce insulin resistance in clinical research studies. The research reviewed here, particularly that relating to hyperinsulinemia, insulin resistance, and cardiovascular disease risk factors, has opened new vistas for the treatment and prevention of NIDDM and atherosclerotic cardiovascular disease. Appropriate exercise clearly is associated with improved insulin sensitivity, modification of CVD risk factors, and lower prevalence of NIDDM. Upper-body obesity, the latest culprit in the field, can also be reduced by exercise. Hyperinsulinemia and insulin resistance can be detected in children, adolescents, and young adults. NIDDM can be prevented, but clearly, intervention needs to commence in childhood, and intensive risk factor intervention in subjects with NIDDM can reduce the risk of atherosclerotic cardiovascular disease. It seems paradoxical that prevention of NIDDM and atherosclerotic cardiovascular disease are now possible even though the biochemical and molecular basis of these disorders is not fully understood.
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PMID:Hyperinsulinemia--how innocent a bystander? 829 79

The history and laboratory examination of the parents of six families with a history of biliary showed that five mothers and one father had cholelithiasis. Two of the mothers also had exogenous obesity and diabetes mellitus, and one mother also had lipid abnormalities. Among the 21 children of the same families, one son had cholelithiasis; 5 children (4 women and one man) had cholelithiasis and exogenous obesity; 10 (9 women and one man) had cholelithiasis, exogenous obesity and diabetes mellitus; two (one man and one woman) had cholelithiasis, exogenous obesity and lipid abnormalities; one son had cholelithiasis and diabetes mellitus, and one son had cholelithiasis and lipid abnormality. Among the 18 grandchildren of these families, 3 (2 women and one man) had cholelithiasis; 5 granddaughters had cholelithiasis and exogenous obesity; 2 grandsons had cholelithiasis, exogenous obesity and diabetes mellitus; 2 grandsons had cholelithiasis and lipid abnormality; one grandson had cholelithiasis, diabetes mellitus and hyperuricemia; one grandson had cholelithiasis, exogenous obesity, lipid abnormalities and hyperuricemia, and one grandson had exogenous obesity and diabetes mellitus. Finally, of the greatgrandchildren, one girl had cholelithiasis.
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PMID:[Familial calculous cholecystopathy]. 847 36

Patients who develop diabetic nephropathy, one of the leading causes of end-stage renal diseases in Western communities, have an increased red cell Li+/Na+ countertransport (CT). Li+/Na+ CT is a membrane function which exchanges intracellular Li for extracellular Na in vitro. High Li+/Na+ CT reflects abnormal kinetic properties of red cell membrane Na/H exchange. A widespread abnormality of Na/H exchange could play a major role in the pathogenesis of diabetic nephropathy as well as of cardiovascular diseases since Na/H exchange is involved in the regulation of cell pH and cell volume; in the cellular response to hormones, mitogens, and growth factors; and in the renal reabsorption of Na and bicarbonate. Li+/Na+ CT is under genetic control and raised in a subgroup of patients with essential hypertension. Among these patients, high Li+/Na+ CT is associated with increased glomerular filtration rate, filtration fraction, proximal fractional Na reabsorption, microalbuminuria, plasma renin activity, and kidney and cardiac volume. Increased Li+/Na+ CT is often associated with hyperlipidemia, hyperuricemia, reduced insulin sensitivity, and obesity. The whole of these observations may explain why patients with diabetes or essential hypertension and increased Li/Na CT are at risk of early renal and cardiac impairment.
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PMID:Red blood cell Li+/Na+ exchange in patients with diabetic nephropathy and essential hypertension: therapeutic implications. 851 86

We now have sufficient knowledge to be able to identify the factors contributing to hyperuricemia in most patients with gout. Some of these factors, such as obesity, a high-purine diet, regular alcohol consumption, and diuretic therapy, may be correctable. In patients with persistent hyperuricemia, regular medication should lower the serum urate concentration to an optimal level. The continuing challenge is to educate patients about correctable factors and the importance of regular medication and ensure their compliance so that attacks of gout do not recur.
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PMID:The management of gout. 861 15


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