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

There is a conflict in previous studies with regard to the relation between adipose tissue mass and total body fluid distribution. This study tested the hypothesis that obesity is accompanied by an increase in the extracellular-to-intracellular fluid ratio above that observed in nonobese subjects. Extracellular fluid was evaluated in obese (n = 39) and nonobese (n = 26) healthy women, using two different dilution volumes, 35SO4 [extracellular water (ECW)] and 24NaCl [exchangeable sodium (Nae)]. Intracellular water (ICW = 3H2O dilution volume-ECW) and total body potassium (TBK; 40K whole body counting) were assumed to represent intracellular fluid. Two independent markers of relative fluid distribution were formulated as ECW/ICW and Nae/TBK. Obese and nonobese women were of similar age and height but differed in body weight and TBW by 67.7 kg and 12.9 liters, respectively. The obese women had significantly larger absolute ECW, Nae, ICW, and TBK compared with the nonobese women (all P less than 0.001). The ratios ECW/ICW and Nae/TBK were significantly higher in obese vs. nonobese women and were highly correlated with each other (r = 0.54, P less than 0.001) in the pooled group of subjects. Fluid volumes are thus increased in obese women, and the expansion is relatively greater for the extracellular compartment. These results have implications in the study of human body composition and may also account in part for the fluid-overload states that often accompany severe obesity.
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PMID:Relative expansion of extracellular fluid in obese vs. nonobese women. 187 82

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

This report deals with three aspects of risk related to blood pressure and high blood pressure. The first aspect of risk concerns distributions of systolic blood pressure (SBP) and diastolic blood pressure (DBP) in the adult population and their relation to long-term risk of morbidity and mortality. By middle age, only a minority (about 20%) of Americans have optimal SBP and DBP levels, less than 120 mm Hg and less than 80 mm Hg, respectively. For the majority with higher levels, risks of major clinical events, including death from cardiovascular diseases and from all causes, are markedly increased. The relations of SBP and DBP with risk are strong, continuous, and graded. Risk is sizable not only for persons with high blood pressure by usual clinical criteria (SBP greater than or equal to 140 mm Hg or DBP greater than or equal to 90 mm Hg), but also for those with "high-normal" blood pressure (e.g., SBP 130-139 mm Hg or DBP 80-89 mm Hg). Thus, the blood pressure problem is a population-wide one and requires for its control a combined population-wide and high-risk strategy. A major component of this strategy must be nutritional-hygienic measures for the primary prevention of the rise in blood pressure during adulthood and of high blood pressure (i.e., primary prevention not only of the complications of high blood pressure but also of high blood pressure itself) through improved lifestyles having the potential to shift downward the blood pressure distribution of the whole population. The second aspect of risk concerns the known risk factors (i.e., aspects of modern lifestyle) leading to the mass occurrence of blood pressure rise during adulthood and of high blood pressure. These risk factors are high salt intake, high dietary sodium/potassium ratio, calorie imbalance and resultant obesity, and high alcohol intake. The extensive data base establishing the role of these common traits in the etiology of the blood pressure/high blood pressure problem is the scientific foundation for efforts to achieve the primary prevention of high blood pressure. The third aspect of risk relates to the combined impact of other risk factors along with blood pressure-high blood pressure in markedly increasing the probabilities of morbidity and mortality (e.g., "rich" diet, diet-dependent serum cholesterol and uric acid, smoking, diabetes, and target-organ damage). Prevention and control of lifestyle-related traits are essential components of the strategy for dealing with the blood pressure-high blood pressure problem.
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PMID:Blood pressure and high blood pressure. Aspects of risk. 188 62

The effect of long-term (12 weeks) oral treatment with sodium orthovanadate on hepatic glycogen metabolizing and lipogenic enzymes was studied in genetically diabetic db/db mice. These mice were characterized by significant (P less than .001) obesity, hyperglycemia, and hyperinsulinemia. Vanadate administration led to significant decreases in body weight (P less than .001) and plasma insulin levels (P less than .01) and the mice became normoglycemic. The total glycogen synthase (EC 2.4.1.11) activity in the livers of diabetic mice showed a 47% increase, which did not undergo any significant change after treatment with vanadate. Hepatic phosphorylase (EC 2.4.1.1) activities (a and total) showed twofold increases in db/db mice when compared with the nondiabetic ones. Vanadate caused significant decreases in phosphorylase a (P less than .02) and total phosphorylase (P less than .001) activities. Glucose-6-phosphate dehydrogenase (EC 1.1.1.49) and malic enzyme (EC 1.1.1.40) in diabetic liver had differential alterations, as indicated by a 50% decrease in glucose-6-phosphate dehydrogenase and 160% increase in malic enzyme activities. Vanadate administration led to normalization of both enzyme activities. In nondiabetic mice, vanadate treatment did not cause changes in any parameter, except for a 46% decrease in plasma insulin levels. This investigation indicates that vanadate can normalize many of the metabolic abnormalities seen in the liver of genetically diabetic db/db mice, a model for non-insulin-dependent diabetes mellitus (NIDDM). Vanadate also causes a decrease in plasma insulin level, along with normalization of plasma glucose, which suggests a partial reversal of insulin resistance.
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PMID:Long-term effects of vanadate treatment on glycogen metabolizing and lipogenic enzymes of liver in genetically diabetic (db/db) mice. 191 Jan 43

This paper attempts to define the theory and practice of a modern approach to the initial workup of the patient with hypertension. The process includes a complete general medical evaluation along with special measures to enable the fullest characterization and clinical differentiation of the disease. The initial workup aims to (a) establish that the hypertension is sustained and should be treated; (b) identify all definable and curable causes for the hypertension; (c) identify the presence and degree of attendant risk factors such as smoking, alcohol use, obesity, diabetes, and abnormal lipid metabolism; (d) characterize the hypertension in terms of its pathophysiology; and (e) assess the presence and degree of target organ damage to the heart, brain, and kidneys. Because all diastolic hypertension is due to arteriolar vasoconstriction, a fundamental strategy of this process is to distinguish between renin-mediated and sodium-related vasoconstrictive forces and to evaluate which is preponderant. The chief instruments of this strategy are the renin-sodium profile and the response of plasma renin activity and blood pressure to specific antirenin system drugs. The captopril test, an important protocol in making this distinction, is primarily a powerful screening tool for confirming the possible presence or absence of curable renovascular disease or curable primary aldosteronism. That renin profiling cannot accurately discriminate between the contributions of either the renin or sodium-volume factors in that large fraction of medium-renin patients is not a viable reason for not performing the test. The test has its greatest strength for identifying sizable numbers of otherwise unrecognizable patients with very high or very low renin concentrations who might have curable disorders and who likely reflect different pathophysiologic vasoconstrictive mechanisms for which entirely different drug therapies are appropriate. However, the baseline renin test is also useful for assessing prognosis and the likelihood of a heart attack and it is valuable for deciding whether to use an anti-renin system drug (for medium and high renin concentrations) as opposed to natriuretic agents (low-renin patients) such as a diuretic or calcium antagonists as the primary step. In our present state of knowledge, the basic diagnostic biochemical workup includes the renin-sodium profile and the 24-h urinary sodium, potassium, and microalbumin excretion rates. This package is further enriched by baseline electrocardiography and echocardiography and the evaluation of glucose and lipid patterns.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Clinical evaluation and differential diagnosis of the individual hypertensive patient. 191 3

Insulin resistance is a critical component underlying the altered glucose homeostasis in a variety of metabolic and non-metabolic disorders. Aging, body fat distribution, obesity, diabetes mellitus or hypertension are well recognized conditions associated with an impaired tissue sensitivity to insulin action. Apart from such constant factors, insulin sensitivity can be acutely modified by independent variables such as physical exercise, dietary factors, alcohol intake or harmless drugs. To evaluate the day-to-day intra-individual variation in insulin sensitivity, glucose homeostasis and lipid profiles, we investigated the insulin sensitivity index (S1) (determined by the minimal model method of Bergman), basal and post-glucose-load insulin and glucose levels, serum total triglyceride and lipoprotein cholesterol fractions in 15 healthy young men (24 +/- 1 year, mean +/- SEM), on two different occasions at an interval of 3 weeks (days 1 and 21), after 3 days of a standard dietary regimen and after an overnight fast. Blood pressure, heart rate, body weight and 24 h urinary sodium excretion were almost identical in the two phases. S1(day 1) varied from 4.2 to 15.8 x 10(-4).min-1 pro microU/ml (mean: 10.2 +/- 0.9) and correlated with S1(day 21) (11.2 +/- 1.2 x 10(-4).min-1 pro microU/ml, r = 0.78, p less than 0.0007). The slope of the relationship did not differ from 1 (1.01, p greater than 0.90), the intercept was close to the origin (0.8, p greater than 0.73) and the coefficient of variation was 14.4%.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Reproducibility of insulin sensitivity measured by the minimal model method. 191 59

Normal male Wistar rats pretreated with insulin for 12 days were studied to determine if chronic insulin treatment would reproduce the cardiovascular changes occurring in obese rats with hyperinsulinemia. After 12 days, plasma insulin rose while plasma glucose fell, but basal pressures recorded while the rats were awake remained unchanged. Depressor and tachycardic responses to isoproterenol were enhanced, thereby suggesting that beta adrenergic responsiveness had been increased. By contrast, cardiovascular responses to angiotensin were unaltered. The same rats were then anesthetized with urethane-chloralose, and reflex responses, elicited by elevating blood pressure with phenylephrine or lowering it with sodium nitroprusside, were compared with those from control rats that had not been treated with insulin. Reflex inhibition of splanchnic nerve activity during phenylephrine infusion was weaker, whereas reflex tachycardia during nitroprusside infusion was stronger in insulin-treated rats. However, cardiovascular and sympathetic responses elicited by electrical stimulation of the posterior hypothalamus were the same whether the rats had been treated with insulin or not. Although these differences imply that hyperinsulinemia cannot be solely responsible for the cardiovascular dysfunction in obesity, our results nonetheless suggest that by increasing beta adrenergic responsiveness and reducing sympathetic inhibition, excess insulin can cause sympathetic predominance even without elevating blood pressure.
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PMID:Sympathetic activation by chronic insulin treatment in conscious rats. 192 Jan 12

Although obesity and alcohol intake as well as dietary sodium, potassium and magnesium are the major non-genetic determinants of blood pressure levels, interest has recently been stimulated in the function of fatty acids and antioxidants in the aetiology of hypertension. In the Kuopio Ischaemic Heart Disease Risk Factor Study both plasma ascorbic acid and serum selenium concentrations had a moderate, independent inverse association, estimated dietary intake of saturated fatty acids had a positive association and estimated dietary intake of linolenic acid had an inverse association with the mean resting blood pressure in 722 Eastern Finnish men with neither self reported hypertension nor cerebrovascular disease. Even though these cross sectional observations do not prove causality, they warrant clinical trials to verify or disprove that dietary fats and antioxidants are factors in the development of hypertension.
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PMID:Dietary fats, antioxidants and blood pressure. 193 Sep 20

Psittacines are often classified as seed eaters despite studies that have established great diversity in food habits in the wild. While seeds are consumed, so are flowers, buds, leaves, fruits and cambium. Some psittacines consume part of greater than 80 species of grasses, forbs, shrubs and trees. In addition, insects may be important. Although there are few controlled studies of the requirements of psittacines, it is probable that most nutrient needs are comparable to those of domesticated precocial birds that have been thoroughly studied. Commercial seed mixes for psittacines commonly contain corn, sunflower, safflower, pumpkin and squash seeds, wheat, peanuts, millet, oat groats and buckwheat, although other seeds may be present. Because hulls/shells comprise 18-69% of these seeds and they are removed before swallowing, a significant proportion of typical seed mixtures is waste. Some of the seeds also are very high in fat and promote obesity. Common nutrient deficiencies of decorticated seeds include lysine, calcium, available phosphorus, sodium, manganese, zinc, iron, iodine, selenium, vitamins A, D, E and K, riboflavin, pantothenic acid, available niacin, vitamin B-12 and choline. Attempts to correct these deficiencies by incorporating pellets into seed mixes are usually thwarted by rejection of the pellets and disproportionate consumption of items that are more highly favored. An extruded diet formulated to meet the projected nutrient needs of psittacines was fed with fruits and vegetables to eight species of psittacines for 1 y. Fledging percentage was increased to 90% from the 66% observed during the previous 2 y when these psittacines were fed seeds, fruits and vegetables. Although this extruded diet was well accepted in a mixture of fruits and vegetables and met nutrient needs, analyses have shown that not all commercial formulated diets are of equal merit.
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PMID:Formulated diets versus seed mixtures for psittacines. 194 Dec 26

Cardiovascular dysfunction associated with obesity was assessed by comparing rats that had been maintained on a regular or high fat diet since weaning. Rats on the high fat diet not only gained weight faster than age-matched controls but also had higher systolic and mean pressures. Development of mild hypertension in obese rats was first detected by indirect tail-cuff measurement and confirmed later by recording intra-arterial pressures directly from indwelling femoral catheters. To assess baroreceptor reflex sensitivity, reflex heart rate responses were elicited by lowering blood pressure with sodium nitroprusside or elevating it with phenylephrine. Initial tests showed that, although reflex tachycardia during depressor responses to sodium nitroprusside did not differ between groups, reflex bradycardia during pressor responses to phenylephrine was weaker in obese than in control rats. Underlying autonomic mechanisms were then examined by repetition of baroreceptor reflex tests after cholinergic blockade with methylatropine or beta-adrenergic blockade with propranolol. Reflex tachycardia was equally inhibited in both groups by either antagonist. By contrast, reflex bradycardia was reduced more in obese than in control rats by beta-adrenergic blockade but was equally reduced by cholinergic blockade. Because residual responses after beta-adrenergic blockade would represent remaining parasympathetic mediation, these results indicate that reflex bradycardia was selectively impaired because of deficient parasympathetic mediation. Considered collectively, our results suggest that impaired parasympathetic mediation of reflex bradycardia could either result from or contribute to the blood pressure elevation in obese rats.
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PMID:Baroreceptor reflex impairment and mild hypertension in rats with dietary-induced obesity. 196 88


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