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

Severly obese subjects and sex- and age-matched controls underwnet physical training during a 6-wk period. Evidence of training was shown in all subjects by increased aerobic power. Before training the obese subjects were characterized by the following abberations: decreased glucose tolerance, hyperinsulinemia, elevated blood glycerol and plasma free fatty acids, and a blunted plasma growth hormone response during glucose tolerance. Noradrenaline output was elevated, a finding of potential interest for the explanation of increased lipolysis, blood pressure, and heart size in obesity. With training the following changes were found:In the controls there was evidence for the beginning of a decrease of adipose tissue mass. In the obese, however, body weight, body fat, or fat cell size did not decrease during training. Plasma insulin decreased, and a corresponding increase of plasma glycerol was seen. Glucose tolerance was not changed, and this, together with decreased plasma insulin, indicated an increase insulin sensitivity of the periphery. Changes in noradrenaline or growth hormone during training could not explain this increased sensitivity. Urinary cortisol output was found to decrease after training in the obese; this might be interpreted as a decrease in cortisol secretion allowing a more effective insulin action on the periphery.
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PMID:Physical training in human hyperplastic obesity. IV. Effects on the hormonal status. 31 26

1. Intra-arterial pressure was recorded continuously in 26 patients with uncomplicated essential hypertension under standardized conditions. Pressure was analysed beat by beat by computer and variability measured as the standard deviation of the normally distributed frequency histogram. 2. Variability was strongly influenced by physical activity, being least during sleep and increasing progressively with bed rest and ambulation. Variability during daytime was not related to time. 3. Systolic variability correlated directly with systolic pressure. An independent inverse relationship with baroreflex sensitivity was observed. Systolic variability tended to increase with obesity. 4. None of the following were related independently with variability: age; race; sex; plasma renin activity; plasma angiotensin II; plasma noradrenaline; plasma adrenaline.
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PMID:Factors determining the variability of arterial pressure in hypertension. 39 78

Excretion of catecholamines and DOPA was impaired in patients with metabolic-alimentary obesity, with ischemic disease of heart, with atherosclerosis and excessive weight. Distinct decrease in content of adrenaline, noradrenaline and DOPA was observed in patients with obesity; the phenomenon was less pronounced in ischemic disease of heart, mainly in aged patients. Correlation was found between the rate of excretion of catecholamines and DOPA and the extent of hyperlipidemia. Dietetics did not normalize completely the impairments studied. Additional administration of pyridoxine caused a favorable effect.
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PMID:[Excretion of catecholamines and DOPA in lipid metabolism disorders]. 59 86

Norepinephrine (NE) levels in the hypothalamus and telencephalon of genetically obese mice with the OBOB and DBDB mutations are significantly higher than those of their lean littermates. Obese mice with the viable yellow mutation failed to show this increase. Restricting the diets of OBOB animals to prevent excessive weight gain does not affect NE levels in the hypothalamus, telencephalon or brainstem.
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PMID:Effects of food restriction and mutation on central catecholamine levels in genetically obese mice. 102 29

The ventral noradrenergic bundle (VB) of the rate brain has been proposed as the substrate for the hyperphagia and obesity produced by ventromedial hypothalamic lesions. To determine the relationship between body weight and damage to the VB, the effects of bilateral electrolytic and 6-hydroxy-dopamine (6-OHDA) lesions of the VB were compared. When rats were fed only a standard laboratory diet, no significant differences were found between groups. When a high-fat diet supplement was introduced, the group with electrolytic lesions became significantly heavier than the control group; however, the 6-OHDA group did not differ from the controls. Norepinephrine depletion was significantly greater following the 6-OHDA than the electrolytic lesions. Both lesions reduced telencephalic dopamine and serotonin only slightly. A second study in which both types of lesions were placed at a rostral ventromedial hypothalamic site yielded the same pattern of results. Diet-dependent increases in body weight were attributed to the destruction of a non-noradrenergic system, which was spared by the relatively selective 6-OHDA lesion but damaged by the nonselective electrolytic lesion.
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PMID:Central noradrenergic neurons: differential effects on body weight of electrolytic and 6-hydroxydopamine lesions in rats. 124 69

Differential temperature measurement between interscapular brown adipose tissue (BAT, Tbat), rectum (Trect) and a subcutaneous point in the back left of the vertebral column (Tsc) was useful for examination of BAT-thermogenesis in glutamate-induced obese Wistar-rats. Positive temperature gradients Tbat-Tsc pointed to a basal BAT-thermogenesis, whereas negative temperature gradients Tbat-Trect did not indicate that heat production in lean and obese rats. One may conclude from this, that inclusion of subcutaneous points outside the BAT improves sensitivity of differential temperature measurements for BAT-thermogenesis. Basal temperatures Tbat, Trect and Tsc were reduced in obese rats compared to lean rats, although thermoinsulation of obese rats is improved on account of their high fat content. This points to a diminished heat production in obese rats. Cold exposure at 4 degrees C elicited an increase of temperature gradients Tbat-Trect in lean as well as in obese rats, with positive values found only in lean rats. However, positive values Tbat-Tsc were calculated for both groups. Increases were noted only in lean rats. Injection of noradrenaline (0.5 mg/kg i.m.) was followed by positive temperature gradients Tbat-Trect and increased positive values for Tbat-Tsc, pointing to a remarkable activation of BAT-thermogenesis in lean and obese rats. These findings confirm, that glutamate-induced obese rats preserved the ability to activate BAT-thermogenesis. There were, however, hints of reduced heat production in BAT of obese rats, thus contributing to obesity despite normophagia.
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PMID:Examination of brown adipose tissue thermogenesis of glutamate-induced obese rats by differential temperature measurements. 129 79

Corticotropin-releasing factor (CRF) has been implicated in the development of obesity in genetically obese rodents. We have investigated the effect of 100 micrograms of intravenous CRF on energy expenditure in women, comparing the response in obese and lean volunteers. In response to CRF, energy expenditure as measured by indirect calorimetry increased rapidly with a peak response in both groups reached by two minutes with a ten minute post-CRF response averaging 9.0% in the lean and 11.0% in the obese. Subsequently, energy expenditure remained elevated for a longer duration in the lean compared to the obese. Overall, the total 30 min cumulative metabolic rise was similar in the lean and obese. The increments in energy expenditure were associated with elevation of plasma noradrenaline levels, suggesting the possible involvement of the sympathetic nervous system. The adrenocorticotrophic (ACTH) and cortisol responses to CRF were similar in obese and lean. Intravenous administration of CRF therefore acutely increases energy expenditure in both lean and obese healthy subjects.
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PMID:The acute effects of corticotropin-releasing factor on energy expenditure in lean and obese women. 132 49

To evaluate the effects of obesity and impaired glucose tolerance on insulin sensitivity, we performed a euglycaemic-hyperinsulinemic clamp at about 350 pmol l-1, combined with 3H-glucose infusion, in 14 obese patients, BMI 36.5 +/- 1.2 and in 12 matched controls, BMI 23.9 +/- 0.4. Six obese patients had normal glucose tolerance (oNGT), and eight had impaired glucose tolerance (oIGT). The ability of insulin to inhibit lipolysis in isolated adipocytes was also studied. Insulin-mediated glucose utilization was more severely impaired in oIGT than in oNGT with respect to the controls (621 +/- 51 vs. 897 +/- 83 vs. 1298 +/- 55 mumol m-2 min-1, P < 0.001). Plasma glycerol was higher in oIGT than in oNGT and in the controls, both fasting (238 +/- 12 vs. 179 +/- 14 vs. 112 +/- 8 mumol l-1, P < 0.001) and during the clamp (175 +/- 21 vs. 120 +/- 12 vs. 36 +/- 6 mumol l-1, P < 0.001). The correlation between glucose utilization and the percent reduction of plasma glycerol during the clamp was significant in the study group as a whole (r = 0.809, P = 0.0001), and in each of the groups separately (oIGT: r = 0.929, P = 0.002; oNGT: r = 0.943, P = 0.036; controls: r = 0.902, P = 0.0001). Inhibition by insulin of noradrenaline-stimulated lipolysis in isolated adipocytes was more severely impaired in oIGT than in oNGT compared with the controls (P < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The glucoregulatory and antilipolytic actions of insulin in abdominal obesity with normal or impaired glucose tolerance: an in vivo and in vitro study. 147 41

Norepinephrine (NE), acting through alpha 2-noradrenergic receptors in the hypothalamic paraventricular nucleus (PVN), has been implicated in the control of feeding behavior and body weight gain. To determine whether this hypothalamic receptor system is disturbed in genetically obese rats, the binding of radioligands to alpha 2-noradrenergic, as well as to alpha 1-noradrenergic, receptors was examined in seven hypothalamic nuclei of obese Zucker rats relative to their lean littermates. Receptor binding procedures, using the alpha 2-noradrenergic agonist [3H]p-aminoclonidine ([3H]PAC) and the alpha 1-noradrenergic antagonist [3H]prazosin, demonstrated that the obese rats, compared to the lean rats, had significantly greater alpha 2-noradrenergic and alpha 1-noradrenergic receptor binding, specifically in the PVN as opposed to other hypothalamic areas examined. Moreover, the obese rats, compared to the lean rats, exhibited greater responsiveness to the effects of food deprivation (48 h), which caused a significant decline in radioligand binding to both alpha 2 and alpha 1 receptors, specifically in the PVN. A decrease in alpha 2-receptor binding after deprivation in the obese rats was also seen in two basal hypothalamic areas, namely, the supraoptic nucleus and arcuate nucleus-median eminence. The possibility exists that these disturbances in hypothalamic alpha-receptors may be involved in the development and/or maintenance of the genetic obesity.
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PMID:Higher alpha-noradrenergic receptors in paraventricular nucleus of obese Zucker rats: decline after food deprivation. 168 67

1. Lipid mobilization during a hypocaloric diet may be enhanced by a pharmacological approach using alpha 2-adrenoceptor antagonists since these drugs are known to increase sympathetic tone and stimulate lipolysis. Studies were undertaken in the dog in order to evaluate the effects of oral yohimbine administration (alpha 2-adrenoceptor antagonist) on heat production, metabolic, endocrinological and cardiovascular parameters. 2. Acute oral yohimbine (0.25 or 0.40 mg kg-1) provoked an increase in plasma non-esterified fatty acids. The drug increased sympathetic nervous system activity as indicated by the increased level of plasma noradrenaline. These effects persisted during the entire experimental period (4 h). The increase in plasma noradrenaline level was two fold higher with the higher dose of yohimbine (0.4 mg kg-1). The plasma adrenaline level was increased only with the higher dose. 3. Yohimbine transiently increased plasma insulin and the effect was dose-dependent. 4. Yohimbine (0.25 mg kg-1) enhanced heart rate and arterial blood pressure. 5. The effect of yohimbine on oxygen consumption, carbon dioxide and heat production was determined by indirect calorimetry. The drug (0.25 mg kg-1) increased O2 consumption and CO2 and heat production 30 min after its administration and the effect persisted over the experimental period. The respiratory quotient, rather low in the fasting animals, remained unchanged. 6. The present work indicates that thermogenesis and lipid mobilization are enhanced during fasting in the dog by alpha 2-adrenoceptor blockade. Yohimbine also induced a transient increase in plasma insulin level and increased heart rate and blood pressure. The lipid mobilization plus the action on thermogenesis observed after yohimbine draw attention to the putative interest of a2-antagonists in the pharmacological treatment of obesity during restricted calorie intake.
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PMID:Thermogenic and lipolytic effect of yohimbine in the dog. 179 15


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