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

The activity of lipoprotein lipase (LPL) was studied in interscapilar brown adipose tissue (BAT), epididymal white adipose tissue (WAT) and in the heart of lean and obese adult Zucker rats maintained at 22 degrees C or adapted to cold (10 degrees C). In WAT the specific activity per gram of tissue was lower in obese than in lean rats but the total activity within the tissue was three-fold higher. Cold acclimation did not modify total activity in either lean or obese rats. In BAT, but not in the heart, both specific and total activities were lower in obese than in lean animals. They were enhanced in both tissues following cold acclimation. Six-hour fasting led to a decrease in specific activity in WAT of lean rats but had no effect in obese animals; an increase was observed in BAT and heart of both genotypes. Insulin administration has no effect on activities in WAT in either 22 or 10 degrees C adapted obese rats. Norepinephrine administration stimulates LPL activity in BAT and heart of all groups. It is concluded that the lack of development of obesity previously observed in obese rats following cold acclimation is not due to a decreased capacity of lipid uptake by WAT. It might in part be due to an increased lipid oxidation in BAT.
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PMID:Effects of cold acclimation on the activity of lipoprotein lipase in adipose tissues of genetically obese Zucker rats. 389 31

Norepinephrine (NE) turnover, an index of sympathetic nervous system (SNS) activity, was measured in interscapular brown adipose tissue (IBAT), heart and pancreas of 3-weeks-old pre-obese monosodium-L-glutamate (MSG) mice and at 6-weeks-old mildly obese MSG mice. In IBAT, rates of NE turnover were slower not only in 3-weeks-old MSG mice but also in older obese MSG mice than in their saline controls. In heart, rates of NE turnover were slower in 6-weeks-old mildly obese MSG mice, but not in pre-obese MSG mice. No significant difference in NE turnover in pancreas was observed at either age. The low NE turnover in IBAT of MSG-treated mice prior to the onset of gross obesity suggests that low SNS activity may be an initial contributor to their high energy efficiency and resultant obesity.
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PMID:Reduced norepinephrine turnover in brown adipose tissue of pre-obese mice treated with monosodium-L-glutamate. 397 2

The possibility that low sympathetic nervous system (SNS) activity in brown adipose tissue (BAT) of 8-wk-old obese (ob/ob) mice results from their gross obesity at that age was investigated. Norepinephrine (NE) turnover, an estimator of SNS activity, was measured in BAT and other organs of 2-wk-old preobese ob/ob mice, and at 4 and 8 wk of age. Rates of NE turnover were 36% slower in BAT of preobese ob/ob mice than in lean littermates and remained slow in their BAT at 4 (-66%) and 8 (-56%) wk of age. In heart, rates of NE turnover were 48% slower in preobese ob/ob mice than in lean littermates, but the difference diminished at 4 (-21%) and 8 (-16%) wk of age. Rates of NE turnover in white adipose tissue, liver, and pancreas of obese mice were generally comparable with rates in these organs of lean mice. Effects of fasting (24 h) and acute cold exposure (14 degrees C for 8 h) were also examined. In general, fasting lowered and cold exposure elevated NE turnover equally in obese and lean mice. Ob/ob mice housed at 23-25 degrees C exhibit low SNS activity in their BAT prior to the onset of gross obesity, even though SNS activity in their BAT responds normally to an acute cold stress. This low SNS activity probably contributes to their subsequent high efficiency of energy retention.
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PMID:Norepinephrine turnover in obese (ob/ob) mice: effects of age, fasting, and acute cold. 613 73

Several studies have suggested that obese subjects have a reduced thermic effect of feeding when compared to normal weight controls. The present study was undertaken to further define this apparent abnormality, and evaluate the role of norepinephrine in the thermic response to food. A test formula meal of 800 calories (85% carbohydrate, 15% protein) was taken by 7 control and 6 moderately obese subjects whose obesity was adult in onset. The rise in resting oxygen consumption following the test meal was greater in the control than in the obese group (p less than 0.01), and there was a significant inverse correlation between the relative degree of obesity and this response to feeding (r = -0.59, p less than 0.05). Norepinephrine concentrations were greater in the obese than in the control group both before (p less than 0.05) and after (p less than 0.05) feeding. No correlations were found between the plasma norepinephrine concentrations and the rise in oxygen consumption after feeding. Four of the 6 obese subjects were restudied after weight reduction. The reduced-obese group showed a trend toward normalization of basal measurements and responses to feeding. It is concluded that the reduced thermic response to feeding seen in the obese subjects studied cannot be directly accounted for by diminished sympathetic nervous system activity as reflected by plasma levels of norepinephrine.
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PMID:Reduced thermic effect of feeding in obesity: role of norepinephrine. 682 82

Norepinephrine (NE) content and turnover rate, and the activity of dopamine-beta-hydroxylase (DBH) were measured in the brown adipose tissue (BAT) of developing Zucker rats of the three genotypes: Fa/Fa and Fa/fa (with a lean phenotype) and fa/fa (phenotypically obese). As early as 15 days of age, namely at a pre-obese stage, BAT NE content and turnover rate are already reduced in fa/fa rats, just like they are at 50 days. The development of DBH activity is completely impaired in fa/fa rats. These results demonstrate that the reduction in sympathetic tone in BAT of fa/fa rats is already present before the onset of phenotypic obesity.
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PMID:Decreased norepinephrine turnover rate in the brown adipose tissue of pre-obese fa/fa Zucker rats. 796

Catecholamines are known to stimulate lipolysis of triglyceride stores in adipose tissue. However, the relationship of sympathoadrenal activity to serum lipid and lipoprotein concentrations remains uncertain. Since obesity, particularly the centripetal form, has recently been shown to be associated with increased urinary excretion of norepinephrine and decreased excretion of epinephrine, the possibility that the sympathoadrenal system is involved in the lipid abnormalities associated with the centripetal form of obesity was investigated. The relationship between 24-hour urinary catecholamine excretion and serum lipid and lipoprotein levels was examined among 615 male participants of the Normative Aging Study. Epinephrine excretion was positively correlated with the high-density lipoprotein cholesterol (HDL-C) level and the ratio of HDL-C to low-density lipoprotein cholesterol ([LDL-C] r = .15, P = .0002, and r = .11, P = .007, respectively) and inversely correlated with the triglyceride level (r = -.14, P = .0005). These relationships remained significant after adjusting for the effects of age, smoking, alcohol intake, adiposity, and insulin level. Epinephrine excretion was not significantly related to levels of total cholesterol or LDL-C. Norepinephrine and dopamine excretion were not significantly related to any lipid variable. These data suggest that (1) epinephrine plays an important role in regulating lipid and lipoprotein metabolism in humans, and (2) decreased adrenal medullary activity may contribute to the dyslipidemia (increased triglycerides and decreased HDL-C) commonly observed among the obese. The sympathoadrenal system therefore, along with hyperinsulinemia, may contribute to the increased cardiovascular risk associated with the insulin resistance syndrome.
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PMID:The relationship of epinephrine excretion to serum lipid levels: the Normative Aging Study. 815 12

The effects of norepinephrine and insulin on glucose transport were investigated in brown adipocytes isolated from obese nondiabetic Lister and Albany (LA/N-cp strain) rats (O-LA), obese diabetic spontaneously hypertensive (SHR/N-cp strain) rats (O-SHR), and from their lean (L) controls to test whether the decreased calorigenic response to norepinephrine of O-SHR adipocytes was specifically associated with alterations in glucose metabolism. Norepinephrine and insulin independently stimulated glucose transport in L-LA, O-LA, and L-SHR brown adipocytes, but their stimulatory effects were markedly reduced in O-SHR cells. Both insulin responsiveness and the total number of insulin receptors were significantly decreased in O-SHR adipocytes but not in O-LA cells. The number of high-affinity beta 1/beta 2-adrenoceptors was significantly increased (+70%) in O-LA adipocytes but was similar in L-SHR and O-SHR cells. These results indicate that 1) major metabolic defects are present in brown adipose tissue (BAT) of O-SHR but not of O-LA, although these two strains are homozygous for the cp allele, 2) postreceptor defects are predominantly involved in O-SHR adipocyte refractoriness to norepinephrine, and 3) a reduced mitochondrial content may represent the principal metabolic alteration explaining the decreased effects of norepinephrine on both thermogenesis and glucose transport. It is postulated that the marked insulin resistance of O-SHR leads to a decreased mitochondriogenesis in BAT, resulting in a diminished tissue thermogenic capacity and reduced glucose metabolism, thereby contributing to obesity and diabetes.
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PMID:Norepinephrine- and insulin-resistant glucose transport in brown adipocytes from diabetic SHR/N-cp rats. 821 49

A 61-year-old woman with hyper-catecholaminemia and hyper-glucocorticoidemia due to a mixed tumor of the right adrenal gland is described. The patient, who had been medicated for hypertension since 1977, complained of thirst and general malaise in 1986. Body weight loss was remarkable. There was neither absolute truncal obesity nor moon face. In September 1986, her blood pressure was 180/110 mmHg and blood glucose level was 400mg/dl. Noradrenaline levels in plasma and in urine were remarkably elevated (1659 pg/ml and 120 micrograms/day, respectively), and adrenaline levels were also high (397 pg/ml in plasma, 34 micrograms/day in urine). Plasma cortisol and urinary 17-OHCS were elevated (39.2 micrograms/dl and 11.9 mg/day, respectively). Plasma ACTH was in the normal range (42.6 pg/ml). Oral administration of neither 1mg nor 8 mg of dexamethasone suppressed plasma cortisol or ACTH levels. Both 131I-metaiodobenzylguanidine and 131I-adosterol accumulated in the right adrenal gland. In 1987 the adrenal tumor (3.0 x 3.5 cm, 30 g) was resected. After the operation, her blood pressure and blood glucose level returned to normal, so that the medication became unnecessary. Histologically it was revealed that the tumor was a mixed adenoma consisting of adreno-medullary and cortical cells (corticomedullary adenoma). The literature on 21 cases of pheochromocytoma associated with Cushing's syndrome was briefly reviewed. Mathison (1969) reported the first case of a mixed tumor of adreno-medullary and cortical cells. So far as we know the present case is the second.
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PMID:[A case of adrenal mixed tumor of pheochromocytoma and adrenocortical adenoma presenting diabetes mellitus and hypertension]. 837 53

The role of brown adipose tissue in total energy balance and cold-induced thermogenesis was studied. Mice expressing mitochondrial uncoupling protein 1 (UCP-1) from the fat-specific aP2 gene promoter (heterozygous and homozygous aP2-Ucp transgenic mice) and their nontransgenic C57BL6/J littermates were used. The transgenic animals are resistant to obesity induced by a high-fat diet, presumably due to ectopic synthesis of UCP-1 in white fat. These animals exhibited atrophy of brown adipose tissue, as indicated by smaller size of brown fat and reduction of its total UCP-1 and DNA contents. Norepinephrine-induced respiration (measured in pentobarbital sodium-anesthetized animals) was decreased proportionally to the dosage of the transgene, and the homozygous (but not heterozygous) transgenic mice exhibited a reduction in their capacity to maintain body temperature in the cold. Our results indicate that the role of brown fat in cold-induced thermogenesis cannot be substituted by increased energy expenditure in other tissues.
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PMID:Brown fat is essential for cold-induced thermogenesis but not for obesity resistance in aP2-Ucp mice. 953 Jan 37

The uncoupling protein (UCP) or thermogenin is a 33 kDa inner-membrane mitochondrial protein exclusive to brown adipocytes in mammals that functions as a proton transporter, allowing the dissipation as heat of the proton gradient generated by the respiratory chain and thereby uncoupling oxidative phosphorylation. Thermogenesis (heat production) in brown adipose tissue, which is activated in response to cold exposure or chronic overeating, depends largely on UCP activity. Norepinephrine, released from sympathetic terminals and acting via beta-adrenoceptors and cAMP, is the main positive regulator of both UCP synthesis and activity. Brown fat thermogenesis plays a critical role in thermoregulation and in overall energy balance, at least in rodents. Manipulation of thermogenesis, whether through UCP or through analogous uncoupling proteins, could be an effective strategy against obesity.
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PMID:The uncoupling protein, thermogenin. 959 49


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