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Query: UMLS:C0155339 (Brown)
 12,436 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Our objective was to find out if central injection of neuropeptide Y (NPY) would alter brown fat thermogenesis and white fat lipoprotein lipase activity. The following three groups of Sprague-Dawley rats received five injections over 24 h into the right lateral ventricle: 1) NPY (5 micrograms/injection) and ad libitum food; 2) NPY (5 micrograms/injection) and food restricted to control intake; 3) saline injection and ad libitum food. The NPY ad libitum-fed group consumed more food than the saline controls or NPY food-restricted animals. Brown fat thermogenic activity, assessed by GDP binding, was decreased relative to saline controls in both NPY-treated groups. White fat lipoprotein lipase activity was greatly increased in both NPY treatment groups compared with saline controls. The NPY effects on brown and white fat were not explained by measures of serum insulin, glucagon, glucose, or other metabolites. In a follow-up experiment, we asked whether food was necessary for expression of the NPY effects. Brown fat mitochondrial GDP binding indicated NPY effect even when no food was ingested. We conclude that intracerebroventricular administration of NPY promotes white fat lipid storage and decreases brown fat thermogenesis in addition to its known effect of stimulating food intake.
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PMID:Effects of intracerebroventricular injection of neuropeptide Y on energy metabolism. 199 19

Young adult male and female Djungarian hamsters were exposed to ambient temperatures of 23 or 0 C for 12 h; half of the animals in each group were treated with iopanoic acid to suppress the peripheral conversion of T4 to the thermotropically active thyroid hormone T3 by the enzyme 5'-deiodinase (5'D). Brown adipose tissue (BAT) mRNA for uncoupling protein (UCP), BAT lipoprotein lipase (LPL) activity, and 5'D activity were measured at the conclusion of the study. A temperature of 0 C produced large rises in 5'D and LPL activities and a similar large increase in UCP mRNA within the 12-h exposure period. When 5'D activity was inhibited with iopanoic acid, mRNA for UCP was reduced, while LPL activity was unaffected. The results show that the optimal production of mRNA for BAT UCP depends on the availability of T3; however, T3 is not required for the cold-induced activation of LPL activity in BAT.
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PMID:Inhibition of 5'-deiodination of thyroxine suppresses the cold-induced increase in brown adipose tissue messenger ribonucleic acid for mitochondrial uncoupling protein without influencing lipoprotein lipase activity. 232 97

Female obese and lean Zucker rats were adrenalectomized (ADX) or sham-operated at 4 wk of age. ADX animals were given daily injections of 0.01, 0.05, 0.50, 1.0, or 2.0 mg hydrocortisone/100 g body wt for 30 days. ADX rats gained less weight than sham-operated controls. Obese ADX rats at the lowest dose (0.01) had a net positive energy gain but lost body fat. As steroid dose increased, obese rats deposited more fat and less protein. Doses of 0.01 and 0.05 mg produced rats that were less fat than sham-operated controls, whereas doses of 0.50, 1.0, and 2.0 mg produced rats of comparable body fat composition. Obese rats were consistently fatter and had a significantly smaller percentage body protein than lean rats at each dose. Body fat elevation was reflected by heavier parametrial and retroperitoneal fat depots and larger fat cells at all doses except the lowest. Compared with sham-operated controls, lean and obese rats at the two lowest replacement doses (0.01, 0.05) exhibited significantly decreased plasma insulin and triglyceride levels and significantly elevated brown adipose tissue protein content and citrate synthase (CS) activity. Obese rats at these doses had significantly reduced adipose tissue lipoprotein lipase (LPL) activity in the retroperitoneal depot and lower food intake. Furthermore, these obese rats had adipose depot weights, cell sizes, LPL activity, and plasma insulin, glucose, and triglyceride comparable to that of lean sham-operated controls. As steroid dose increased (0.5, 1.0, 2.0), plasma insulin and triglyceride and food intake markedly increased only in obese rats. Adipose tissue LPL activity appeared unaffected by dose. Brown adipose tissue protein content and CS activity significantly decreased as dose increased in both lean and obese rats. At all doses of replacement obese rats were more responsive to steroid than were lean rats. Obese rats receiving 0.01 mg had comparable fat depot weights, cell sizes, and plasma insulin and triglyceride as lean rats receiving 50 times as much steroid per day (0.50 mg). These results suggest glucocorticoids play an important role in the early development of obesity in the Zucker rat and support the hypothesis that obese rats are more responsive to glucocorticoids than are lean rats.
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PMID:Effect of adrenalectomy and glucocorticoid replacement on development of obesity. 351 71

Brown fat lipoprotein lipase activity did not change in the first two weeks of pregnancy whereas it decreased on day 18 of gestation and was lower during late pregnancy and lactation. Fatty acid synthesis rate, measured in vivo with (3H)H2O, showed a progressive increase until day 18 of gestation followed by a decrease on day 20 of pregnancy and a reduced lipogenesis rate throughout lactation. The early reduction in the pathways of fatty acid uptake and synthesis in brown fat during the breeding cycle of the rat suggests the possibility that a decline in the substrate supply was a factor contributing to the reduced thermogenic activity of brown adipose tissue after parturition.
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PMID:Changes in brown adipose tissue lipoprotein lipase activity and lipogenesis rate during pregnancy and lactation in the rat. 379 Jan 43

Brown fat thermogenesis is increased after a single test meal. This study was conducted to determine whether lipoprotein lipase activity is higher in brown adipose and other tissues after a single large meal. Rats were trained to eat two large meals per day. Two hours after consuming a test meal, lipoprotein lipase activity was measured in interscapular brown adipose tissue, retroperitoneal and epididymal white adipose tissue, gastrocnemius and soleus skeletal muscles and heart. After a high carbohydrate test meal, lipoprotein lipase activity in white adipose tissue pads was higher (P less than 0.05) and that in brown adipose tissue was lower (P less than 0.05) than in these tissues from the meal-deprived group. Muscle lipoprotein lipase did not change significantly. A high fat test meal did not significantly alter lipoprotein lipase activity in brown adipose tissue, white adipose tissue, gastrocnemius or soleus when compared to the meal-deprived control, but heart lipoprotein lipase activity was significantly elevated. These findings indicate that after a single test meal lipoprotein lipase activity in brown adipose tissue is not higher than that from the meal-deprived group and therefore, lipoprotein lipase may not play a rate-limiting role in moving free fatty acids into this tissue in the postprandial state.
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PMID:Meal-induced changes in lipoprotein lipase activity in brown fat and other tissues of rats. 395 Jul 70

Gonadal steroids affect energy balance and adiposity in a variety of mammalian species. For example, estradiol acts via multiple, redundant mechanisms to reduce body weight and adiposity. The steroid can act directly in the brain to decrease food intake and stimulate voluntary exercise. Sex hormones may act concurrently in non-neural peripheral tissues to alter metabolic processes and energy balance. White adipose tissue estrogen receptors may mediate estradiol-induced decreases in lipoprotein lipase activity and lipid storage. Finally, estradiol increases energy expenditure independent of any effects on voluntary exercise. Brown adipose tissue is a potential site for estradiol-induced thermogenesis.
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PMID:Gonadal influences on adiposity. 406 26

Brown adipose tissue (BAT) is known to be responsible for heat production in newborn and adult hibernating mammals. In rats and mice, BAT has been demonstrated to possess a much higher glycerokinase activity than white adipose tissue (WAT). It has been speculated that this high activity may cause the futile cycle of triglyceride breakdown and resynthesis to be activated, thus contributing to heat production. However, at present very little information is available regarding the location, function, and quantitative importance of BAT in adult human subjects. Our objective in this study was to locate BAT in human subjects and to characterize it biochemically, especially with respect to the enzyme glycerokinase. We have looked for histologically identifiable BAT in 32 human subjects and found it in 12 subjects. Most of the BAT samples were obtained from perirenal adipose depots in children undergoing surgery. Some of the samples were almost totally comprised of BAT cells, whereas others were a mixture of BAT cells and WAT cells. The glycerokinase activity per gram of tissue was higher in BAT than in WAT in all the subjects where the above comparison was made. The activity per mg protein or per microgram DNA was higher in most BAT samples. In one pure BAT specimen, the basal lipolytic rate and the lipoprotein lipase activity were measured and they were both higher in BAT than in the WAT obtained from the same patient. These results show that human brown adipose tissue possesses an enzymatic profile very similar to that of rodent brown adipose tissue.
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PMID:Glycerokinase activity in human brown adipose tissue. 630 16

To delineate the factors that may affect triglyceride capture in brown adipose tissue, we have determined the lipoprotein lipase activity (LPS) under conditions known to modulate this activity in other tissues. Acclimation temperature (28 degree C or 5 degree C) had no effect on circadian variations of white adipose tissue and heart LPL activity, LPL activity in brown adipose tissue of 28 degree C rats was similar to that in white adipose tissue (peak activity between 21:00 and 07:00 h), whereas LPL activity of the former was four times higher in 5 degree C rats and rhythmicity was altered (peak activity at 17:00 h as for heart). Brown adipose tissue LPL activity was increased in 28 degree C rats but not in 5 degree C rats after a single injection of insulin to fasting animals. A single injection of dexamethasone increased brown adipose tissue LPL activity only in 5 degree C rats, whereas enzyme activity was increased in both 28 degree C and 5 degree C rats by a single injection of norepinephrine to fed animals. These variations were discussed with relation to the role of brown adipose tissue at 5 degrees C and 28 degrees C.
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PMID:Circadian rhythm and hormonal sensitivity of lipoprotein lipase activity in cold acclimated rats. 701 9

Brown adipocytes cultured from newborn combined-lipase-deficient (cld/cld) mice and castanospermine (CST)-treated 3T3-L1 adipocytes synthesize lipoprotein lipase (LPL) which is inactive and retained in the endoplasmic reticulum (ER) [Masuno, Blanchette-Mackie, Chernick and Scow (1990) J.Biol. Chem. 265, 1628-1638; Masuno, Blanchette-Mackie, Schultz, Spaeth, Scow and Okuda (1992) J. Lipid Res.33, 1343-1349]. Brefeldin A (BFA), which is known to block protein transport from ER and translocate Golgi components to ER, was used here to study the effect of translocated Golgi enzymes on LPL retained in ER of cld/cld and CST-treated mouse brown adipocytes. Brown adipocytes cultured from newborn normal mice contained 3000-5000 m-units of LPL activity/mg of DNA and secreted 35 m-units of LPL activity/mg of DNA per h. BFA at 10 micrograms/ml doubled LPL activity in normal cells within 2 h as it stopped completely secretion of active LPL. LPL in mouse cells has two N-oligosaccharide chains per subunit. Analyses with SDS/PAGE and immunoblotting showed that about one-third of LPL subunits in untreated normal cells were totally endo-beta-N-acetylglucosaminidase (endo H)-resistant, one-third were partially endo H-resistant, and one-third were totally endo H-sensitive. BFA decreased to zero the proportion of subunits which were totally endo H-resistant, while it increased the proportion which were partially endo H-resistant. Thus, BFA blocked processing of one oligosaccharide chain per subunit to endo H-resistance. Sucrose-gradient centrifugation studies showed that BFA increased the proportion of LPL subunits in normal cells which were present as active dimers. LPL activity in cld/cld adipocytes was 120 m-units/mg of DNA and that in normal adipocytes treated with CST was 430 m-units/mg of DNA. Most LPL subunits in such cells were totally endo H-sensitive and some were partially endo H-resistant, but none were totally endo H-resistant. Some of the subunits, in both cld/cld and CST-treated cells, were present as inactive LPL dimers. BFA increased LPL activity in cld/cld cells to 2100 m-units/mg of DNA and that in CST-treated cells to 2600 m-units/mg of DNA within 2 h. BFA increased in both groups the proportion of LPL subunits which were partially endo H-resistant. BFA also increased the proportion which were present as active dimers. Immunofluorescence studies in normal and cld/cld adipocytes showed that BFA caused retention of LPL in large tubular and spherical structures and in ER, but not in Golgi. When BFA was withdrawn and protein synthesis was blocked with cycloheximide, LPL in normal cells was transferred to Golgi within 30 min and disappeared within 60 min, whereas LPL in cld/cld cells was retained in large vesicles and ER. The findings indicate that BFA enabled synthesis of active LPL in cld/cld and CST-treated cells via translocation of Golgi components to ER. Also, cld/cld cells synthesized LPL which could be processed to active lipase and the enzymes needed for activation of the lipase were present in Golgi of such cells. Production of inactive LPL in cld/cld adipocytes probably results from their inability to transport LPL from ER to Golgi.
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PMID:Brefeldin A enables synthesis of active lipoprotein lipase in cld/cld and castanospermine-treated mouse brown adipocytes via translocation of Golgi components to endoplasmic reticulum. 869 53

To investigate the effects of prolonged dietary sodium restriction on lipid metabolism, male rats weighing 35 to 40 g (just weaned) were fed either a low-salt (LSD) or a normal salt diet (NSD) and used in metabolic experiments after 1, 2, or 3 months of diet consumption. After 2 and 3 months on the diet, LSD rats showed increased amounts of lipid in carcass and retroperitoneal tissue. In both LSD and NSD, extending the feeding period from 2 to 3 months resulted in a marked reduction in the in vivo rates of adipose tissue fatty acid synthesis that was accompanied by increases in liver lipogenesis and in the activity of adipose tissue lipoprotein lipase (LPL). However, these increases were more marked in LSD rats. Thus, in vivo rates of liver fatty synthesis and LPL activity in LSD rats, which were already higher (by about 35% and 20%, respectively) than in controls after 2 months, attained levels 50% higher than those in NSD animals after another month on the diet. Brown adipose tissue (BAT) thermogenic capacity, estimated after 2 and 3 months by the tissue temperature response to norepinephrine (NE) injection and by guanosine diphosphate (GDP) binding to BAT mitochondria, did not change in controls, but was significantly reduced in LSD rats. This raises the possibility that a decrease in overall energy expenditure, together with an LPL-induced increased uptake of preformed fatty acids from the circulation, may account for the excessive lipid accumulation in LSD rats. Taken together, the data indicate that prolonged dietary sodium restriction exacerbates normal, age-related changes in white and BAT metabolism.
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PMID:Dietary sodium restriction exacerbates age-related changes in rat adipose tissue and liver lipogenesis. 1289 76


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