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 12,436 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Several techniques for the identification of the young obese Zucker rat were developed and tested. A procedure utilizing biopsies of hypodermal adipocytes was successful in identifying the obese phenotype in large litters of 7-d and older rats. This technique involves sizing and counting fat cells in esterase stained cryostat sections of skin biopsies. Another procedure involved measuring times to cessation of spontaneous activity upon acute exposure to a cold environment. As early as 3 d, obese rats become inactive (in the cold) in a significantly shorter time when compared to the lean rat. This technique was not a discriminating test for the identification of the obese genotype at 3 d of age. A preliminary analysis of brown fat histology and histochemistry indicated larger and more lipid filled brown adipocytes in the obese animal when compared to lean animals at 10 and 14 d of age. Brown fat from young obese animals was histochemically similar to brown fat in lean rats.
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PMID:Techniques for identification of the young obese Zucker rat and some observations on brown adipose tissue morphology and histochemistry in the young obese Zucker rat. 664 57

Nonshivering thermogenesis was originally defined as a cold-induced increase in heat production not associated with the muscle activity of shivering. Recent research shows it to be a metabolic process located primarily in brown adipose tissue and controlled by the activity of the sympathetic nervous supply of this tissue. Another stimulus to sympathetic nervous activity, the ingestion of food, promotes diet-induced thermogenesis in brown adipose tissue. Brown adipose tissue grows and regresses in accordance with the extent to which it is stimulated, either by cold or by diet, and the capacity of the animal for cold-induced nonshivering thermogenesis and diet-induced thermogenesis increases or decreases accordingly. In certain hibernators another stimulus, photoperiod, promotes growth or regression of brown adipose tissue. The neural regulation of thermogenesis in brown adipose tissue is thus not only part of the central control mechanisms involved in thermoregulation but also part of those involved in the regulation of energy balance. In hibernators , such as the hamster, the neural regulation of thermogenesis in brown adipose tissue includes, in addition, central components that control the function of brown adipose tissue during entry into and arousal from hibernation and pineal or melatonin-related components that control its growth in response to photoperiod. In animals which become intermittently torpid, such as the mouse, the regulation includes in addition central components that control the function of brown adipose tissue during entry into and arousal from torpor. The central neural components involved in control of thermoregulation are better understood than are those involved in the regulation of energy balance. Studies of animal with hypothalamic obesity indicate that the control of diet-induced thermogenesis in brown adipose tissue requires the participation of the ventromedial region of the hypothalamus whereas the control of cold-induced nonshivering thermogenesis does not. The importance of comparative studies in different species is emphasized since any neural model for the control of brown adipose tissue thermogenesis is likely to apply in detail only to the species for which it was developed.
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PMID:Nonshivering thermogenesis. 672 94

Brown adipose tissue is a major thermogenic effector of cold-induced nonshivering thermogenesis. Previous studies indicate that melatonin and/or short photoperiod are involved in the increase in brown fat deposition seen in certain cold-acclimated rodents. The present study was undertaken, in part, to determine whether the pineal is a necessary component in the cold-induced increase in thermogenic capacity characteristic of the cold-acclimated laboratory rat. Under a 12L:12D light cycle, pinealectomized rats did not differ from sham-operated rats in their ability to increase brown fat deposition in the cold (5 degrees C). Moreover, in a subsequent set of experiments performed at 9 degrees C, intact rats maintained at a short photoperiod (9L:15D) exhibited the same degree of brown fat hypertrophy/hyperplasia as did those kept at a long photoperiod (15L:9D). These data thus indicate that: (a) the intact pineal is not necessary for the cold-induced increase in brown adipose tissue occurring in the cold-acclimated rat; and (b) photoperiod does not significantly modulate the magnitude of this increase.
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PMID:Photoperiod and pinealectomy do not affect cold-induced deposition of brown adipose tissue in the Long-Evans rat. 683 6

Brown adipose tissue, a well known effector of regulatory thermogenesis found in mammals, is unique in its ability to steadily increase its heat production several fold for very long periods of time. It constitutes a shunt of energy flow between food intake and heat dissipation, it is activated through its sympathetic nerve supply. There are evidence in the rat, that brown adipose tissue is activated following overfeeding, thus decreasing food efficiency and determining resistance to obesity. Genetically obese (ob/ob) mice fed and kept at 22 degrees C lack the possibility of activating their brown fat energy shunt; they are known to be poorly resistant to cold stress despite their large insulation. This is taken as a further circumstantial evidence of an overlap in thermal and food efficiency regulatory systems in rodents through sympathetically controlled brown fast as a common effector.
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PMID:Is there a sympathetic regulation of the efficiency of energy utilization? 701 32

Brown adipose tissue is an important site of cold-induced nonshivering thermogenesis in many mammals. The plasma membrane-bound Na+-K+-ATPase has been shown to be significantly involved in this thermogenesis although its exact role is unknown at present. Evidence that coupling of oxidative phosphorylation to electron transport may become loosened during thermogenesis has prompted an investigation of potential roles of the Na+-K+ pump that would be compatible with altered respiratory coupling. One such role is that of modulating norepinephrine (NE)-induced lipolysis and hence provision of free fatty acids to the mitochondria. Under such conditions, inhibition of the pump would reduce NE-induced respiration by limiting substrate availability. If, in fact, the primary role of the pump in NE-induced thermogenesis is to facilitate substrate availability, provision of exogenous substrate should bypass this involvement and ameliorate the ouabain inhibition of respiration. In the present study, this possibility was examined by determining the effect of an exogenous substrate, butyrate, on the contribution of the Na+-K+ pump to NE-stimulated respiration of isolated hamster brown adipocytes. Although exogenous butyrate was able to serve as a substrate for brown adipocyte respiration, its presence had no significant effect on the ouabain sensitivity of NE-induced rates of oxygen consumption. That is, ouabain (1 mM) inhibited the NE-evoked thermogenesis of the adipocytes by 77.7 +/- 6.5% in the absence of butyrate (2 mM) and by 73.4 +/- 9.9% in its presence. It appears, therefore, that the contribution of the Na+-K+ membrane pump to brown fat thermogenesis does not simply reflect modulation of NE-evoked lipolysis.
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PMID:Effects of butyrate on ouabain-sensitive respiration of hamster brown adipocytes. 705 78

Brown adipose tissue (BAT) is an important site of adaptive changes in thermogenesis in the rat. The sympathetic nervous system, which richly supplies BAT, is thought to play an important role in the regulation of BAT thermogenesis because catecholamines stimulate and beta adrenergic blocking agents inhibit oxygen consumption in this tissue. The present studies were carried out to assess directly sympathetic activity in BAT in response to cold exposure and to changes in dietary intake, both of which alter heat production in the rat. Sympathetic activity was determined from the rate of norepinephrine (NE) turnover in interscapular brown adipose tissue (IBAT) after preliminary experiments validated the use of NE turnover techniques in IBAT. Acute exposure to 4 degrees C increased NE turnover in IBAT 4- to 12-fold compared with ambient temperature controls, depending upon the interval over which the turnover measurement was made, while in the heart NE turnover doubled in response to the same cold stimulus. In animals exposed to cold continuously for 10 d before study, NE turnover measurements in IBAT and in the heart were elevated comparably to those obtained during acute exposure. Alterations in feeding were also associated with changes in NE turnover in IBAT. Fasting for 2 d decreased NE turnover in IBAT (-35% from 29.2+/-4.2 ng NE/h to 18.9+/-5.9) and in heart (-52%). In animals fed a "cafeteria" diet, a model of voluntary overfeeding in the rat, NE turnover was increased in both IBAT (+108% from 24.8+/-4.5 ng NE/h to 51.7+/-6.8) and heart (+66%). Because ganglionic blockade exerted a greater effect on NE turnover in IBAT in cafeteria-fed rats than in controls, the increase in NE turnover in IBAT with this overfeeding regimen reflects enhanced central sympathetic outflow. Thus NE turnover techniques can be satisfactorily applied to the assessment of sympathetic nervous system activity in IBAT. The experiments reported here demonstrate changes in sympathetic activity in IBAT that parallel known adaptive changes in heat production in the rat. These studies, therefore, support the concept that the increased thermogenesis of chronic cold exposure and of cafeteria feeding occur by similar mechanisms and imply an important role for the sympathetic nervous system, mediated in part through BAT, in the regulation of energy balance in the rat.
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PMID:Effect of diet and cold exposure on norepinephrine turnover in brown adipose tissue of the rat. 706 45

Brown adipose tissue (BAT) of rats is known to grow in response to acclimation to cold. The growth is accompanied by changes in mitochondrial polypeptide composition (an increase in the relative proportion of a polypeptide of molecular weight 32,000, known to be associated with the thermogenic proton conductance pathway). The mediator of the change in mitochondrial polypeptide composition is unknown. The objective of these experiments was to find out whether any of the pituitary hormones might be the mediator. Treatment of rats with growth hormone failed to alter BAT size or mitochondrial polypeptide composition. BAT grew and the change in BAT mitochondrial polypeptide composition occurred in cold-acclimated hypophysectomized rats, maintained on thyroxine and corticosterone to ensure their survival in the cold. It is concluded that none of the pituitary hormones is the mediator for the cold-induced change in BAT mitochondrial polypeptide composition or is required to exert a direct effect on BAT for cold-induced BAT growth to occur. It also seems unlikely that more than a maintenance amount of glucocorticoids is required for normal cold-induced growth of BAT; these hormones are thus also unlikely to mediate the change in BAT mitochondrial polypeptide composition. The requirement for no more than a maintenance amount of thyroxine for BAT growth and for the cold-induced change in BAT mitochondrial polypeptide composition confirms previous conclusions drawn from studies on cold-acclimated thyroidectomized rats.
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PMID:Growth of interscapular brown adipose tissue in cold-acclimated hypophysectomized rats maintained on thyroxine and corticosterone. 712 89

The onset of thermogenesis in response to cold exposure in individual mice was studied using a sensitive close circuit system for measuring their rate of oxygen consumption. On the day of birth, exposure to a cool environment did not stimulate an increase in oxygen consumption, but 48 h later the majority of mice respond by doubling their metabolic rate in response to a fall from 36 to 31 degrees C in ambient temperature. When 5 mice huddled together an ambient temperature drop from 36 to 23 degrees C was required to provoke the same response. Brown adipose tissue is present at birth but the cells are relatively small and contain little fat. By the second day they are three times larger and contain far more fat. The onset of thermogenesis appears to await the development of brown adipose tissue.
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PMID:Onset of thermogenesis in response to cold in newborn mice. 713 88

To determine the effects of cafeteria feeding on brown (BAT) and white (WAT) adipose tissue cellularity, thermogenesis and body composition, male Sprague-Dawley rats were fed a cafeteria or a Purina chow diet for 52 days postweaning. Interscapular BAT (IBAT) was removed from subgroups of rats on each diet, and the animals continued on the same regimens. The IBAT weight of rats fed cafeteria diets was 160% of controls after 3 days and 220% after 52 days of the dietary regimens, and brown adipocyte numbers were 130 and 300% those of stock diet-fed rats, respectively, during the same period. Brown adipocyte diameters were initially greater in rats fed cafeteria diet than in rats fed stock diet but were similar after 52 days. Norepinephrine-stimulated thermogenesis was greater in rats fed cafeteria diets than in rats fed stock diet and was intermediate between the two in the IBAT-lipectomized group fed cafeteria diet. Surgical reduction of IBAT resulted in hypertrophy of WAT and an improved efficiency of weight gain, whereas body composition, WAT cellularity, and the efficiency of weight gain of similarly operated rats fed stock diet were unaltered from those of unoperated animals fed stock diet. These results are consistent with the development of a nutritionally induced hyperplasia and/or differentiation of BAT similar to that which follows cold acclimatization. BAT may play an active role in the expenditure of excess energy during periods of overnutrition, and thereby influence an animal's propensity for fatness.
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PMID:Effect of cafeteria feeding on brown and white adipose tissue cellularity, thermogenesis, and body composition in rats. 714 7

Cold-adapted (CA) and warm-adapted (WA) rats (5 and 28 degrees C) were infused with noradrenaline (4 microgram.kg-1.min-1) for 15 min. Blood was collected from Sulzer's vein coming from brown adipose tissue and analyzed for total carnitine, free carnitine, and beta-hydroxybutyrate content, before and up to 45 min after the infusion. Acylcarnitine (total minus free carnitine) levels increased more and total carnitine levels decreased more in the CA group than in the WA group. beta-Hydroxybutyrate content increased to the same extent (from about 0.16 to 0.8 mM) in both groups. Brown fat was found not to release carnitine into the circulation after NA infusion. Twenty minutes after the end of the infusion brown fat retained both ketones and acylcarnitine in the CA rats only.
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PMID:Brown adipose tissue and carnitine in cold-adapted rats. 723 52


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