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

Mice selectively bred for either high or low levels of thermoregulatory nest building were cold-acclimated (5 degrees C) for 3 weeks without nesting material; then body weight and food intake were measured. The mice selected for low nest building (Lows) of both sexes showed lower feed efficiencies than the high nest-building mice (Highs), although their body weights were not significantly different (Table 1). This adds to a large body of evidence which suggests that nest building and feed efficiency were influenced by a common mechanism (Lacy et al. 1978; Sulzbach and Lynch 1984; Lynch et al. 1981; Lynch and Roberts 1984). Brown adipose tissue mitochondrial GDP binding and cytochrome c oxidase activity were measured in the above mice. In females, the Lows had 100% higher levels of total GDP binding than the Highs, while no difference between the lines was seen in males. Thus in the High females, lower energy expenditure through brown fat thermogenesis may account for their greater feed efficiency. In males, the genetic differences in feed efficiency must be due to differences in either thermogenesis in tissues other than brown fat, or mechanisms which reduce heat loss.
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PMID:Genetic association between nest building and brown adipose tissue thermogenesis in female house mice. 303 34

Seasonal acclimation of nonshivering thermogenesis and brown adipose tissue was studied in wild bank voles (Clethrionomys glareolus), yellow necked field mice and wood mice (Apodemus flavicollis, A. sylvaticus). Both, voles and mice increased their capacity for nonshivering thermogenesis during winter. Thermogenic properties of brown fat (cytochrome c oxidase activity, mitochondrial protein content, GDP-binding of brown fat mitochondria) showed similar changes during seasonal acclimation; Clethrionomys and Apodemus spp. both showed lowest thermogenic properties in the summer during August, a rapid increase during fall, and highest levels of thermogenic activity in the winter months. With regard to changes in body weight and brown fat mass these species show different strategies for seasonal acclimation. In Clethrionomys a reduction of body mass in the winter was found, both in the wild population as well as in individual animals housed in the laboratory. A. flavicollis showed a reduction of body weight during fall, whereas A. sylvaticus maintained a constant body mass throughout the year. Brown fat mass and cellularity increased in the Apodemus spp. during winter, in parallel with the thermogenic properties of brown fat, whereas in Clethrionomys brown fat mass and cellularity remained seasonally constant. These species live in the same habitat and were trapped in the same area. It is concluded that seasonal improvements of in vivo and in vitro thermogenesis are very similar in these species, although the physiological basis for this improvement is different in Clethrionomys and Apodemus.
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PMID:Seasonal acclimation of bank voles and wood mice: nonshivering thermogenesis and thermogenic properties of brown adipose tissue mitochondria. 304 8

Brown adipose tissue has earlier been suggested as an important site of the diet-induced thermogenesis that results from cafeteria feeding in rats. The aim of the present communication has been to see if any defined component of this diet can mimic the effects of the diet on the trophic response of brown fat and if these effects are mediated by the sympathetic nervous system. Rats fed a lipid emulsion did not show hypertrophy of brown adipose tissue. Rats fed a glucose solution, whether voluntarily or by force feeding, showed a clear trophic response of brown fat, as seen by the morphology of the tissue and its increased wet weight, increased protein content, increased total and specific cytochrome c oxidase activity, and increased mitochondrial guanosine diphosphate binding. Chemical sympathectomy of young rats by guanethidine prior to glucose feeding impaired the glucose-induced effects on brown fat. beta-Adrenergic blockade in adult rats also tended to depress the glucose effect. Consequently we conclude that chronic glucose ingestion can mimic cafeteria feeding with respect to the trophic response of brown fat and that an intact sympathetic nervous system is required for the mediation of the glucose effect to the brown adipose tissue.
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PMID:Trophic response of rat brown fat by glucose feeding: involvement of sympathetic nervous system. 629 8

Brown fat hypertrophy in the rat resulting from cold adaptation is shown here to involve increased mitochondrial, peroxisomal, and lysosomal enzyme activities. Mitochondrial activity in homogenates of brown fat was estimated as cytochrome c oxidase. After 4 wk in the cold (+5 C), the total activity was 3-fold higher than in control rats, although the specific activity was somewhat lower. Peroxisomal activity was followed as cyanide-insensitive palmitoyl-CoA-dependent NAD+ reduction (palmitoyl-CoA oxidase) and as catalase. The total activity of both palmitoyl-CoA oxidase and catalase was more than 10-fold higher than in controls and the specific activity about 3-fold higher. Acid phosphatase, used as a lysosomal marker, showed a 6-fold higher total activity and almost twice as high specific activity. The relatively greater increase in peroxisomes and lysosomes compared with mitochondria indicates an involvement in thermogenesis also for these organelles.
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PMID:Cold adaptation in the rat: increased brown fat peroxisomal beta-oxidation relative to maximal mitochondrial oxidative capacity. 743 8

The aerobic purification of Pseudomonas nautica 617 nitrous oxide reductase yielded two forms of the enzyme exhibiting different chromatographic behaviors. The protein contains six copper atoms per monomer, arranged in two centers named Cu(A) and Cu(Z). Cu(Z) could be neither oxidized nor further reduced under our experimental conditions, and exhibits a 4-line EPR spectrum (g(x)=2.015, A(x)=1.5 mT, g(y)=2.071, A(y)=2 mT, g(z)=2.138, A(z)=7 mT) and a strong absorption at approximately 640 nm. Cu(A) can be stabilized in a reduced EPR-silent state and in an oxidized state with a typical 7-line EPR spectrum (g(x)=g(y)= 2.021, A(x) = A(y)=0 mT, g(z) = 2.178, A(z)= 4 mT) and absorption bands at 480, 540, and approximately 800 nm. The difference between the two purified forms of nitrous oxide reductase is interpreted as a difference in the oxidation state of the Cu(A) center. In form A, Cu(A) is predominantly oxidized (S = (1)/(2), Cu(1.5+)-Cu(1.5+)), while in form B it is mostly in the one-electron reduced state (S = 0, Cu(1+)-Cu(1+)). In both forms, Cu(Z) remains reduced (S = 1/2). Complete crystallographic data at 2.4 A indicate that Cu(A) is a binuclear site (similar to the site found in cytochrome c oxidase) and Cu(Z) is a novel tetracopper cluster [Brown, K., et al. (2000) Nat. Struct. Biol. (in press)]. The complete amino acid sequence of the enzyme was determined and comparisons made with sequences of other nitrous oxide reductases, emphasizing the coordination of the centers. A 10.3 kDa peptide copurified with both forms of nitrous oxide reductase shows strong homology with proteins of the heat-shock GroES chaperonin family.
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PMID:Purification, characterization, and preliminary crystallographic study of copper-containing nitrous oxide reductase from Pseudomonas nautica 617. 1074 77

The in vivo cellular impact of age-associated mitochondrial DNA mutations is unknown. We hypothesized that mitochondrial DNA deletion mutations contribute to the fiber atrophy and loss that cause sarcopenia, the age-related decline of muscle mass and function. We examined 82,713 rectus femoris muscle fibers from Fischer 344 x Brown Norway F1 hybrid rats of ages 5, 18, and 38 months through 1000 microns by serial cryosectioning and histochemical staining for cytochrome c oxidase and succinate dehydrogenase. Between 5 and 38 months of age, the rectus femoris muscle in the hybrid rat demonstrated a 33% decrease in mass concomitant with a 30% decrease in total fibers at the muscle mid-belly. We observed significant increases in the number of mitochondrial abnormalities with age from 289 +/- 8 ETS abnormal fibers in the entire 5-month-old rectus femoris to 1094 +/- 126 in the 38-month-old as calculated from the volume density of these abnormalities. Segmental mitochondrial abnormalities contained mitochondrial DNA deletion mutations as revealed by laser capture microdissection and whole mitochondrial genome amplification. Muscle fibers harboring mitochondrial deletions often displayed atrophy, splitting and increased steady-state levels of oxidative nucleic damage. These data suggest a causal role for age-associated mitochondrial DNA deletion mutations in sarcopenia.
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PMID:Mitochondrial DNA deletion mutations colocalize with segmental electron transport system abnormalities, muscle fiber atrophy, fiber splitting, and oxidative damage in sarcopenia. 1115 48

We hypothesized that cardiac aging in the rat involves mitochondrial genetic damage and mitochondrial enzymatic dysfunction of individual cardiomyocytes as has been demonstrated previously only in primate myocardium. Myocardium from Fischer 344 x Brown Norway F(1)hybrid rats of ages 5, 18 and 36-38 months was examined for mitochondrial genetic and enzymatic abnormalities. In-vivo hemodynamic measurements revealed age-related changes of left ventricular function while histological evaluation demonstrated an increase in percent area fibrosis from 7%+/-5 in the 5-month-old hearts to 38%+/-2 in the subendocardium of the left ventricle of 38-month-old rats. Mitochondrial genomes lacking 8000 to 9000 bp of primary sequence were detected in tissue homogenates from right and left ventricular myocardium and the abundance of these deleted genomes increased with age. In-situ histochemical staining of serial cryomicrotome sections of myocardial tissue revealed individual cardiomyocytes displaying abnormal, primarily absent, activities of cytochrome c oxidase and succinate dehydrogenase. The area density of histochemically-abnormal cardiomyocytes increased from 0.05 per mm(2)to 0.3 per mm(2)between 5 and 36-38 months of age in the left ventricle, and they were localized primarily to the left ventricular subendocardium. The presence of age-related mitochondrial genetic and enzymatic abnormalities in the Fischer 344 x Brown Norway F(1)hybrid rat heart suggests the role of mitochondrial dysfunction, secondary to mtDNA mutations, in age-related cardiomyocyte loss and subsequent cardiac aging.
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PMID:Age-associated changes in function, structure and mitochondrial genetic and enzymatic abnormalities in the Fischer 344 x Brown Norway F(1) hybrid rat heart. 1181 61

We compared responses of the fast extensor digitorum longus (EDL) and tibialis anterior (TA) muscles in young (15-week) and aging (101-week) male Brown Norwegian rats to 50 days of chronic low-frequency stimulation (CLFS, 10 Hz, 10 hours/day). After 50 days of CLFS, the EDL muscles of the young (22-week) and aging (108-week) rats displayed similar increases in type IIA fibers, relative concentration of myosin heavy chain MHCIIa, elevations in mitochondrial citrate synthase and 3-hydroxyacyl-CoA dehydrogenase activities, and similar decreases in glycolytic enzyme activities (glyceraldehydephosphate dehydrogenase, lactate dehydrogenase). TA muscle in young rats contained a few cytochrome c oxidase negative (COX-) type I fibers. Their number was approximately 2-fold elevated by CLFS. Conversely, aging muscle, which contained a slightly higher amount of COX- fibers than young TA muscle, responded to CLFS with a significant decrease in COX- fibers. The appearance of small COX-positive type I fibers in stimulated aging muscle indicated that regenerating type I fibers "diluted" the COX-deficient fiber population.
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PMID:Adaptive potentials of skeletal muscle in young and aging rats. 1191 26

Biological aging is associated with functional deficits at the cellular, organ, and system levels. The pituitary gland, the central organ of the neuroendocrine system, has been shown to play an important role in the aging process. To gain a better understanding of its functional changes with aging, we compared the gene expression profiles of the anterior pituitary of young and old Brown Norway rats, focusing on the major pituitary hormone genes. We also explored the effects of caloric restriction, an intervention shown to delay or inhibit age-associated pathologic and biologic changes in a number of systems and organisms, on the expression of these genes. Of the total of 1176 genes arrayed on each of the six membranes per group that we used, 542 (46%) were detectable in the anterior pituitary of young and old rats. Significance analysis of microarrays (SAM) of these 542 detectable genes revealed 28 genes that changed significantly with age, among which 24 decreased and 4 increased. Among the five major hormone genes on the membrane, growth hormone (GH) and prolactin decreased with age, the glycoprotein hormone common alpha subunit gene increased, and follicle-stimulating hormone-beta subunit (FSH-beta) and thyrotropin-beta (TSH-beta) subunit did not change. Among these genes, the three found to change by array analysis were confirmed to do so by Northern blot analysis. For the two genes among the five that were not selected (i.e. did not change) by array analysis, TSH-beta also showed no significant change by Northern blot; but the other, FSH-beta, showed significant increase. Thus, of the five genes checked by Northern blot analysis, the results were consistent with the array data in four cases. Short-term caloric restriction (5 weeks) of young adult animals resulted in 19 genes being significantly down-regulated, while no significantly up-regulated genes were identified. Among the genes that were down-regulated were GH, gonadotropin releasing hormone receptor (GnRH-R), three cytochrome c oxidase subunits and two heat shock proteins. With long-term (21 month) caloric restriction, about 30% of the genes that changed with aging (8/28) were prevented from doing so, and none of the age-related changes was enhanced with long-term caloric restriction. The genes that showed most significant rescue were neuropeptide Y, GnRH-R, DNA-binding protein inhibitor Id-3, and nerve growth factor-induced protein I-B. These results indicate that long-term caloric restriction can partially prevent some of the age-related changes in gene expression in the anterior pituitary of Brown Norway rats, suggesting a benefit of this regimen to be the slowing of the aging process. The fact that fewer than 30% genes derived benefit also suggests that the effect of caloric restriction is rather limit, which is consistent with the thesis that caloric restriction may slow, but not prevent, the aging process.
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PMID:Gene expression by the anterior pituitary gland: effects of age and caloric restriction. 1524 22

Brown adipose tissue (BAT) physiology and imaging have recently attracted considerable attention. BAT is characterized both by enhanced perfusion and increased mitochondrial activity. (99m)Tc-sestamibi is a lipophilic cationic tracer that concentrates in mitochondria. Data on the accumulation of (99m)Tc-sestamibi in BAT are currently lacking. This study investigates the in vivo (99m)Tc-sestamibi uptake in rat BAT. (99m)Tc-sestamibi was administered in male Wistar rats of various age and body size. (99m)Tc-sestamibi uptake was measured in vitro in BAT and white fat (WF) together with cytochrome c oxidase activity. Both (99m)Tc-sestamibi uptake and cytochrome c oxidase activity were higher in BAT than in WF (P<0.05). (99m)Tc-Sestamibi uptake in both BAT and WF was negatively related to body weight (r = -0.96 and -0.89, respectively) as was the BAT/WF uptake ratio (r = -0.85). These data show a higher (99m)Tc-sestamibi uptake in BAT compared to WF, in agreement with the high mitochondrial content and respiratory activity of the former. The strong negative correlation between (99m)Tc-sestamibi uptake in BAT and body weight (negative allometry), is in accordance to increased needs of thermogenesis in smaller animals. Implications of increased (99m)Tc-sestamibi uptake in BAT in radionuclide imaging are also discussed.
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PMID:Assessment of brown adipose tissue activity in rats by 99mTc-sestamibi uptake. 1649 7


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