ライフサイエンスコーパス: brown fat

1 higher maximum standardized uptake values of brown fat.

2 to be female and thinner than those without brown fat.

3 an and maximum standardized uptake values of brown fat.

4 and P301S mice, preventing lipid vacuoles in brown fat.

5 se heart, skeletal muscle, liver, kidney and brown fat.

6 es while obesity increases its expression in brown fat.

7 ogenesis was observed in skeletal muscle and brown fat.

8 heir altered mitochondrial metabolism in the brown fat.

9 nd determining the balance between white and brown fat.

10 hological and biochemical characteristics of brown fat.

11 l muscle and, unexpectedly, to interscapular brown fat.

12 es in ZAG mRNA and protein levels in WAT and brown fat.

13 .c., and mammary gland) and in interscapular brown fat.

14 g in muscle and beta-adrenergic signaling in brown fat.

15 process that we hypothesize to be in foci of brown fat.

16 ility shift assay with nuclear extracts from brown fat.

17 key event for triggering heat production in brown fat.

18 tically up-regulated during thermogenesis in brown fat.

19 tes, similar to cold-exposed or fish oil-fed brown fat.

20 s, salivary gland, intestine, white fat, and brown fat.

21 RNA titers were highest in heart, lung, and brown fat.

22 tially controls the formation of thermogenic brown fat.

23 hree cell types: melanocytes, platelets, and brown fat.

24 in thermogenesis and fatty acid oxidation in brown fat.

25 d the state of current knowledge about human brown fat.

26 ng of lipolysis and lipogenesis in activated brown fat.

27 ral fat, and promoted additional browning in brown fat.

28 has been linked to greater thermogenesis by brown fat.

29 enlargement and "whitening" of interscapular brown fat.

30 ated in serum from obese mice (ob/ob, db/db, brown-fat ablated, gold-thioglucose treated, high-fat fe

31 stly increased in mice with toxigene-induced brown fat ablation uncoupling protein diphtheria toxin A

32 Brown fat activates uncoupled respiration in response to

33 their tail surface was reduced, normalizing brown fat activity and energy expenditure.

34 How tumours induce brown fat activity is unknown.

35 ecent studies also have indicated that human brown fat activity levels correlate with leanness.

36 he increase in adiposity and the decrease in brown fat activity observed during the normal aging proc

37 Brown fat activity was markedly decreased in FIGIRKO mic

38 in turn leads to compensatory alterations in brown fat activity.

39 Does human brown fat actually combust fat to release heat?

40 ia and the presence of uncoupling protein 1, brown fat adipocytes can be termed as energy inefficient

41 ancement of energy expenditure, promotion of brown fat adipogenesis by thiazolidinediones could contr

42 not only a role for the insulin receptors in brown fat adipogenesis, the data also suggest a novel ro

43 significant difference in the prevalence of brown fat among ethnic groups.

44 function in 30 transgenic mice with reduced brown fat and 30 matched wild-type controls.

45 p7 knockout embryos show a marked paucity of brown fat and an almost complete absence of UCP1.

46 ession pattern distinct from either white or brown fat and are preferentially sensitive to the polype

47 creasing energy metabolism via activation of brown fat and browning of white fat, but intact liver in

48 gh developmental expression of either NRF-1 (brown fat and developing brain) or myogenin (striated mu

49 butions with highest levels of expression in brown fat and heart, their mRNAs are differentially regu

50 ns projecting to the NTS, rapidly stimulates brown fat and increases energy expenditure but does not

51 ing, it also decreases energy expenditure in brown fat and increases enzymatic activity associated wi

52 Classic brown fat and inducible beige fat both dissipate chemica

53 This cofactor is cold inducible in brown fat and interacts with multiple transcription fact

54 mammalian organs, with highest expression in brown fat and kidney.

55 m in the major metabolic organs of white and brown fat and liver.

56 so abrogates the ability of mice to regulate brown fat and maintain core body temperature.

57 ly expressed in adipose tissues, enriched in brown fat and markedly increased during brown adipocyte

58 R agonists additively enhanced expression of brown fat and mitochondrial markers in a p38 MAPK-depend

59 ehog signaling increases glucose uptake into brown fat and muscle.

60 al proliferation and respiratory activity in brown fat and skeletal muscle are directed by the transc

61 ation of progenitor cells that gives rise to brown fat and skeletal muscle but not white fat.

62 graph analyses of mitochondria isolated from brown fat and skeletal muscle).

63 ch is expressed in several tissues including brown fat and skeletal muscle, and that activates mitoch

64 certain aspects of adaptive thermogenesis in brown fat and skeletal muscle, hepatic gluconeogenesis,

65 elevated upon cold exposure of mice in both brown fat and skeletal muscle, key thermogenic tissues.

66 ce and activity are significantly reduced in brown fat and skeletal muscles of Ews-deficient mice.

67 mously regulates adipose lineage commitment, brown fat and smooth muscle cell formation, and systemic

68 ge largely overlaps with the Myf5 lineage in brown fat and subcutaneous white fat, but exhibits gende

69 pression in white fat and UCP1 expression in brown fat and that resistance to obesity is correlated w

70 ARgamma and PBP expression overlapped in the brown fat and urogenital sinus at stage E15.5 of embryog

71 reased expression of genes characteristic of brown fat and were intolerant to cold exposure.

72 onstrate that Akt2 is especially abundant in brown fat and, to a lesser extent, skeletal muscle and l

73 racteristics of those with and those without brown fat, and correlate these characteristics with the

74 d glycerol release and oxygen consumption in brown fat, and decreases fat oxidation and glycerol rele

75 atly reduced in muscle, minimally reduced in brown fat, and not reduced at all in liver.

76 rmomyotome gives rise to dermis, muscle, and brown fat, and that Wnt signalling normally instructs ce

77 Brown fat appeared to be completely absent from all expe

78 ptical changes are identified when white and brown fat are assessed in vivo.

79 Although the functions of white fat and brown fat are increasingly well understood, their develo

80 ear localization of transcription factors in brown fat are reduced during post-natal development.

81 duodenal lipid sensing activates a gut-brain-brown fat axis to determine brown fat temperature, and t

82 an obesogenic diet indicates that UCP1-based brown fat-based thermogenesis plays no role in so-called

83 xpression of adipogenic genes common to both brown fat (BAT) and white fat (WAT), and the expression

84 pose tissue specifically increases classical brown fat (BAT) mass, but not white fat (WAT) mass.

85 The Hdac1 level is lower in mouse brown fat (BAT) than white fat, is suppressed in mouse B

86 ase our proneness to obesity - provided that brown fat becomes activated not only by cold but also th

87 This has revitalized interest in brown fat biology and has driven the discovery of many n

88 As we enter into a new era of brown fat biology, the next challenge will be to develop

89 ol 3-phosphate oxidation by skeletal muscle, brown fat, brain, and heart mitochondria with an emphasi

90 e due in part to increased glucose uptake in brown fat, browning of white fat, and overall increased

91 show an age-dependent loss of interscapular brown fat but increased expression of uncoupling protein

92 n PRDM16 caused minimal effects on classical brown fat but markedly inhibited beige adipocyte functio

93 Adult humans have brown fat, but the amounts and activities are substantia

94 Brown fat can increase energy expenditure and protect ag

95 Brown fat can reduce obesity through the dissipation of

96 r of nuclear receptors, termed PGC-1, from a brown fat cDNA library.

97 These data implicate LRP130 in brown fat cell development and differentiation.

98 Notably, brown fat cell development common to both PGC-1 coactiva

99 n relating to the transcriptional control of brown fat cell development.

100 adipose tissue upon cold exposure and during brown fat cell differentiation.

101 gase for PGC-1alpha and negatively regulates brown fat cell metabolism.

102 expression, suppress RNF34 expression in the brown fat cell, indicating a physiological relevance of

103 metabolism and adaptive thermogenesis in the brown fat cell.

104 cification and developmental cues specifying brown-fat cell fate remain poorly understood.

105 In response to cold or exercise, brown fat cells also emerge in the white adipose tissue

106 These brown fat cells are subject to further up-regulation of

107 Recent data suggests that brown fat cells arise in vivo from a Myf5-positive, myob

108 Despite intact PGC-1 coactivator expression, brown fat cells deficient for LRP130 exhibit attenuated

109 rom murine brown fat precursors and in human brown fat cells differentiated from human neck brown pre

110 ls respond to cool temperatures, but classic brown fat cells do not.

111 , while the opposite effects are observed in brown fat cells ectopically expressing wild-type RNF34 b

112 Indeed, the number of UCP1-positive brown fat cells in intermuscular fat in 129 mice is >700

113 In brown fat cells, knockdown of RNF34 increases the endoge

114 fferentiated cells, such as motor neurons or brown fat cells, to control the expression of genes that

115 ss-talk between constitutive and recruitable brown fat cells.

116 ll fate switch from myoblastic precursors to brown fat cells.

117 l fate switch between skeletal myoblasts and brown fat cells.

118 myoblasts induces their differentiation into brown fat cells.

119 t data suggest the existence of two types of brown fat cells: constitutive BAT (cBAT), which is of em

120 in brown adipocytes causes a severe loss of brown fat characteristics and induces muscle differentia

121 6 from brown fat precursors causes a loss of brown fat characteristics and promotes muscle differenti

122 suggest that there are two distinct types of brown fat: classical brown fat derived from a myf-5 cell

123 wn adipocyte differentiation and enriched in brown fat compared with other organs.

124 ow that LRP130 is preferentially enriched in brown fat compared with white, and induced in a PGC-1-de

125 In rodents, UCP1 activity and brown fat contribute importantly to whole-body energy ex

126 a suggesting that irisin stimulates white-to-brown fat conversion have led to the hypothesis that it

127 metabolism, at least partially, via a heart-brown fat cross-talk involving FGF21.

128 and PGC-1alpha, increased expression of the brown-fat-defining marker uncoupling protein 1 (UCP1) an

129 provide evidence that previously identified brown fat deposits in adult humans are composed of beige

130 Bnip3 is reciprocally regulated in white and brown fat depots of diet-induced obesity and leptin-defi

131 ical manipulations or the transplantation of brown fat depots, these methods are difficult to use for

132 e two distinct types of brown fat: classical brown fat derived from a myf-5 cellular lineage and UCP1

133 Da zinc finger protein that robustly induces brown fat determination and differentiation.

134 RDM16 is a zinc-finger protein that controls brown fat determination by stimulating brown fat-selecti

135 ents and that transgenic mice with decreased brown fat develop obesity demonstrates the importance of

136 iven the discovery of many new regulators of brown fat development and function.

137 containing 7b (Zbtb7b) as a potent driver of brown fat development and thermogenesis and cold-induced

138 tal cold, the functions of ILC2s in beige or brown fat development are poorly defined.

139 ter understand PGC-1 coactivator function in brown fat development, we explored the metabolic role of

140 gous) domain-containing 16 (PRDM16) drives a brown fat differentiation program, but the mechanisms by

141 ression of miR-365, a miRNA known to promote brown fat differentiation; however, introduction of othe

142 Finally, Prdm16-deficient brown fat displays an abnormal morphology, reduced therm

143 Whether brown fat engages other tissues through secreted factors

144 These results establish Nrg4 as a brown fat-enriched endocrine factor with therapeutic pot

145 s including induction of early regulators of brown fat fate PRDM16 and PGC-1alpha, increased expressi

146 ts establish SYK as an essential mediator of brown fat formation and function.

147 ient to disrupt white fat formation, but not brown fat formation and/or maintenance, although it is r

148 that the PRDM16-C/EBP-beta complex initiates brown fat formation from myoblastic precursors, and may

149 ntifies miR-34a as an inhibitor of beige and brown fat formation, providing a potential target for tr

150 d BAT mass and lipid content during neonatal brown fat formation.

151 specific BAF chromatin remodeling complex to brown fat gene enhancers, thereby regulating chromatin a

152 adipocytes, as demonstrated by increases in brown fat gene expression, mitochondrial content, and un

153 lpha, which are key regulators promoting the brown fat gene program.

154 ent of the BAF complex that was required for brown fat gene programming and mitochondrial function.

155 d that the mechanisms of Foxa3 modulation of brown fat gene programs involve the suppression of perox

156 Brown fat generates heat through uncoupled respiration,

157 Brown fat generates heat via the mitochondrial uncouplin

158 iR-150 attenuates the elevated expression of brown fat genes caused by KSRP deletion.

159 allowing this complex to powerfully activate brown fat genes, such as PGC-1alpha itself.

160 The maximum standardized uptake value of brown fat had a significant inverse correlation with age

161 Those with brown fat had significantly lower body weight (147.5 lb

162 To date, the metabolic action of brown fat has been primarily attributed to its role in f

163 Brown fat has been proposed to contain beta4-AR, as evid

164 udies examining the effects of TZDs on human brown fat have been reported.

165 s that elicit the transformation of white to brown fat have potentially profound benefits in the trea

166 entral role in nonshivering thermogenesis in brown fat; however, its role in beige fat remains unclea

167 set of insulin signaling in skeletal muscle, brown fat, hypothalamus, hippocampus, and prefrontal cor

168 fic chromatin remodeling complex to activate brown fat identity genes.

169 A high capacity to induce brown fat in areas of traditional white fat had no impac

170 However, the role of brown fat in humans is less clear.

171 velop obesity demonstrates the importance of brown fat in maintaining nutritional homeostasis.

172 in mouse embryonic fibroblasts or in vivo in brown fat in mice.

173 We found that brown fat in normal human bone marrow contains this prot

174 PURPOSES: To assess the prevalence of brown fat in patients with cancer, compare demographic c

175 Given the importance of brown fat in the control of energy metabolism in rodents

176 Brown fat, in all of its dimensions, can increase energy

177 one markedly induced molecular signatures of brown fat, including the key thermogenic gene Ucp1.

178 xpression of several genes characteristic of brown fat, including uncoupling protein 1.

179 he first robust method of visualizing murine brown fat independent of its activation state.Current ap

180 The mammalian brown fat inducible thioesterase variant 2 (BFIT2), also

181 mber 1 (Them1; synonyms Acot11, StarD14, and brown fat inducible thioesterase) is a long-chain fatty

182 Brown fat is a specialized tissue that can dissipate ene

183 Because of this, energy expenditure in brown fat is capable of ranging over many orders of magn

184 That adult humans possess brown fat is now accepted - but is the brown fat metabol

185 Brown fat is specialized for energy expenditure and has

186 Brown fat is specialized for energy expenditure, a proce

187 role for retinoid metabolism in white versus brown fat is unknown.

188 etween strains were minimal in interscapular brown fat, large differences occurred in white fat tissu

189 eads to induction of pockets of multilocular brown fat-like cells in remaining white adipose depots,

190 technology optimized to establish functional brown fat-like depots in vivo.

191 ivity by EPO is associated with induction of brown fat-like features in white adipocytes, as demonstr

192 ntagonist impaired EPO-mediated induction of brown fat-like gene expression and uncoupled respiration

193 Prdm16 is a cell-autonomous determinant of a brown fat-like gene program and thermogenesis in subcuta

194 regulate expression of genes that control a brown fat-like program in white adipose tissue, energy e

195 ystem to unlock the therapeutic potential of brown fat-like tissue expansion.

196 ulate UCP1 expression and a broad program of brown-fat-like development.

197 demonstrate that EWS is essential for early brown fat lineage determination.

198 Sarcoma (EWS), is essential for determining brown fat lineage during development.

199 hese data indicate that PRDM16 specifies the brown fat lineage from a progenitor that expresses myobl

200 arise from early muscle progenitors, but how brown fat lineage is determined is not completely unders

201 Thus, cells of the brown fat lineage were detectable in all human adipose d

202 e drug differentially affected the brain and brown fat lipidome of control and P301S mice, preventing

203 cing body weight and percentage gonadal fat, brown fat, liver, and heart were also identified.

204 ermogenic adipocyte formation and identified Brown fat lncRNA 1 (Blnc1) as a nuclear lncRNA that prom

205 ry pathway through which Zbtb7b recruits the brown fat lncRNA 1 (Blnc1)/heterogeneous nuclear ribonuc

206 significantly decreased expression levels of brown fat markers, decreased p38 MAPK phosphorylation, a

207 IGIRKO mice had markedly decreased white and brown fat mass and were completely resistant to high fat

208 in FIGIRKO mice despite a >85% reduction in brown fat mass.

209 s the possibility that calorie combustion in brown fat may be of significance for our metabolism and,

210 sm and, correspondingly, that the absence of brown fat may increase our proneness to obesity - provid

211 Mice with reduced brown fat may serve as a new model for the cardiovascula

212 ensatory mechanism, aimed at restoring total brown-fat-mediated thermogenic capacity in the body, is

213 ssess brown fat is now accepted - but is the brown fat metabolically active?

214 en Id1/PGC1alpha and Id1/Ebf2 in controlling brown fat metabolism, which has significant implications

215 etwork important for PGC-1alpha function and brown fat metabolism.

216 h sympathetic overactivity and regulation of brown fat metabolism.

217 y via a sympathetically-mediated increase in brown fat metabolism; (2) reduced thermogenesis probably

218 ses in mitochondrial thermogenic proteins in brown fat, mice lacking YY1 in this tissue are strongly

219 ndistinguishable de-energization of isolated brown fat mitochondria by fatty acids in UCP1-deficient

220 embrane potential and oxygen consumption, in brown fat mitochondria from UCP1-deficient mice.

221 ocumented fluorodeoxyglucose (FDG) uptake in brown fat (n = 298).

222 also noted enlarged skeletal muscle fibres, brown fat necrosis and calcification of cardiac tissue.

223 In skeletal muscle and in brown fat, neither UCP2 nor UCP3 expression was affected

224 the testis and high levels of expression in brown fat, neurons, and myometrium.

225 P kinase kinase 3, despite the expression in brown fat of MKK3, -4, and -6.

226 ubiquitously expressed and is induced in the brown fat of UCP-deficient mice.

227 Brown fat, on the other hand, dissipates chemical energy

228 even after removal of the main interscapular brown fat pad.

229 All white fat depots and brown fat pads were severely reduced in size, and exhibi

230 nally, Prdm16 haploinsufficiency reduced the brown fat phenotype in white adipose tissue stimulated b

231 tor thermogenesis in BAs derived from murine brown fat precursors and in human brown fat cells differ

232 Loss of PRDM16 from brown fat precursors causes a loss of brown fat characte

233 se tissue (BAT) are constitutively committed brown-fat progenitors, Sca-1(+) cells from skeletal musc

234 a is sufficient to induce a fully functional brown fat program in naive fibroblastic cells, including

235 As brown fat promotes energy dissipation, myokines that eli

236 uellet et al. demonstrate that metabolism in brown fat really is increased when adult humans are expo

237 d cold-induced transcriptional remodeling in brown fat, rendering mice sensitive to cold temperature,

238 at catecholamine-stimulated thermogenesis in brown fat requires beta-adrenergic elevations in cyclic

239 c and cellular aspects of recent progress in brown fat research.

240 er than 20% of axillary lymph nodes, livers, brown fat samples, kidneys, or blood samples throughout

241 ntified the histone reader protein DPF3 as a brown fat-selective component of the BAF complex that wa

242 trols brown fat determination by stimulating brown fat-selective gene expression, while suppressing t

243 but the mechanisms by which PRDM16 activates brown fat-selective genes have been unclear.

244 The expression of brown fat-selective genes is increased in subcutaneous/i

245 Interestingly, expression of known brown fat-selective genes such as PRDM16 was strongly co

246 ctive genes, but the expression of classical brown fat-selective genes were nearly undetectable.

247 l and catecholamine-stimulated expression of brown fat-selective genes.

248 ective genes, but not with that of classical brown fat-selective genes.

249 omplex, and recruits it to superenhancers at brown fat-selective genes.

250 binding is highly enriched at a broad set of brown fat-selective genes.

251 ntal change in chromatin architecture at key brown fat-selective genes.

252 adipocyte number and increased expression of brown fat-selective markers in white adipose tissue.

253 own of TRPP3 repressed the expression of the brown fat signature genes uncoupling protein (UCP)-1 and

254 , a region that controls sympathetic tone to brown fat, skin blood vessels, and heart.

255 efficiently develop into adipose tissue with brown fat-specific characteristics.

256 y which EBF2 regulates chromatin to activate brown fat-specific genes in adipocytes were unknown.

257 containing 16 (PRDM16) induces expression of brown fat-specific genes in brown and beige adipocytes,

258 M16 is a transcription factor that activates brown fat-specific genes while repressing white fat and

259 Uncoupling protein-1 (UCP1) is a brown fat-specific mitochondrial inner membrane protein

260 complex, is recruited to the enhancer of the brown fat-specific uncoupling protein 1 (Ucp1) gene thro

261 activator of transcription 5, as well as the brown-fat-specific markers PPARgamma coactivator 1 alpha

262 genesis as a consequence of high sympathetic brown fat stimulation.

263 in misty gray lean mutant mice not producing brown fat suggest that white adipocytes convert into fat

264 he prominent involvement of heart, lung, and brown fat suggests that these sites may be important tis

265 ates a gut-brain-brown fat axis to determine brown fat temperature, and thereby reveal a previously u

266 ration of lipids into the duodenum increases brown fat temperature.

267 pids abolished the lipid-induced increase in brown fat temperature.

268 ta indicate that the actions of CGP 12177 in brown fat that have been attributed to novel beta-AR (i.

269 ull mice show a loss of glycogen and reduced brown fat that is consistent with malnutrition leading t

270 mediator of the cAMP signaling mechanism of brown fat that promotes thermogenesis.

271 preferendum, tail-skin vasoconstriction, and brown fat thermogenesis), thus suggesting that TRPM8 is

272 ovel regulator of mitochondrial function and brown fat thermogenesis.

273 olished duodenal lipid-induced activation of brown fat thermogenesis.

274 ysis and have recently been shown to control brown fat thermogenesis.

275 d the ability of duodenal lipids to increase brown fat thermogenesis.

276 beige or white adipose tissue contributes to brown fat thermogenic function or compensates for partia

277 asal expression of UCP1, but, like classical brown fat, they respond to cyclic AMP stimulation with h

278 Like endogenous brown fat, this synthetic brown fat tissue acts as a sin

279 ponse to thermogenic stimuli, peroxisomes in brown fat tissue (BAT) undergo selective remodeling and

280 Like endogenous brown fat, this synthetic brown fat tissue acts as a sink for glucose uptake, as d

281 ing cells purified from Ebf2(GFP) embryos or brown fat tissue did not express myoblast or dermal cell

282 and PDE3B mRNA levels in heart and white and brown fat tissues of JCR:LA-cp rats revealed that PDE3B

283 660-673) outline mechanisms by which the brown fat transcription factor early B-cell factor 2 (EB

284 and PBP are differentially expressed in the brown fat, transitional epithelium of the urinary bladde

285 ulate iron metabolism only in the kidney and brown fat, two tissues in which the endogenous expressio

286 a protein highly homologous to the mammalian brown fat uncoupling protein (UCP).

287 Uptake of FDG in brown fat was demonstrated in 298 of 6867 (4.33%) patien

288 e receptors mediating CGP 12177 responses in brown fat was examined using wild-type mice and mice lac

289 Brown fat was hypertrophic and contained fat-laden cells

290 Prevalence of brown fat was significantly higher in female (5.9% [211

291 roglitazone in aP2/DTA mice, whose white and brown fat was virtually eliminated by fat-specific expre

292 However, in brown fat, we observed a 2-3-fold increase in the expres

293 Control patients (n = 298) without brown fat were chosen and matched for age, sex, and mont

294 Patients with brown fat were more likely to be female and thinner than

295 erature, whereas gene expression patterns in brown fat were not altered.

296 ld exposure up-regulates SIRT3 expression in brown fat, whereas elevated climate temperature reduces

297 genes are upregulated in eWAT, as is Ucp1 in brown fat, while liver triglyceride accumulation is atte

298 progenitor cells, ScaPCs) residing in murine brown fat, white fat, and skeletal muscle.

299 ce displayed enlarged but pale interscapular brown fat with decreased expression of genes characteris

300 In this study, we evaluated the presence of brown fat within human HO lesions.