ライフサイエンスコーパス: brown adipocyte

1 equired for marker gene expression in mature brown adipocytes.

2 nd promoted lipolysis in T37i differentiated brown adipocytes.

3 tenance as well as in the differentiation of brown adipocytes.

4 cantly stimulate p38 MAPK phosphorylation in brown adipocytes.

5 ficiency reduces the thermogenic activity of brown adipocytes.

6 ll markers and uniformly differentiated into brown adipocytes.

7 ines and is localized in the mitochondria of brown adipocytes.

8 AV-mediated transgene expression in white or brown adipocytes.

9 , oxidative metabolism, and thermogenesis in brown adipocytes.

10 etase long-chain family member 1 (Acsl1), in brown adipocytes.

11 GC-1alpha, and MED1 on the UCP-1 enhancer in brown adipocytes.

12 elopment of adipose tissue containing mostly brown adipocytes.

13 s in either MEF adipocytes or differentiated brown adipocytes.

14 and dose-dependent manner in both white and brown adipocytes.

15 de is stimulation of UCP1 gene expression in brown adipocytes.

16 ce could be fully differentiated into mature brown adipocytes.

17 ll surface area and membrane turnover in rat brown adipocytes.

18 lls might be regulated in tissues other than brown adipocytes.

19 rmally responsive to adrenergic signaling in brown adipocytes.

20 t beta3-AR gene expression preferentially to brown adipocytes.

21 E-1 in extracts prepared from differentiated brown adipocytes.

22 ghts into the regulation of thermogenesis by brown adipocytes.

23 UCP1 expression in pre-adipocytes and mature brown adipocytes.

24 a was located in the mitochondrial matrix in brown adipocytes.

25 and the BAF chromatin remodeling complex in brown adipocytes.

26 ing uncoupled respiration (thermogenesis) in brown adipocytes.

27 olarization by promoting potassium efflux in brown adipocytes.

28 tion-induced BAT-specific gene expression in brown adipocytes.

29 s an autocrine activator of Gq signalling in brown adipocytes.

30 PGC1alpha, COX8B and ATP5B in differentiated brown adipocytes.

31 enhances differentiation of human and murine brown adipocytes.

32 in NT-PGC-1alpha-expressing PGC-1alpha(-/-) brown adipocytes.

33 ased ex vivo adipogenic differentiation into brown adipocytes.

34 submaximal beta-adrenoceptor stimulation of brown adipocytes, a PDE3 inhibitor alone could potentiat

35 In differentiated brown adipocytes, activation of Wnt signaling suppresses

36 tures exist in rodents and humans: classical brown adipocytes and beige (also referred to as brite) a

37 Both classical brown adipocytes and brown-like beige adipocytes are con

38 5 precursors are not the exclusive source of brown adipocytes and contribute more to the mature white

39 We confirm expression of PD-L1 on brown adipocytes and demonstrate that signal intensity d

40 ng to URE1 of nuclear extracts from cultured brown adipocytes and from the brown adipose tissue of co

41 mRNA and protein were detectable in isolated brown adipocytes and gradually decreased during differen

42 Expression of the Ucp1 gene is unique in brown adipocytes and is regulated tightly.

43 ncoupling protein (UCP) is expressed only in brown adipocytes and is responsible for the unique therm

44 BAT development in mice at E15.5, with fewer brown adipocytes and lower mitochondrial protein compare

45 Brown adipocytes and muscle and dorsal dermis descend fr

46 ates the supply of active thyroid hormone to brown adipocytes and other D2-expressing cells.

47 These results suggest a role for VEGF in brown adipocytes and preadipocytes to promote survival,

48 regulation of mitochondrial transcription in brown adipocytes and provide new insight into the transc

49 Mitochondrial function was investigated in brown adipocytes and skeletal muscle in the mice.

50 that PPARgamma is a key regulatory factor in brown adipocytes and suggest that PPARgamma functions no

51 ay important roles in the differentiation of brown adipocytes and that the N terminus of IRS-1 is mor

52 ld during differentiation of cultured murine brown adipocytes and that VEGF receptor-2 is phosphoryla

53 duction of UCP1 and PGC-1alpha expression in brown adipocytes and the restoration of cold intolerance

54 ene signatures that were unique to classical brown adipocytes and to beige cells induced by a specifi

55 Rs) are expressed predominantly on white and brown adipocytes, and acute treatment of mice with CL 31

56 N303R/S332G) to activate ATGL in Cos7 cells, brown adipocytes, and artificial lipid droplets.

57 ells, interscapular brown adipose tissue for brown adipocytes, and ear mesenchymal stem cells for whi

58 and IRS-2 to aPKC activation in immortalized brown adipocytes, and further suggest that IRS-1 and IRS

59 that is mediated by cold-activated beige and brown adipocytes, and it entails increased uptake of car

60 ted exclusively by beta3-ARs in white and/or brown adipocytes, and that beta3-ARs in other tissue sit

61 beta 3-Adrenergic receptors are found on brown adipocytes, and treatment with beta 3-selective ag

62 g using anti-VEGFR2 antibody DC101 increased brown adipocyte apoptosis, as determined by cell number

63 soluble Flt1, resulted in 7-fold increase in brown adipocyte apoptosis, mitochondrial degeneration, a

64 Brown adipocytes are located in dedicated depots and exp

65 Brown adipocytes are located in specific deposits or can

66 While classical brown adipocytes are located mainly in dedicated BAT dep

67 chondrial respiration and heat production in brown adipocytes are the transcriptional coactivator PGC

68 ocytes convert into fat-oxidizing cells when brown adipocytes are unavailable, providing a compensato

69 Postnatal brown adipocytes arise from early muscle progenitors, bu

70 Current evidence indicates that brown adipocytes arise from Myf5(+) dermotomal precursor

71 Rodents possess two types of UCP-1 positive brown adipocytes arising from distinct developmental lin

72 re to nesfatin-1 promoted differentiation of brown adipocytes as revealed by a significant increase i

73 s accompanied by a corresponding increase in brown adipocytes as revealed by immunohistology with ant

74 r with respect to expression in white versus brown adipocytes as well as their ability to be stimulat

75 tion, apelin increases the basal activity of brown adipocytes, as evidenced by the increased PGC1alph

76 To understand the nature of adult human brown adipocytes at single cell resolution, we isolated

77 Adrenergic stimulation of brown adipocytes (BA) induces mitochondrial uncoupling,

78 Brown adipocytes (BAs) are specialized for adaptive ther

79 ed how cold stress induces the appearance of brown adipocytes (BAs) in brown and white adipose tissue

80 heat production as the signature function of brown adipocytes (BAs), particularly at the single cell

81 b1) and downstream targets including Ucp1 in brown adipocytes (BATs).

82 As early as 24 hours later, brown adipocytes began accumulating in the lesional area

83 ergically-stimulated membrane trafficking in brown adipocytes, but that ATP responses are initiated b

84 Activation of brown adipocytes by beta-AR agonism or 8-bromo-cyclic AM

85 VDU1, but not VDU2, is markedly increased in brown adipocytes by norepinephrine or cold exposure, fur

86 diHOME increased fatty acid (FA) uptake into brown adipocytes by promoting the translocation of the F

87 Loss of EHMT1 in brown adipocytes causes a severe loss of brown fat chara

88 expression of Prdm16, which determines beige/brown adipocyte cell fate.

89 carbon for de novo fatty acid synthesis in a brown adipocyte cell line.

90 hese proteins in more detail, we established brown adipocyte cell lines from wild type and various IR

91 f IRS-1 in adipocyte biology, we established brown adipocyte cell lines from wild-type and IRS-1 knoc

92 Attainment of a brown adipocyte cell phenotype in white adipocytes, with

93 antify fluxes in these pathways we incubated brown adipocyte cells in [U-(13)C]glutamine or [5-(13)C]

94 th mitochondrial biogenesis can increase the brown adipocyte character of white fat.

95 factor 2 (EBF2) is an essential mediator of brown adipocyte commitment and terminal differentiation.

96 it the greatest inducible capacity to become brown adipocytes compared with cells isolated from mesen

97 Task1(-/-)-mouse-derived brown adipocytes, compared with wild-type mouse-derived

98 Primary brown adipocyte cultures in vitro confirmed that miRNAs

99 distinct developmental lineages: "classical" brown adipocytes develop during the prenatal stage where

100 that, in absence of IL-33 or ST2, beige and brown adipocytes develop normally but fail to express an

101 n a cell-autonomous manner, independently of brown adipocyte development or differentiation.

102 Brown adipocyte development within white adipose tissue

103 ied miR-182 and miR-203 as new regulators of brown adipocyte development.

104 ctive signals that act in concert to specify brown adipocyte development.

105 markedly abolished the high level of UCP1 in brown adipocytes differentiated from the preadipocytes.

106 Finally, in brown adipocytes differentiated in culture, MLL4 identif

107 tyrosine kinase (SYK) is upregulated during brown adipocyte differentiation and activated by beta-ad

108 -specific miRNAs that are upregulated during brown adipocyte differentiation and enriched in brown fa

109 eveal an important role of BMP7 in promoting brown adipocyte differentiation and thermogenesis in viv

110 genesis has classically been associated with brown adipocyte differentiation and thermogenesis, our r

111 we report that apelin-APJ signaling promotes brown adipocyte differentiation by increasing the expres

112 body recognition studies identified distinct brown adipocyte differentiation stage-specific, NRRE-1-p

113 RT1-related transcriptional signature during brown adipocyte differentiation that may contribute to s

114 icroRNAs (miRNAs) as essential regulators of brown adipocyte differentiation, but whether miRNAs are

115 inding activities and MCAD expression during brown adipocyte differentiation, cardiac development, an

116 elineating the transcriptional regulation of brown adipocyte differentiation, cellular lineage specif

117 Whether BSCL2 directly participates in brown adipocyte differentiation, development, and functi

118 d in brown fat and markedly increased during brown adipocyte differentiation.

119 we explored the metabolic role of LRP130 in brown adipocyte differentiation.

120 criptional induction of the MCAD gene during brown adipocyte differentiation.

121 ontrol of a pivotal metabolic pathway during brown adipocyte differentiation.

122 enuated phosphorylation of S6K and S6 during brown adipocyte differentiation.

123 ow that BSCL2 expression is increased during brown adipocyte differentiation.

124 ic stimulation, and is down-regulated during brown adipocyte differentiation.

125 Brown adipocytes display phenotypic plasticity, as they

126 cytes, compared with wild-type mouse-derived brown adipocytes, displayed an impaired beta3-adrenergic

127 the authors show that PD-L1 is expressed on brown adipocytes, does not change upon BAT activation, a

128 in transcription that occur in interscapular brown adipocytes during development.

129 obese mice restored vascularity, ameliorated brown adipocyte dysfunction, and improved insulin sensit

130 ctivator (PGC) 1beta in PGC-1alpha-deficient brown adipocytes eliminated their response to hypoxia.

131 Enforced expression of SIRT3 in the HIB1B brown adipocytes enhances the expression of the uncoupli

132 Isolated UCP1 KO brown adipocytes exhibited defective induction of uncoup

133 e levels of TFAM expression, PGC-1alpha(-/-) brown adipocytes expressing NT-PGC-1alpha had higher exp

134 mtDNA-encoded ETC genes than PGC-1alpha(-/-) brown adipocytes expressing PGC-1alpha, suggesting a dir

135 Thus, Fabp3(-/-) brown adipocytes fail to oxidize exogenously supplied fa

136 induce human and mouse adipocytes to acquire brown adipocyte features, including a capacity for therm

137 rized, facilitating delivery of nutrients to brown adipocytes for heat production.

138 by which PRDM16, the principal regulator of brown adipocyte formation and function, can simultaneous

139 ntaining protein 16, a key factor present in brown adipocytes found in depots.

140 eta(3a)-AR displayed Galpha(i/o) coupling in brown adipocytes from caveolin-1 knock-out mice or in wi

141 To determine the differences between brown adipocytes from interscapular brown tissue (iBAT)

142 ranslocation was confirmed in differentiated brown adipocytes from perilipin null mice expressing an

143 r Them2 in heat production, cultured primary brown adipocytes from Them2(-/-) mice exhibited increase

144 KEY POINTS: Maternal high-fat diet impairs brown adipocyte function and correlates with obesity in

145 Maternal obesity impairs offspring brown adipocyte function and correlates with obesity in

146 xpression of Ucp1 and other genes regulating brown adipocyte function in response to beta-adrenergic

147 ies targeting cAMP/PKA signaling to regulate brown adipocyte function, viability, and metabolic homeo

148 ipose tissue differentiation, also regulates brown adipocyte function.

149 e is known about the factors involved in the brown adipocyte gene regulatory program.

150 Nat8l knockdown in brown adipocytes has no impact on cellular triglyceride

151 Transient brown adipocytes have been shown to be a critical regula

152 However, Lcn2(-/-) brown adipocytes have normal norepinephrine-stimulated p

153 Lcn2(-/-) differentiated brown adipocytes have significantly decreased expression

154 associated with mitochondrial abundance and brown adipocyte identity were increased, and basal lipol

155 ergic and insulin signaling systems in mouse brown adipocytes immortalized by SV40 T infection.

156 y weight, smaller fat stores, lipid-depleted brown adipocytes, improved glucose tolerance, and elevat

157 ordinately induced during differentiation of brown adipocytes in culture.

158 ocytes but differ from conventional white or brown adipocytes in decreased expression of genes involv

159 ture, in part through conversion of white to brown adipocytes in inguinal fat.

160 dipose tissue (WAT) are similar to classical brown adipocytes in that they can burn lipids to produce

161 Given the role of brown adipocytes in the enhancement of energy expenditur

162 Presently, we have used immortalized brown adipocytes in which either IRS-1 or IRS-2 has been

163 In brown adipocytes in which either IRS-1 or IRS-2 was knoc

164 Induction of brown adipocytes in white fat depots by adrenergic stimu

165 or ion and substrate cycling associated with brown adipocytes in white fat depots, are induced in UCP

166 identify genes controlling the induction of brown adipocytes in white fat tissues.

167 MP-dependent regulation of multiple genes in brown adipocytes, including Ucp1, occurred through the p

168 Compared with controls, Gpat4(-/-) brown adipocytes incorporated 33% less fatty acid into t

169 ctopic activation of type I IFN signaling in brown adipocytes induces mitochondrial dysfunction and r

170 was initiated to identify genes that control brown adipocyte induction in white fat depots in mice.

171 those with an enhanced capacity for Ucp1 and brown adipocyte induction in white fat preferentially lo

172 reveals that this UCP1 is in mitochondria of brown adipocytes interspersed between muscle bundles.

173 In contrast to the white adipocyte, the brown adipocyte is characterized by abundant mitochondri

174 8 mitogen-activated protein kinase (MAPK) in brown adipocytes is an indispensable step in the transcr

175 Brown adipocytes isolated from hypothyroid mice replaced

176 To test this hypothesis genetically, brown adipocytes lacking PDE3B were examined for their r

177 adipocytes, but rather a specialized form of brown adipocyte-like cells, which have a unique function

178 followed by a shift toward a more favorable, brown adipocyte-like metabolic state characterized by up

179 , nesfatin-1 promotes the differentiation of brown adipocytes likely through the mTOR dependent mecha

180 mitment of mesenchymal progenitor cells to a brown adipocyte lineage, and implantation of these cells

181 We identified Cox7a1, well-known as brown adipocyte marker gene, as a cold-responsive protei

182 se training also increases expression of the brown adipocyte marker uncoupling protein 1 (UCP1) in bo

183 IRS-1 appears to be an important mediator of brown adipocyte maturation.

184 provides further evidence for regulation of brown adipocyte metabolism by Wnt signaling.

185 thylase 1), a histone demethylase, regulates brown adipocyte metabolism in two ways.

186 to investigate the role of NT-PGC-1alpha in brown adipocyte mitochondria.

187 As seen in the brown adipocytes observed during HO in the mouse, these

188 P-r during cold stress may be to deplete the brown adipocyte of guanine nucleotides, converting them

189 ew tool for studying thermogenic function in brown adipocytes of both murine and human origins.

190 ly, transgenic re-expression of beta3-ARs in brown adipocytes only (BAT-mice) failed to rescue, in an

191 e and brown adipocytes (WAT+BAT-mice), or in brown adipocytes only (BAT-mice).

192 fold proteins of the JIP family expressed in brown adipocytes, only JIP2 co-immunoprecipitates p38alp

193 ue transcriptional regulators of the primary brown adipocyte phenotype are unknown, limiting our abil

194 T to take on a more-white rather than a more-brown adipocyte phenotype.

195 c nervous system is critical for maintaining brown adipocyte phenotypes in classic brown adipose tiss

196 Brown adipocytes play important roles in the regulation

197 Brown adipocytes produced lower amounts of hypoxia-induc

198 is a lipid droplet (LD)-protein enriched in brown adipocytes promoting the enlargement of LDs, which

199 Loss of DPF3 in brown adipocytes reduced chromatin accessibility at EBF2

200 or deletion of TSC1 decreased expression of brown adipocyte-related genes UCP1, UCP3, PGC1alpha and

201 quired for the feature maintenance of mature brown adipocytes remains unknown.

202 tch that determines lineage specification of brown adipocytes remains unknown.

203 the differentiation and lipid metabolism of brown adipocytes remains unknown.

204 Thus, differentiation of brown adipocytes requires a timed and regulated expressi

205 ta) while the normal sympathetic response of brown adipocytes requires TR alpha.

206 nectin and Pgc1alpha expression in white and brown adipocytes, respectively.

207 vestigated the mechanisms by which white and brown adipocytes respond to hypoxia.

208 beta-Adrenergic activation in brown adipocytes results in a dissociation of HDAC1 from

209 etyltransferase reporters in differentiating brown adipocytes revealed that a known nuclear receptor

210 Mice lacking insulin receptors in brown adipocytes show an age-dependent loss of interscap

211 Ucp1 was linked with an elevation of cAMP in brown adipocytes, similar to cold-exposed or fish oil-fe

212 PGC-1alpha and PGC-1alpha in PGC-1alpha(-/-) brown adipocytes similarly induced expression of nuclear

213 Surprisingly, we found that, in brown adipocytes, some NT-PGC-1alpha localizes to mitoch

214 -1.0 of the marine UCP gene is required for brown adipocyte-specific expression.

215 in obese individuals, and corrected impaired brown adipocyte-specific gene expression in white adipos

216 se tissue but also induces the expression of brown adipocyte-specific genes and proteins in white adi

217 esis due to the targeted inactivation of the brown adipocyte-specific mitochondrial uncoupling protei

218 itional factors in HIB-1B cells required for brown adipocyte-specific UCP expression.

219 , whereas activating Wnt signaling in mature brown adipocytes stimulates their conversion to white ad

220 T that developed consisted of SYK-expressing brown adipocytes that had escaped homozygous Syk deletio

221 a mice developed markedly enlarged white and brown adipocytes that were fully differentiated.

222 Therefore, in the brown adipocyte the recently described scaffold protein

223 In Dio2(-/-) brown adipocytes, the acute norepinephrine-, CL316,243-,

224 rom UCP1-based nonshivering thermogenesis in brown adipocytes, the identity of thermogenic mechanisms

225 s a direct transcriptional target of EBF2 in brown adipocytes, thereby establishing a regulatory modu

226 ucts can activate PPARalpha and PPARdelta in brown adipocytes, thereby expanding the oxidative capaci

227 at increased TRIP-Br2 significantly inhibits brown adipocytes thermogenesis.

228 Thus, HDAC1 negatively regulates the brown adipocyte thermogenic program, and inhibiting Hdac

229 te that HDAC1 is a negative regulator of the brown adipocyte thermogenic program.

230 uces premature activation of differentiating brown adipocytes through cyclic AMP (cAMP)/protein kinas

231 T development ultimately causes apoptosis of brown adipocytes through inflammation, resulting in BAT

232 l TASK1 controls the thermogenic activity in brown adipocytes through modulation of beta-adrenergic r

233 ofile G protein-coupled receptors (GPCRs) in brown adipocytes to identify druggable regulators of BAT

234 Cultured myotubes and primary brown adipocytes treated with a class I-specific HDAC in

235 hat obesity-induced inflammation upregulates brown adipocytes TRIP-Br2 expression via the ER stress p

236 Our results indicate that dynamics of brown adipocytes turnover during reversible transition f

237 represents a plausible explanation as to why brown adipocytes ultimately specialize in lipid cataboli

238 odels, we propose a model in which activated brown adipocytes use their intracellular triglyceride st

239 vates BAT, presumably by directly activating brown adipocytes via the PKA pathway, suggesting a novel

240 Mitochondrial uncoupling induced by NE in brown adipocytes was reduced by inhibition of mitochondr

241 enic re-expression of beta3-ARs in white and brown adipocytes (WAT+BAT-mice), demonstrating that each

242 3-ARs are expressed exclusively in white and brown adipocytes (WAT+BAT-mice), or in brown adipocytes

243 BP3 gain- and loss-of-function approaches in brown adipocytes, we detected a correlation between FABP

244 esis in vivo By deleting GR in precursors of brown adipocytes, we found unexpectedly that GR is dispe

245 Primary brown adipocytes were additionally examined for their bi

246 We found that brown adipocytes were smaller and exhibited profound del

247 toplasm to nuclear translocation of CRTC3 in brown adipocytes, where it recruits C/EBPbeta to enhance

248 r to fully induce UCP1 mRNA and lipolysis in brown adipocytes, whereas neither PDE inhibitor alone ha

249 BMPs in soft tissue stimulates production of brown adipocytes, which drive the early steps of heterot

250 e in knockout mice had increased features of brown adipocytes, which, along with an increase in norma

251 Treatment of primary brown adipocytes with CL or forskolin induced the expres

252 rses the attenuation of thermogenic genes in brown adipocytes with impaired respiratory capacity, whi

253 The treatment of differentiated T37i brown adipocytes with salsalate increased uncoupled resp

254 ological or genetic inhibition of HSL and in brown adipocytes with stable knockdown of ATGL.

255 bility to expand the number and activity of "brown adipocytes" within white fat depots.

256 ing protein 1 (UCP1), a definitive marker of brown adipocytes, within HO-containing tissues but not n

257 ulation of more and larger lipid droplets in brown adipocytes without impacting either mitochondrial