ライフサイエンスコーパス: brown adipocyte

1 PGC1alpha, COX8B and ATP5B in differentiated brown adipocytes.

2 enhances differentiation of human and murine brown adipocytes.

3 white adipocytes, and thermogenic beige and brown adipocytes.

4 ced overactivation of catabolic responses in brown adipocytes.

5 ased ex vivo adipogenic differentiation into brown adipocytes.

6 equired for marker gene expression in mature brown adipocytes.

7 nd promoted lipolysis in T37i differentiated brown adipocytes.

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

9 cantly stimulate p38 MAPK phosphorylation in brown adipocytes.

10 ficiency reduces the thermogenic activity of brown adipocytes.

11 ll markers and uniformly differentiated into brown adipocytes.

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

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

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

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

16 elopment of adipose tissue containing mostly brown adipocytes.

17 and KLF15 expression in both mouse and human brown adipocytes.

18 e and Opn3-dependent molecular signatures in brown adipocytes.

19 s in either MEF adipocytes or differentiated brown adipocytes.

20 ipocytes, while increasing these measures in brown adipocytes.

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

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

23 ce could be fully differentiated into mature brown adipocytes.

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

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

26 t screen of nearly 12,000 compounds in mouse brown adipocytes.

27 rmally responsive to adrenergic signaling in brown adipocytes.

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

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

30 ghts into the regulation of thermogenesis by brown adipocytes.

31 b-a protein that lacks a signal peptide-from brown adipocytes.

32 MAT adipocytes are not UCP1-expressing beige/brown adipocytes.

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

34 ), lipids shown to activate thermogenesis in brown adipocytes.

35 , oxidative metabolism, and thermogenesis in brown adipocytes.

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

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

38 isoproterenol treatments of BAT and primary brown adipocytes.

39 and the BAF chromatin remodeling complex in brown adipocytes.

40 ing uncoupled respiration (thermogenesis) in brown adipocytes.

41 olarization by promoting potassium efflux in brown adipocytes.

42 mia due to exaggerated catabolic activity in brown adipocytes.

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

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

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

46 In differentiated brown adipocytes, activation of Wnt signaling suppresses

47 Evidence in mature brown adipocytes also suggests mTORC2 acts through ACLY

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

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

50 5 precursors are not the exclusive source of brown adipocytes and contribute more to the mature white

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

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

53 (including un-coupled respiration) in mouse brown adipocytes and human brown and white adipocytes.

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

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

56 nificantly reduced differentiation of murine brown adipocytes and mitochondrial biogenesis and respir

57 Brown adipocytes and muscle and dorsal dermis descend fr

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

75 ORC2 substrates; however, deleting Rictor in brown adipocytes appears to drive lipid catabolism by pr

76 It was presumed that brown adipocytes are composed of a homogeneous cell popu

77 Brown adipocytes are located in dedicated depots and exp

78 Brown adipocytes are located in specific deposits or can

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

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

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

82 Postnatal brown adipocytes arise from early muscle progenitors, bu

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

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

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

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

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

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

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

90 Adrenergic stimulation of NCLX-null brown adipocytes (BA) induces a profound mitochondrial C

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

92 Brown adipocytes (BAs) are a potential cell source for t

93 Brown adipocytes (BAs) are specialized for adaptive ther

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

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

96 By analyzing the developmental dynamics of brown adipocytes (BAs), we found that BAs size enlargeme

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

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

99 BCL6) as a critical regulator of dormancy in brown adipocytes but not for their commitment, different

100 eity, not only differences between white and brown adipocytes, but also differences in white adipose

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

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

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

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

105 understanding the pathophysiological role of brown adipocytes can provide effective strategies deline

106 Brown adipocytes carrying a defective mutation in Opn3's

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

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

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

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

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

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

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

114 s3 on isoproterenol (ISO)-treated 3T3-L1 and brown adipocyte cells.

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

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

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

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

119 ose uptake and efficiently promotes white-to-brown adipocyte conversion.

120 At the cellular level, Opn3-KO brown adipocytes cultured in darkness had decreased gluc

121 Primary brown adipocyte cultures in vitro confirmed that miRNAs

122 Conversely, addition of 3-HIB to white and brown adipocyte cultures increases fatty acid uptake and

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

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

125 These data provide a roadmap for brown adipocyte development and indicate that BAs genera

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

127 Brown adipocyte development within white adipose tissue

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

150 that LSD2 functions during earlier phases of brown adipocyte differentiation.

151 Brown adipocytes display phenotypic plasticity, as they

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

153 Brown adipocytes dissipating energy as heat have emergin

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

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

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

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

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

159 Isolated UCP1 KO brown adipocytes exhibited defective induction of uncoup

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

182 isolated and expanded to generate autologous brown adipocyte implants.

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

184 Stress-inducible IL-6 is produced from brown adipocytes in a beta-3-adrenergic-receptor-depende

185 ordinately induced during differentiation of brown adipocytes in culture.

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

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

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

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

190 stinct characteristics from the conventional brown adipocytes in their molecular signature, regulatio

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

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

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

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

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

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

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

198 abeling experiments, we found that activated brown adipocytes increased labeling of pyruvate and TCA

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

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

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

202 he essential mTORC2 subunit Rictor in murine brown adipocytes inhibits de novo lipid synthesis, promo

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

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

205 8 mitogen-activated protein kinase (MAPK) in brown adipocytes is an indispensable step in the transcr

206 However, the transplantation of brown adipocytes is currently impeded by poor efficiency

207 Brown adipocytes isolated from hypothyroid mice replaced

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

209 phic "megamitochondria" with altered MAMs in brown adipocytes lacking the Sel1L-Hrd1 protein complex

210 ogenesis, as conditional deletion of Mpc1 in brown adipocytes leads to impaired cold adaptation.

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

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

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

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

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

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

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

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

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

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

221 In brown adipocytes, mTORC2 regulates glucose and lipid met

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

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

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

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

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

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

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

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

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

231 Brown adipocytes play important roles in the regulation

232 Brown adipocytes produced lower amounts of hypoxia-induc

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

234 Brown adipocytes provide a metabolic defense against env

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

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

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

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

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

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

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

242 nin 3beta, and forced expression of S100b in brown adipocytes rescues the defective sympathetic inner

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

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

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

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

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

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

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

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

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

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

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

254 bosyltransferase (Nampt) knockout (ANKO) and brown adipocyte-specific Nampt knockout (BANKO) mice bec

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

256 previously uncharacterized subpopulation of brown adipocytes that display distinct characteristics f

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

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

259 mitochondria-enriched thermogenic fat cells (brown adipocytes) that play a crucial role in the regula

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

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

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

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

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

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

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

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

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

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

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

271 hanistically, BCL6 remodels the epigenome of brown adipocytes to enforce brown and oppose white adipo

272 Although dormancy is a regulated response in brown adipocytes to environmental warmth, its transcript

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

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

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

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

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

278 During differentiation, both white and brown adipocytes upregulate BCAA utilization and release

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

280 cell-autonomous, light-sensing mechanism in brown adipocytes via Opn3-GPCR signaling that can regula

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

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

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

284 3-ARs are expressed exclusively in white and brown adipocytes (WAT+BAT-mice), or in brown adipocytes

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

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

287 Based on the developmental dynamics of brown adipocytes, we propose that the murine iBAT has tw

288 Primary brown adipocytes were additionally examined for their bi

289 Mice with ERAD deficiency in brown adipocytes were cold sensitive and exhibited mitoc

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

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

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

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

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

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

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

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

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

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

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

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