ライフサイエンスコーパス: beige

1 that are termed 'brite' (brown-in-white) or 'beige'.

2 track and manipulate beige progenitors and 'beiging'.

3 ther transient p53 inhibition can rescue WAT beiging.

4 MA-marked progenitors appeared essential for beiging.

5 ipocytes in scWAT, also known as browning or beiging.

6 re separate from the process of browning and beiging.

7 ilitated the increase of mitochondria during beiging.

8 keletal muscle, and cold acclimation induces beige adipocyte biogenesis in adipose tissue.

9 eratures early in life influence the mode of beige adipocyte biogenesis upon cold exposure later in l

10 in response to external cues by stimulating beige adipocyte biogenesis; however, the developmental o

11 Maternal resveratrol promotes beige adipocyte development in offspring white adipose t

12 Our model of human beige adipocyte development provides a new and scalable

13 a master transcriptional repressor of brown/beige adipocyte differentiation and thermogenesis, and p

14 s of the transcription factor Foxp1 in brown/beige adipocyte differentiation and thermogenesis.

15 Relevant human models for beige adipocyte differentiation are essential to impleme

16 g protein alpha as a regulator of glycolytic beige adipocyte differentiation through a myogenic inter

17 Beige adipocyte differentiation within white adipose tis

18 pression in mesenchymal stem cells decreases beige adipocyte differentiation, while increasing extrac

19 reveal that miR-327 targets FGF10 to prevent beige adipocyte differentiation.

20 l to track and manipulate beige progenitors, beige adipocyte formation and function.

21 moderate alcohol intake on thermogenic brown/beige adipocyte formation and glucose and lipid homeosta

22 ate alcohol intake induces thermogenic brown/beige adipocyte formation and promotes glucose and lipid

23 ine regulatory signaling loop that regulates beige adipocyte formation and suggests that the miR-327-

24 found that dietary resveratrol (RES) induces beige adipocyte formation in adult mice.

25 atal beige adipocytes inhibited cold-induced beige adipocyte formation in adult mice.

26 standing the molecular mechanisms regulating beige adipocyte formation may lead to the development of

27 Here, we found that cold-induced beige adipocyte formation requires Adrb1, not Adrb3, act

28 ion of a BMP7-ROCK signaling axis regulating beige adipocyte formation via control of the G-actin-reg

29 ate alcohol intake induces thermogenic brown/beige adipocyte formation via elevating retinoic acid si

30 ates distinct sets of genes during brown and beige adipocyte formation.

31 n enhances beta3-adrenergic-receptor-induced beige adipocyte formation.

32 mulating adipocytes, although an increase in beige adipocyte gene expression is observed.

33 ose tissue (WAT) increases the expression of beige adipocyte genes in the winter.

34 pose tissue origin can shift towards a brown/beige adipocyte phenotype.

35 use single-cell RNA sequencing to identify a beige adipocyte precursor cell that gives rise to thermo

36 arkers, including UCP1, increased numbers of beige adipocyte precursors, and expanded UCP1-expressing

37 Here we report that human brite/beige adipocyte progenitors proliferate in response to p

38 WAT aging in mice impairs cold-induced beige adipocyte recruitment (beiging), which has been at

39 ion sensitizes aged white adipose tissue for beige adipocyte recruitment by blocking mitophagy.

40 Furthermore, we demonstrated that beige adipocyte renaissance was governed by liver kinase

41 beiging characteristics, a phenomenon termed beige adipocyte renaissance.

42 Here we report a type of beige adipocyte that has a critical role in chronic cold

43 sympathetic nervous system drives brown and beige adipocyte thermogenesis through the release of nor

44 kin-33 is a critical controller of brown and beige adipocyte thermogenesis.

45 suppressed by cold and other stimulators of beige adipocyte thermogenesis.

46 is associated with diminished generation of beige adipocytes ('beige adipogenesis'), a thermogenic a

47 Human beige adipocytes (BAs) have potential utility for the de

48 We suggest a unified model in which beige adipocytes (UCP1(+) multilocular cells) in rodents

49 s in finely tuning the metabolic activity of beige adipocytes according to extracellular metabolic co

50 ired for efficient utilization of glucose by beige adipocytes activated by the canonical beta3-adrene

51 erant NOD-scid IL2rg(null) (NSG) mice, brite/beige adipocytes activated in vitro enhance systemic glu

52 ng with the appearance of multilocular brown/beige adipocytes and elevated thermogenic gene expressio

53 indicate that Gq signalling regulates brown/beige adipocytes and inhibition of Gq signalling may be

54 ate mapped into the majority of cold-induced beige adipocytes and SMA-marked progenitors appeared ess

55 t developmental origins of white, brown, and beige adipocytes and their role in metabolic physiology

56 Uncoupling protein 1(+) beige adipocytes are dynamically regulated by environmen

57 Brown and beige adipocytes are specialized cells that express unco

58 aled that the MCT1 is expressed in inducible beige adipocytes as the emergence of uncoupling protein

59 Lsd1 maintains beige adipocytes by controlling the expression of peroxi

60 Beige adipocytes can form through de novo adipogenesis;

61 agonist is sufficient to rescue the loss of beige adipocytes caused by Lsd1 ablation.

62 Brown and beige adipocytes combust nutrients for thermogenesis and

63 rmogenic function of uncoupling protein 1(+) beige adipocytes contributed to metabolic fitness in adi

64 Brown and beige adipocytes convert chemical energy into heat throu

65 Beige adipocytes depend on mitochondrial oxidative phosp

66 ise understanding of the cellular origins of beige adipocytes emanating in response to physiological

67 In vitro, beige adipocytes exhibit uncoupled mitochondrial respira

68 type 2 immune responses, licenses brown and beige adipocytes for uncoupled respiration.

69 In this study, we show that beige adipocytes formed postnatally in subcutaneous ingu

70 Moreover, beige adipocytes from AdKO IWAT displayed enhanced brown

71 gic receptor (beta3-AR) is observed in brown/beige adipocytes from both lines of mice.

72 icient protocol to generate functional human beige adipocytes from human induced pluripotent stem cel

73 Activation of thermogenic beige adipocytes has recently emerged as a promising the

74 Activated beige adipocytes have therapeutic potential due to their

75 Recent studies indicate the existence of beige adipocytes in adult humans, making this cell type

76 Here, we review the role of brown and beige adipocytes in lipoprotein metabolism and atheroscl

77 development and cold-induced recruitment of beige adipocytes in mammals.

78 fer our perspective on the natural origin of beige adipocytes in mice.

79 ion also inhibited the formation of juvenile beige adipocytes in the inguinal fat pad.

80 ronmental cold stimulates the recruitment of beige adipocytes in the white adipose tissue (WAT) of mi

81 ral reports have described the generation of beige adipocytes in vitro, their potential utility in ce

82 ter inform therapeutic strategies to recruit beige adipocytes in vivo.

83 ecruitment of uncoupling protein 1 (UCP1)(+) beige adipocytes in WAT, a process known as beiging or b

84 Id1 in BAT thermogenesis and programming of beige adipocytes in white adipose tissue (WAT).

85 e formation of uncoupling protein 1-positive beige adipocytes in white adipose tissue, and increased

86 Ablation of these postnatal beige adipocytes inhibited cold-induced beige adipocyte

87 standing mechanisms by which a population of beige adipocytes is increased in white adipose tissue (W

88 f TET1 in the thermogenic gene regulation of beige adipocytes is largely DNA demethylase-independent.

89 ate glycolytic beige fat, a subpopulation of beige adipocytes mediated by GABPalpha emerging in the a

90 n adult animals, peri-weaning development of beige adipocytes occurs in a temperature- and sympatheti

91 particular, with time, thermogenic-competent beige adipocytes progressively gain a white adipocyte mo

92 To date, the origin of beige adipocytes remains enigmatic.

93 Activation of energy-dissipating brown/beige adipocytes represents an attractive therapeutic st

94 Molecular profiling of beige adipocytes shows them to be similar to primary BAs

95 and energy-dissipating function mediated by beige adipocytes that express the uncoupling protein UCP

96 LE3 regulates thermogenic gene expression in beige adipocytes through inhibition of EBF2 transcriptio

97 ient to rescue the age-related transition of beige adipocytes to white adipocytes in vivo, whereas lo

98 ms controlling the age-related transition of beige adipocytes to white adipocytes remain unclear.

99 ls, uncoupling protein-1 (UCP1) in brown and beige adipocytes uncouples fatty acid oxidation from ATP

100 ntial of the SMA-tracked progenitors to form beige adipocytes was accompanied by an inability to main

101 cold exposure stimulates the recruitment of beige adipocytes within white adipose tissue.

102 ression, the role of lactate transporters on beige adipocytes' ongoing metabolic activity remains poo

103 ot entirely resemble either classic brown or beige adipocytes, but rather a specialized form of brown

104 tein used in several studies as a marker for beige adipocytes, showed elevated levels of thermogenic

105 of uncoupling protein 1 (UCP1) in brown and beige adipocytes, the principal sites for uncoupled resp

106 ipid mobilization and oxidation in brown and beige adipocytes, where the harnessed energy is dissipat

107 odents and humans; cold induces formation of beige adipocytes, whereas warm temperature and nutrient

108 Cold temperatures induce formation of beige adipocytes, which convert glucose and fatty acids

109 3) inhibits mitochondrial gene expression in beige adipocytes.

110 ates mature white adipocytes to convert into beige adipocytes.

111 tes in maintaining properties of preexisting beige adipocytes.

112 ntrols differentiation of preadipocytes into beige adipocytes.

113 enerate Adrb3-induced, but not cold-induced, beige adipocytes.

114 vascular (Acta2+) cells to form cold-induced beige adipocytes.

115 d promotes preadipocyte differentiation into beige adipocytes.

116 stimulates UCP1-independent thermogenesis in beige adipocytes.

117 Nor did they express factors present in beige adipocytes.

118 are necessary for development of functional beige adipocytes.

119 of the thermogenic gene program in brown and beige adipocytes.

120 s of thermogenic fat cells, termed brown and beige adipocytes.

121 ing, which feeds the oxidative metabolism of beige adipocytes.

122 e of this protein as a functional marker for beige adipocytes.

123 tes suggesting MCT1 as a marker of inducible beige adipocytes.

124 genic genes, including Ucp1 and Ppargc1a, in beige adipocytes.

125 olism in mitochondrial dynamics in brown and beige adipocytes.

126 ntrolling adaptive thermogenesis in brown or beige adipocytes.

127 ring white adipocytes to energy-catabolizing beige adipocytes.

128 umans, the presence of brite or beige (brite/beige) adipocytes is correlated with a lean, metabolical

129 pregnancy and lactation could promote brown/beige adipogenesis and protect against HFD-induced adipo

130 romal-vascular (SV) cells revealed increased beige adipogenesis associated with increased thermogenic

131 inflammation-driven inhibitory mechanism of beige adipogenesis in obesity that required direct adhes

132 d cycle of inflammation-driven impairment of beige adipogenesis in obesity.

133 ton dynamics contribute to the inhibition of beige adipogenesis in WAT, and also promotes age-related

134 resulted in elevated expression of UCP1 and beige adipogenesis of subcutaneous AT in obesity.

135 ipose progenitors, the effects of alcohol on beige adipogenesis were largely abolished.

136 diminished generation of beige adipocytes ('beige adipogenesis'), a thermogenic and energy-dissipati

137 redominantly from progenitors (i.e., de novo beige adipogenesis) upon the first exposure to cold temp

138 ifferent beta-adrenergic receptors to induce beige adipogenesis.

139 of PDGFRbeta also enhances white, brown, and beige adipogenesis.

140 commitment but not the maintenance phase of beige adipogenesis.

141 ase-2 is distinctively involved in brown and beige adipogenic differentiation.

142 tity during the differentiation of brown and beige adipogenic progenitors in mice.

143 hese molecules in modulating white and brown/beige adipogenic tissue development and activity.

144 eta3-AR agonist mirabegron, which stimulates beige adipose formation in subcutaneous white adipose ti

145 e identify arginine/creatine metabolism as a beige adipose signature and demonstrate that creatine en

146 The study of beige adipose tissue (BeAT) has recently gained populari

147 However, beige adipose tissue also develops during the peri-weani

148 ed a drug screening platform utilizing human beige adipose tissue and identified non-canonical activa

149 Brown adipose tissue (BAT) and beige adipose tissue combust fuels for heat production i

150 Increasing thermogenic brown and beige adipose tissue futile cycling may be an important

151 al and developmental regulation of brown and beige adipose tissue, as well as critical physiological

152 Brown and beige adipose tissues can catabolize stored energy to ge

153 Brown and beige adipose tissues can dissipate chemical energy as h

154 Brown and beige adipose tissues contain thermogenic fat cells that

155 Brown and beige adipose tissues have been identified as potential

156 s (ROS) initiates thermogenesis in brown and beige adipose tissues.

157 ect effects on adipocytes and elicitation of beige adipose.

158 We find that, in absence of IL-33 or ST2, beige and brown adipocytes develop normally but fail to

159 g process that is mediated by cold-activated beige and brown adipocytes, and it entails increased upt

160 gy-storing white adipocytes, and thermogenic beige and brown adipocytes.

161 uncoupling protein 1 (UCP1), a biomarker of beige and brown adipogenesis, remains unclear.

162 dministration of a beta3-agonist and reduces beige and brown adipose metabolic rate.

163 2 protein (Nbeal2) belongs to the family of beige and Chediak-Higashi (BEACH) domain proteins.

164 Here, we show that three types of Beige and Chediak-Higashi (BEACH)-domain proteins contri

165 ase 2A, and the yeast kinase TOR1) or BEACH (beige and Chediak-Higashi) domains.

166 ation of energy expenditure and promotion of beige and white fat activation.

167 energy expenditure and oxygen consumption in beige and white fat depots.

168 ntiated adipocytes restored cold-induced WAT beiging and augmented whole-body energy expenditure and

169 tophagy in aged white adipocytes impedes WAT beiging and may be therapeutically targeted to improve i

170 Tregs in female mice in promoting adipocyte beiging and thermogenesis in SAT, in part by slanting M2

171 treatment for 7 days increased SAT adipocyte beiging and thermogenic gene expression in male or femal

172 tures and then interconvert between "dormant beige" and "active beige" phenotypes (i.e., beige cell a

173 acid synthesis and oxidation in mouse brown, beige, and white adipose tissues; however, the cellular

174 Notably, CD81 is not only a beige APC marker but also required for de novo beige fat

175 This beige APC population is proliferative and marked by cell

176 a key sensor of external inputs and controls beige APC proliferation and whole-body energy homeostasi

177 2 types of thermogenic adipocytes, brown and beige, are thought to be of different origins but share

178 ine organ and site of lipid storage, whereas beige AT is primarily white but contains some cells that

179 the basis of its function as white, brown or beige (brite)(1).

180 In humans, the presence of brite or beige (brite/beige) adipocytes is correlated with a lean

181 s therefore drive the proliferation of human beige/brite adipocyte progenitors, and activated beige/b

182 ing protein UCP1 expression and expansion of beige/brite adipocytes (so-called browning) in white adi

183 characterized by the accumulation of Ucp1(+) beige/BRITE adipocytes (termed 'browning').

184 Beige/brite adipocytes are induced within white adipose

185 e/brite adipocyte progenitors, and activated beige/brite adipocytes can affect systemic glucose homeo

186 he mesenchymal progenitors that give rise to beige/brite adipocytes express a unique set of cytokines

187 ogeneity is a distinct property of activated beige/brite adipocytes that might be under epigenetic co

188 ABSTRACT: Promoting beige/brite adipogenesis and thermogenic activity is con

189 Because resulting beige/brite cells exhibit antiobesity and antidiabetic e

190 positive, which is a defining feature of the beige/brite phenotype, while displaying uncoupled respir

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

192 that BMAT adipocytes are not UCP1-expressing beige/brown adipocytes.

193 lted in the up-regulation of thermogenic and beige/brown markers (UCP1, PRDM16, ZIC-1 and TBX1) and i

194 white adipose differentiation inhibited the beige/brown markers, suggesting the presence of multipot

195 ssues of 28-wk-old (aged) mice with impaired beiging capability.

196 ded to visualize de novo adipogenesis versus beige cell activation in mice.

197 beige" and "active beige" phenotypes (i.e., beige cell activation) upon subsequent changes in enviro

198 Whether beige cells arise through de novo differentiation from r

199 , the intervention induced the appearance of beige cells in iWAT, associated with a marked increase i

200 tivation of UCP1 in ectopic tissues, such as beige cells in iWAT, may be an interesting therapeutic a

201 aging, associated with increased amounts of beige cells in subcutaneous white adipose tissue (sWAT)

202 rgy expenditure and the number of brown-like/beige cells in white adipose tissue (WAT).

203 the white adipose tissue (WAT; also known as beige cells), a process known as browning.

204 at the adult stage, but cold restored their beiging characteristics, a phenomenon termed beige adipo

205 through de novo adipogenesis; however, how "beiging" characteristics are maintained afterward is lar

206 ion and highlights a concomitant increase of beige differentiation marker and a decrease in extracell

207 bly but whether these two stimuli may induce beiging differently at cellular and molecular levels rem

208 ogical significance of the CHRNA2 pathway in beige fat biogenesis and energy homeostasis.

209 ige APC marker but also required for de novo beige fat biogenesis following cold exposure.

210 inal white adipose tissue concomitantly with beige fat cell decline.

211 ansition and identify Lsd1 as a regulator of beige fat cell maintenance.

212 anonical thermogenic mechanism through which beige fat controls whole-body energy homeostasis via Ca(

213 In the absence of UCP1, beige fat dynamically expends glucose through enhanced g

214 velopment and thermogenesis and cold-induced beige fat formation.

215 white adipose tissue is sufficient to induce beige fat gene expression in vivo.

216 e we show that the development of functional beige fat in the inguinal subcutaneous adipose tissue (i

217 This beige fat is distinct from conventional beige fat with r

218 (APs) and their subsequent commitment to the beige fat lineage.

219 BAT and beige fat oxidized fatty acids to fuel Ucp1-mediated the

220 These beige fat progenitors are marked by PDGFRalpha, Sca1, an

221 n factor EGR1 as a negative regulator of the beige fat program.

222 We recently identified a new beige fat regulatory pathway mediated via the nicotinic

223 mogenesis in brown fat; however, its role in beige fat remains unclear.

224 Beige fat serves as a substantial metabolic sink that di

225 Brown and beige fat share a remarkably similar transcriptional pro

226 st UCP1-independent thermogenic mechanism in beige fat that involves enhanced ATP-dependent Ca(2+) cy

227 t thermogenesis through the SERCA2b pathway; beige fat thereby functions as a 'glucose sink' and impr

228 hibition of SERCA2b impairs UCP1-independent beige fat thermogenesis in humans and mice as well as in

229 It has been suggested that beige fat thermogenesis is tightly controlled by epigene

230 Conversely, activation of BAT and beige fat through cold exposure suppressed alcoholic liv

231 This beige fat is distinct from conventional beige fat with respect to developmental origin and regul

232 hat CHRNA2 signaling may activate glycolytic beige fat, a subpopulation of beige adipocytes mediated

233 We therefore refer to it as glycolytic beige fat.

234 es of excised white, brown, and cold-induced beige fat.

235 he cell-intrinsic plasticity to give rise to beige fat.

236 nal acetyltransferase Naa10p, for harnessing beige-fat biogenesis and improving whole-body energy hom

237 strate that creatine enhances respiration in beige-fat mitochondria when ADP is limiting.

238 Beyond thermogenesis, brown and beige fats engage other metabolic tissues via secreted f

239 Lack of Id1 increases beige gene and Ucp1 expression in the WAT in response to

240 together with a number of BAT selective and beige gene markers.

241 ling in transcriptional control of brown and beige gene programs and illustrate a pituitary-adipose s

242 he hypothesis that mast cells promote SC WAT beiging in response to cold.

243 ent study, repeated cold application induced beiging in subcutaneous white adipose tissue (SC WAT) of

244 findings show that HFpEF is associated with beiging in white AT and with dysfunctional brown AT.

245 ytes from IIA+ mice were much more prone to "beiging," including increased expression of brown adipos

246 The antibody also causes profound beiging, increases cellular mitochondrial density, activ

247 inal white adipose tissues were subjected to beige induction, these cells showed a dramatic rise in m

248 LPS-Responsive-Beige-like Anchor (LRBA) is a PBW protein whose immune f

249 LPS-responsive beige-like anchor (LRBA) protein deficiency in humans ca

250 tients revealed an absence of LPS-responsive beige-like anchor (LRBA) protein expression, a known cau

251 LPS-responsive beige-like anchor protein (LRBA) and cytotoxic T lymphoc

252 s with severe presentation of LPS-responsive beige-like anchor protein (LRBA) deficiency, but long-te

253 )(oxP/loxP)), results in the accumulation of beige-like thermogenic adipocytes within multiple viscer

254 ascular mural cells tracked the cold-induced beige lineage.

255 ed with smaller adipocyte size and increased beiging markers (ucp-1, cidea, and eva) in white AT.

256 ouse model of chronic infection, 5 of 6 SCID/beige mice (83.3%) were cured after treatment with a sin

257 d uPA/severe combined immunodeficient (SCID)/beige mice challenged with HBV in vivo, immune induction

258 ction of chemically induced diabetes in SCID-Beige mice for 3 months.

259 SCID-beige mice injected via the tail vein with ERK clones we

260 t murine hosts and could only form tumors in beige mice lacking NK cells.

261 Hypothyroidism was generated in SCID-beige mice using an iodine-deficient diet containing 0.1

262 In streptozotocin-induced diabetic SCID/beige mice, the injection of 750 rat islet equivalents e

263 In this study, using Lyst-mutant beige mice, we show that lysosomal trafficking regulator

264 orly vascularized subcutaneous space of SCID-Beige mice.

265 l aorta of a severe combined immunodeficient Beige mouse model supports normal blood flow and vessel

266 on, (d) adipocyte apoptosis, (e) browning or beiging of adipose tissue, and (f) energy metabolism.

267 press beta3-ARs, these data suggest that the beiging of SC WAT by mirabegron reduces adipose tissue d

268 2 in adipocytes are mediated by the browning/beiging of white adipose tissue.

269 cting downstream PGC1alpha levels leading to beiging of white fat.

270 bcutaneous transplantation of skin into SCID/beige or athymic nude mice at 2 independent sites.

271 rmation of these cells, alternatively called beige or brite adipocytes, are incompletely understood.

272 beige adipocytes in WAT, a process known as beiging or browning that regulates caloric expenditure.

273 e, muscle and mural lineages, three proposed beige origins.

274 is very important in the development of the beige phenotype and activation of its thermogenic progra

275 iR-327 to WATs significantly compromises the beige phenotype and thermogenesis.

276 gulates UCP1 expression and acquisition of a beige phenotype in differentiated mouse WAT-PDGFR-alpha(

277 n differentiated SV cells reproduced the pro-beige phenotype of ROCK2(+/-) SV cells.

278 rconvert between "dormant beige" and "active beige" phenotypes (i.e., beige cell activation) upon sub

279 etic tools to fate map, track and manipulate beige progenitors and 'beiging'.

280 d mice may be useful to track and manipulate beige progenitors, beige adipocyte formation and functio

281 adipocytes is causative of age-impaired WAT beiging remains unknown.

282 We studied the seasonal beiging response in SC WAT from lean humans.

283 and are an important immune cell type in the beiging response of WAT.

284 ber of immune mediators are important in the beiging response.

285 lly, two stimuli have been used to trigger a beiging response: cold temperatures and beta3-adrenergic

286 Taken together, TET1 is a potent beige-selective epigenetic breaker of the thermogenic ge

287 Subjects with the most SC WAT beiging showed the greatest improvement in beta cell fun

288 adipocytes are insulin sensitive and display beige-specific markers and functional properties, includ

289 pes of adipose tissue (AT)-brown, white, and beige-that differ with stage of development, species, an

290 The transcriptomic signature of "brite/beige" thermogenic adipocytes reveals mechanisms for iro

291 While lactate is known to induce beiging through the regulation of Ucp1 gene expression,

292 , suggesting that mast cells promote adipose beiging through the release of histamine or other produc

293 to the mechanism controlling the age-related beige-to-white adipocyte transition and identify Lsd1 as

294 tissue morphology, glucose homeostasis, and beige-to-white adipocyte transition were unaffected in v

295 gical blockade of PDGFR-alpha impair the WAT-beige transition.

296 These two beiging triggers have been used interchangeably but whet

297 Cold exposure decreased p53 in beiging WAT of young mice but not in aged mice.

298 ically, cold exposure repressed autophagy in beiging WAT of young mice yet increased autophagy in age

299 To identify factors that promote or inhibit beiging, we performed multiplex analysis of gene express

300 rs cold-induced beige adipocyte recruitment (beiging), which has been attributed to the senescence of