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 MA-marked progenitors appeared essential for beiging.

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

5 roduction of enkephalin peptides that elicit beiging.

6 ere evaluated: Swiss, BALB/c, C57BL/6, nude, beige, A/J, and GKO.

7 y genes and pathways that regulate brown and beige adipocyte biology have now been identified, provid

8 Thus, an increase in beige adipocyte content in WAT browning would raise ener

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

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

11 Stimulating beige adipocyte development, or WAT browning, increases

12 as a nuclear lncRNA that promotes brown and beige adipocyte differentiation and function.

13 found that KCNK3 and MTUS1 were required for beige adipocyte differentiation and thermogenic function

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

15 Beige adipocyte differentiation within white adipose tis

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

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

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

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

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

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

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

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

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

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

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

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

28 n classical brown fat but markedly inhibited beige adipocyte function in subcutaneous fat following c

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

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

31 ckout mice exhibit upregulated expression of beige adipocyte marker genes, particularly during an HFD

32 ure genes, including Ucp1 and Pgc1alpha, and beige adipocyte markers Tmem26 and CD137.

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

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

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

36 beiging characteristics, a phenomenon termed beige adipocyte renaissance.

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

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

39 inating from distinct progenitors, brown and beige adipocytes acquire remarkably similar molecular an

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

41 and functional characteristics of brown and beige adipocytes and discuss emerging questions, with a

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

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

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

45 th classical brown adipocytes and brown-like beige adipocytes are considered as promising therapeutic

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

47 These findings indicate that PRDM16 and beige adipocytes are required for the "browning" of whit

48 Brown and beige adipocytes are specialized cells that express unco

49 f BAT-selective genes and for development of beige adipocytes both in vitro and in vivo.

50 Beige adipocytes burn fat and dissipate the energy as he

51 Lsd1 maintains beige adipocytes by controlling the expression of peroxi

52 Beige adipocytes can form through de novo adipogenesis;

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

54 Brown and beige adipocytes combust nutrients for thermogenesis and

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

56 Brown and beige adipocytes convert chemical energy into heat throu

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

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

59 Moreover, beige adipocytes from AdKO IWAT displayed enhanced brown

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

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

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

63 onstrated that Lou/C animals express UCP1 in beige adipocytes in inguinal white adipose tissue (iWAT)

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

65 than miR-378 per se, suppresses formation of beige adipocytes in subcutaneous WAT.

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

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

68 Beige adipocytes in white adipose tissue (WAT) are simil

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

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

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

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

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

74 dedicated BAT depots of rodents and infants, beige adipocytes sporadically reside with white adipocyt

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

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

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

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

79 ble form of thermogenic adipocytes (that is, beige adipocytes).

80 ion of brown fat-specific genes in brown and beige adipocytes, although the underlying transcription-

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

82 ls in subcutaneous fat generate and activate beige adipocytes, producing thermogenesis.

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

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

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

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

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

88 he development of physiologically functional beige adipocytes.

89 c1 as a driver of thermogenesis in brown and beige adipocytes.

90 ates mature white adipocytes to convert into beige adipocytes.

91 fat deposits in adult humans are composed of beige adipocytes.

92 t appear to result in thermogenically active beige adipocytes.

93 tes in maintaining properties of preexisting beige adipocytes.

94 ntrols differentiation of preadipocytes into beige adipocytes.

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

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

97 d promotes preadipocyte differentiation into beige adipocytes.

98 stimulates UCP1-independent thermogenesis in beige adipocytes.

99 Nor did they express factors present in beige adipocytes.

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

101 However, "beige" adipocytes also exist in WAT.

102 he developmental origin of these "brite" or "beige" adipocytes is unclear.

103 nduced 'browning' of subcutaneous fat, most 'beige' adipocytes stem from de novo-differentiated adipo

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

105 t animals differentiated into brown-like (or beige) adipocytes.

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

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

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

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

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

111 ifferent beta-adrenergic receptors to induce beige adipogenesis.

112 ntegral feedback regulator of both white and beige adipogenic commitment and differentiation, and res

113 Beige adipose cells are a distinct and inducible type of

114 functional adaptations to cold of brown and beige adipose depots are examined using quantitative mit

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

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

117 Brown and beige adipose tissue is specialized for heat production

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

119 Cs) into lipid-accumulating, UCP1-expressing beige adipose tissue.

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

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

122 Thermogenic brown and beige adipose tissues dissipate chemical energy as heat,

123 Brown and beige adipose tissues have been identified as potential

124 ative and thermogenic functions in brown and beige adipose tissues modulate rates of energy expenditu

125 ect effects on adipocytes and elicitation of beige adipose.

126 atic lipid accumulation in HCV-infected SCID-beige/Alb-uPa mice.

127 s and humans: classical brown adipocytes and beige (also referred to as brite) adipocytes.

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

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

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

131 study identifies miR-34a as an inhibitor of beige and brown fat formation, providing a potential tar

132 2 protein (Nbeal2) belongs to the family of beige and Chediak-Higashi (BEACH) domain proteins.

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

134 th the vesicle trafficking-associated BEACH (Beige and Chediak-Higashi) domain protein family and by

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

136 e different functional domains of BEACH (for beige and human Chediak-Higashi syndrome) proteins, such

137 ad of severe combined immunodeficient (SCID)/Beige and nonobese diabetic (NOD)/SCID/IL-2gamma-recepto

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

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

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

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

142 We have used the beige (Bg) mouse, which is deficient in endosome biogene

143 letely abolished in the immunodeficient SCID/beige (bg) variant.

144 developmental shift from energy-dissipating beige (brite) adipocytes to energy-storing white adipocy

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

146 al muscle, and has alternatively been called beige, brite or inducible BAT.

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

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

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

150 Beige/brite adipocytes are induced within white adipose

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

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

153 cytes while suppressing differentiation into beige/brite adipocytes.

154 nd pre-adipocyte differentiation into mature beige/brite adipocytes.

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

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

157 ng protein-1 (characteristic of both BAT and beige/brite cells), this study did not show "browning" o

158 te that human BAT may be primary composed of beige/brite cells.

159 Brown and beige/brite fats generate heat via uncoupled respiration

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

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

162 ted the preadipocytes to assume an oxidative beige/brown adipose phenotype including markers of incre

163 white adipogenic differentiation reactivated beige/brown markers, suggesting that increased BMP4 pref

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

165 increased BMP4 preferentially regulates the beige/brown phenotype.

166 ulation of adipose tissue, white, brown, and beige, can potentially lead to the development of a new

167 ore, histological analyses showed that a new beige cell marker, CITED1, was selectively expressed in

168 regulated and secreted from muscle to induce beige cell markers and the browning of WAT in Mstn(-/-)

169 correlated with that of the newly identified beige cell-selective genes, but not with that of classic

170 early all the human BAT abundantly expressed beige cell-selective genes, but the expression of classi

171 of a newly discovered type of adipocyte, the beige cell.

172 s selectively expressed in the UCP1-positive beige cells as well as in human BAT.

173 Induction of beige cells causes the browning of white fat and improve

174 Beige cells have a gene expression pattern distinct from

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

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

177 ogy and transcriptional control of brown and beige cells in rodents and the state of current knowledg

178 yperinsulinemic clamps, suggesting a role of beige cells in this process.

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

180 unique to classical brown adipocytes and to beige cells induced by a specific PPARgamma agonist rosi

181 Beige cells resemble white fat cells in having extremely

182 Beige cells' inducible characteristics make them a promi

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

184 cible 'brown-like' adipocytes, also known as beige cells, develop in white fat in response to various

185 Here, we report the isolation of "beige" cells from murine white fat depots.

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

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

188 We found that neurons lacking the BEACH (beige-Chediak/Higashi) domain protein Neurobeachin (Nbea

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

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

191 e efferent circuit controlling biogenesis of beige fat and provide support for its targeting to treat

192 e IL-4Ralpha in PDGFRalpha(+) APs to promote beige fat biogenesis.

193 Classic brown fat and inducible beige fat both dissipate chemical energy in the form of

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

195 criptional mechanisms that control brown and beige fat cell development.

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

197 The activities of brown and beige fat cells reduce metabolic disease, including obes

198 White and beige fat cells respond to cool temperatures, but classi

199 P1(+) adipocytes, including the discovery of beige fat cells, a new thermogenic cell type.

200 escribed the cloning and characterization of beige fat cells, the thermogenic "brown-like" cells that

201 vation of both classical brown and inducible beige fat cells.

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

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

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

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

206 ent is the physiologic stimulus for inducing beige fat in mice and humans, the events that lead from

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

208 fficient to promote the growth of functional beige fat in thermoneutral mice.

209 The biogenesis of beige fat is poorly understood.

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

211 tion of IL-4 to thermoneutral mice increases beige fat mass and thermogenic capacity to ameliorate pr

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

213 om the sensing of cold to the development of beige fat remain poorly understood.

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

215 e depots, which express markers of brown and beige fat such as uncoupling protein 1 and transmembrane

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

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

218 and the expression of genes associated with beige fat thermogenesis and anti-inflammatory cytokines.

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

220 Here, we identify the efferent beige fat thermogenic circuit, consisting of eosinophils

221 derived ceramides, which directly compromise beige fat thermogenic function.

222 In murine beige fat, cold exposure stimulates mitochondrial creati

223 Beige fat, which expresses the thermogenic protein UCP1,

224 ion of miR-34a increased coexpression of the beige fat-specific marker CD137 and the browning marker

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

226 signaling impairs cold-induced biogenesis of beige fat.

227 rmogenic adipose tissue, also referred to as beige fat.

228 converts white fat into the more thermogenic beige fat.

229 t into the microbiota-fat signaling axis and beige-fat development in health and metabolic disease.

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

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

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

233 rowth of pancreatic tumors grafted into SCID-Beige immunocompromised mice.

234 te Ucp1 expression in vitro and that promote beiging in vivo.

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

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

237 IL-33-elicited ILC2s was sufficient to drive beiging independently of the adaptive immune system, eos

238 27 deficiency, lipopolysaccharide-responsive beige-like anchor (LRBA) deficiency, activated PI3KD syn

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

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

241 A truncating mutation in LPS-responsive beige-like anchor (LRBA), which abolished protein expres

242 mutation in the gene encoding LPS-responsive beige-like anchor (LRBA), which was previously implicate

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

244 coding the lipopolysaccharide-responsive and beige-like anchor protein) cause a syndrome of autoimmun

245 ation in LRBA (lipopolysaccharide responsive beige-like anchor protein).

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

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

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

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

250 creatic tumors and improved survival of SCID beige mice carrying A549 human lung tumors compared with

251 to newborn severe combined immunodeficiency-beige mice exposed to 90% O2 from birth; sham controls r

252 retards tumor growth in immunodeficient SCID/Beige mice following transplantation of primary tumor B

253 as few as 100 cells) injected s.c. into SCID/Beige mice formed tumors, and in one case, SKNBE(2)C iCS

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

255 ear skin of C57BL/6 and immunodeficient SCID/Beige mice resulted in tumor formation in only the latte

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

257 s infusion of CD19-targeted nTregs into SCID-Beige mice with systemic Raji tumors traffic to sites of

258 Xenotransplantation of SCID/Beige mice with U87 cells and GSDCs gave rise to tumors

259 7 infected severe combined immunodeficiency-beige mice, and the parasites did not recur in these imm

260 -231 xenograft growth and metastasis in SCID/beige mice, implicating a critical role for macrophages

261 to the liver of retrorsine (RS)-treated SCID/beige mice, naive hAECs differentiated into hepatocyte-l

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 cted SCID (severe combined immunodeficiency)-Beige mice.

265 hotopically implanted into the lungs of SCID-beige mice.

266 zoledronic acid proved highly toxic to SCID Beige mice.

267 mised SCID (severe combined immunodeficient)-Beige mice.

268 plantation into the cleared fat pads of SCID/Beige mice.

269 rs of severe combined immunodeficient (SCID)/beige mice.

270 taylorii to cause chronic infection in SCID/BEIGE mice.

271 rm tumors in severe combined immunodeficient-beige mice.

272 in a severe combined immunodeficient (SCID)/beige mouse host.

273 ety of T4 immunotherapy in vivo using a SCID beige mouse model.

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

275 ise training on mitochondrial function, the "beiging" of WAT, regulation of adipokines, metabolic eff

276 nic responses to diet and cold exposure and 'beiging' of white adipose tissue.

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

278 It is unclear, however, how beige or white adipose tissue contributes to brown fat t

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

280 s develop during the prenatal stage whereas "beige" or "brite" cells that reside in white adipose tis

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

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

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

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

285 robial mat communities referred to as black, beige, pink and button mats on the surfaces of the throm

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

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

288 issue homeostasis and promote adipose tissue beiging, protecting against obesity and metabolic dysfun

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

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

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

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

293 r model in Severe Combined Immune Deficiency-beige (SCID-bg) mice, should be attributed to the extrav

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

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

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

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

298 These two beiging triggers have been used interchangeably but whet

299 IL-33-induced beiging was dependent on ILC2s, and IL-33 treatment or t

300 of Tregs on CAR-modified T cells in the SCID-Beige xenotransplant model, we isolated, genetically tar