ライフサイエンスコーパス: adipocyte

1 This impairs insulin signaling in adipocytes.

2 e brown adipocytes and human brown and white adipocytes.

3 d by pharmacological inhibition in mammalian adipocytes.

4 adipocytes, and thermogenic beige and brown adipocytes.

5 nic fibroblasts (MEFs) after reprograming to adipocytes.

6 -type ES cells are the only source of mature adipocytes.

7 enesis, a process carried out by thermogenic adipocytes.

8 eractivation of catabolic responses in brown adipocytes.

9 tion did not prevent the formation of mature adipocytes.

10 more abundant in differentiated, thermogenic adipocytes.

11 ced by modulators of cAMP levels in isolated adipocytes.

12 last functions and promote browning of white adipocytes.

13 ls (MSCs), which can also differentiate into adipocytes.

14 king functional G(i) proteins selectively in adipocytes.

15 required for recycling of lipids released by adipocytes.

16 n AMPK-mediated signaling in both muscle and adipocytes.

17 enesis and robust expression in mature human adipocytes.

18 hich feeds the oxidative metabolism of beige adipocytes.

19 cts in mouse RAW264.7 macrophages and 3T3-L1 adipocytes.

20 e observed with mice lacking P2Y(6)R only in adipocytes.

21 scued HSPC mobilization, but it increased BM adipocytes.

22 litazone failed to downregulate Cxcl12 in BM adipocytes.

23 F15 expression in both mouse and human brown adipocytes.

24 cular bone with age without change in marrow adipocytes.

25 t two distinct classes of subcutaneous white adipocytes.

26 Opn3-dependent molecular signatures in brown adipocytes.

27 y and triggers Ca(2+) cycling selectively in adipocytes.

28 that drive transcriptional reprogramming in adipocytes.

29 ggesting MCT1 as a marker of inducible beige adipocytes.

30 elevant cell types, namely preadipocytes and adipocytes.

31 ling in mature osteoblasts, osteoclasts, and adipocytes.

32 confirmed by biochemical assays in mammalian adipocytes.

33 ids shown to activate thermogenesis in brown adipocytes.

34 rentiation of 3T3-L1 murine fibroblasts into adipocytes.

35 nses in ovarian cancer cells cocultured with adipocytes.

36 ly increase RSPO3 expression in subcutaneous adipocytes.

37 hat integrates functional mature human white adipocytes.

38 oterenol treatments of BAT and primary brown adipocytes.

39 ells, but not in perivascular adipose tissue adipocytes.

40 e to exaggerated catabolic activity in brown adipocytes.

41 cells cocultured with primary human omental adipocytes.

42 ecessary for development of functional beige adipocytes.

43 inely tuning the metabolic activity of beige adipocytes according to extracellular metabolic conditio

44 or efficient utilization of glucose by beige adipocytes activated by the canonical beta3-adrenergic s

45 idomic, and genetic experiments in mice that adipocytes adjacent to skin injury initiate lipid releas

46 ght to determine how STAT1 activity in white adipocytes affects insulin sensitivity.

47 shift toward an increased number of smaller adipocytes, along with an improved adipogenic potential.

48 The marrow adipocyte also has an endocrine role in whole body homeo

49 Evidence in mature brown adipocytes also suggests mTORC2 acts through ACLY to inc

50 gle-cell RNA sequencing revealed that dermal adipocytes alter their fate and generate ECM-producing m

51 Adipocytes and adipose tissue derived cells have been in

52 tegravir and raltegravir can directly impact adipocytes and adipose tissue.

53 Using primary rat adipocytes and cultured 3T3-L1 adipocytes, we observed t

54 egulation of mitochondrial activity in mouse adipocytes and fly fat bodies with downregulated PI3K, w

55 lammatory features in both myeloid cells and adipocytes and hint at an underappreciated contribution

56 uding un-coupled respiration) in mouse brown adipocytes and human brown and white adipocytes.

57 ished obese adipose tissue leads to enlarged adipocytes and increased body weights in transgenic mice

58 ith reduced lower-body fat, enlarged gluteal adipocytes and insulin resistance.

59 lls) to a noncanonical trans-signaling mode (adipocytes and muscle) with increased expression of the

60 ith primary cultures of differentiated human adipocytes and muscle.RESULTSThe clinical effects of mir

61 F9, as potent inducers of UCP1 expression in adipocytes and preadipocytes.

62 e, adiponectin, is secreted by primary mouse adipocytes and protects fibroblasts from radiation-induc

63 t, we review the extensive crosstalk between adipocytes and resident innate immune cells as well as t

64 -inducible genetic lineage tracing of mature adipocytes and single-cell RNA sequencing revealed that

65 Functional validation in human adipocytes and skeletal muscle cells (SKMCs) confirmed t

66 1(high) While TRAIL was equally expressed in adipocytes and stromal vascular fraction (SVF), TL1A was

67 rstanding of both the heterogeneity of white adipocytes and their link to normal metabolism and disea

68 n downstream of autocrine FGF21 expressed by adipocytes and upstream of endocrine FGF21 expressed by

69 e uptake and oxidative catabolism in primary adipocytes and white adipose tissue of nitrate-treated r

70 At the same time, data in endothelial cells, adipocytes, and elsewhere suggest BETs also help regulat

71 te that generated osteoblasts, chondrocytes, adipocytes, and macrophages.

72 re adipogenic and differentiated into mature adipocytes, and the deletion of Pdgfra in developmental

73 ee distinct cell types: energy-storing white adipocytes, and thermogenic beige and brown adipocytes.

74 BM adipocytes are another source of CXCL12 that blunts mobi

75 It was presumed that brown adipocytes are composed of a homogeneous cell population

76 Adipocytes are critical for ovarian cancer cells to home

77 Adipocytes are the primary parenchymal cell type in adip

78 to investigate the relationship between mean adipocyte area and obesity-related traits, and identify

79 After meta-analysis, we found that mean adipocyte area positively correlated with body mass inde

80 id accumulation in adipose stem cells and/or adipocytes as observed in vivo.

81 hat the MCT1 is expressed in inducible beige adipocytes as the emergence of uncoupling protein 1 afte

82 subset possessed a lower-level expression of adipocyte-associated genes and significantly over 100-fo

83 at promotes the differentiation of MSCs into adipocytes at the expense of osteoblasts.

84 al adipose tissue lipolysis independently of adipocyte-autonomous ATGL, and thereby worsen organ fail

85 ysfunction upon dietary challenges caused by adipocyte-autonomous regulation in vivo.

86 ohol-induced adipose atrophy and how altered adipocyte autophagy contributes to alcohol-induced liver

87 Human beige adipocytes (BAs) have potential utility for the developm

88 nalyzing the developmental dynamics of brown adipocytes (BAs), we found that BAs size enlargement par

89 nt role of Tregs in female mice in promoting adipocyte beiging and thermogenesis in SAT, in part by s

90 CL treatment for 7 days increased SAT adipocyte beiging and thermogenic gene expression in mal

91 Here, we show that MCP-1 produced by omental adipocytes binding to its cognate receptor CCR-2 on ovar

92 sponse to external cues by stimulating beige adipocyte biogenesis; however, the developmental origin

93 rkers related to intermediary metabolism and adipocyte biology (fatty acid binding protein-4 and grow

94 5c contributes to male/female differences in adipocyte biology and highlight X-escape genes as a crit

95 Bone marrow adipocytes (BMAd) have recently been implicated in accel

96 gonism desensitizes GIPR activity in primary adipocytes, both differentiated in vitro and adipose tis

97 dipose tissue dysfunction affecting not only adipocytes but also immune cell function.

98 ipose tissue during pancreatitis and entered adipocytes by multiple mechanisms, hydrolyzing adipose t

99 KBTBD2 maintains insulin sensitivity in adipocytes by restricting the abundance of p85alpha.

100 eath Bcl-2 family member, and activation and adipocyte cell death both in vitro and in vivo Here, we

101 e costly techniques have focused on damaging adipocyte cell membranes, hydrolyzing triglycerides (TGs

102 and identify genetic factors associated with adipocyte cell size.

103 iple myeloma and in vitro using myeloma cell-adipocyte cocultures.

104 oxidant stress, but expression of NaKtide in adipocytes completely prevented the worsening.

105 These data suggest that the redox state of adipocytes controls the development of uremic cardiomyop

106 A group of cells that can become adipocytes controls the formation of blood vessels in th

107 aling, but sustained Cxcl12 expression by BM adipocytes could limit full recovery of HSPC mobilizatio

108 Adipocyte culture yielded the same conclusion.

109 At the cellular level, Opn3-KO brown adipocytes cultured in darkness had decreased glucose up

110 ersely, addition of 3-HIB to white and brown adipocyte cultures increases fatty acid uptake and modul

111 ne creates localized pH gradients that drive adipocyte death and saponification of TGs.

112 Mechanistically, we found evidence that adipocyte death triggered MGC formation.

113 Furthermore, mature dermal adipocytes dedifferentiate into migratory extracellularm

114 l a complex structure with distinct types of adipocyte, depot-specific differences, a biologically si

115 In this study, luciferase expressing human adipocyte derived stem cells (ADSC) were labelled with g

116 The adipocyte-derived hormone adiponectin has a broad spectr

117 Leptin is an adipocyte-derived hormone with pleiotropic functions aff

118 y gland biology is emerging, but the role of adipocyte-derived lipids in tissue homeostasis and repai

119 However, how seipin regulates adipocyte development and function remains incompletely

120 These data provide a roadmap for brown adipocyte development and indicate that BAs generated fr

121 ARgamma) is a nuclear receptor essential for adipocyte development and the maintenance of the alterna

122 Adipocyte DICER is required for whole-body metabolic ada

123 vity were assessed in human proliferating or adipocyte-differentiated adipose stem cells after long-t

124 lar matrix remodeling, which is critical for adipocyte differentiation and adipose tissue expansion.

125 FAM13A expression, which in turn, regulates adipocyte differentiation and contribute to changes in b

126 ed to impaired induction of early markers of adipocyte differentiation in cultured cells.

127 Adipocyte differentiation is driven by waves of transcri

128 mediators was increased, whereas markers of adipocyte differentiation were decreased.

129 annexin A3 (AnxA3), a negative regulator of adipocyte differentiation, is down-regulated in RCC and

130 To study the role of beta-actin in adipocyte differentiation, we conducted RNA sequencing o

131 y (ATAC-Seq), gene expression (RNA-Seq), and adipocyte differentiation.

132 In this study, we demonstrated that 3T3L1 adipocytes differentiation increased ROS and protein S-g

133 These new insights into adipocyte-driven IR may assist development of AT-targete

134 Adipocyte dysfunction links obesity to insulin resistanc

135 sts of immune cells, fibroblasts, pericytes, adipocytes, endothelial and neuronal cells, and the extr

136 -canonical p53 function in the regulation of adipocyte energy homeostasis and indicate that the dysre

137 Last, serum sex hormone and adipocyte estrogen/testosterone receptor expression prof

138 In vitro, beige adipocytes exhibit uncoupled mitochondrial respiration a

139 decrease in adipogenesis, and the resulting adipocytes exhibited lower accumulation of lipid droplet

140 ipogenic induction, both male and female MFR adipocytes exhibited lower PPARgamma, ADRP, and adiponec

141 ion, we found that, unlike other cell types, adipocytes expressed mRNA efficiently at 4 and 24 h afte

142 posure stimulates the formation of brownlike adipocytes expressing UCP1 (uncoupling-protein-1) in sub

143 Adipocyte-extrinsic insulin resistance was observed in l

144 s of KBTBD2 in adipocytes, some features are adipocyte-extrinsic.

145 d on the acquisition of a novel capacity for adipocyte FAO in a background of extant UCP1.

146 Besides cytoplasmic lipase-dependent adipocyte fat mobilization, the metabolic role of lysoso

147 metabolomics documented that 5-PAHSA primes adipocytes for glucose metabolism in a different way fro

148 We show that the isolated adipocyte fraction, but not the total undigested adipose

149 oaches; CellProfiler, Adiposoft and floating adipocytes fractions, all run blindly on two external co

150 activity of Tregs reduced or disappeared in adipocytes from eWAT or gWAT.

151 -R mRNA expression in subcutaneous abdominal adipocytes from subjects treated with pioglitazone.

152 which correlates with impacts on thermogenic adipocyte function and presumably other biological proce

153 Adipocyte function in regulating bone marrow, skin, musc

154 ardiac physiology, neuronal development, and adipocyte function.

155 Our data support the concept that adipocyte G(i) signaling is essential for maintaining eu

156 Drug-mediated activation of adipocyte G(i) signaling may prove beneficial for restor

157 In addition, multiple myeloma cells altered adipocyte gene expression and cytokine secretory profile

158 herapy on GIP-mediated insulin secretion and adipocyte GIP-R expression in subjects with well-control

159 ht gain in DIO mice, demonstrating a role of adipocyte GIPR in the regulation of adiposity in vivo.

160 IFNbeta-sensing promotes adipocyte glycolysis, while glycolysis inhibition impede

161 activation of G(i) signaling selectively in adipocytes greatly improved glucose homeostasis and insu

162 of HIV proteins and antiretroviral agents on adipocyte health, genetic factors, increased microbial t

163 ion of the type I IFN axis and activation of adipocyte IFNAR signaling contributes to obesity-associa

164 ose tissue reduces expression of TGFbeta1 in adipocytes, impairs local sympathetic innervation and ca

165 Subcutaneous adipocytes in KO mice show a size distribution shift tow

166 opment and cold-induced recruitment of beige adipocytes in mammals.

167 We identify a rare subpopulation of adipocytes in mice that increases in abundance at higher

168 t MGCs are specialized for clearance of dead adipocytes in obesity.

169 studies have shown that Lcn2 is secreted by adipocytes in response to inflammation and is categorize

170 recursor cell that gives rise to thermogenic adipocytes in subcutaneous adipose tissue.

171 ; average R2 across cohorts = 0.49) and that adipocytes in subcutaneous depots are larger than their

172 bers of osteoblasts, osteoclasts, and marrow adipocytes in Tg mice, suggesting independence of EPO si

173 tal cold stimulates the recruitment of beige adipocytes in the white adipose tissue (WAT) of mice and

174 heal by regenerating new hair follicles and adipocytes in their center.

175 characteristics from the conventional brown adipocytes in their molecular signature, regulation, and

176 Mechanistically, RBP4 treatment of human adipocytes in vitro directly stimulated basal lipolysis.

177 we have demonstrated this mechanism in human adipocytes in vitro, and correlations from our flux stud

178 ports have described the generation of beige adipocytes in vitro, their potential utility in cell the

179 ue exhibit reduced bone and increased marrow adipocytes; in contrast, transgenic mice (Tg) with osteo

180 It has been known adipocytes increase p53 expression and activity in obesi

181 partially by inhibiting MCP-1 secretion from adipocytes independent of direct effects on cancer cells

182 hint at an underappreciated contribution of adipocyte inflammation in disease pathogenesis.

183 ysis inhibition impeded IFNbeta-driven intra-adipocyte inflammation.

184 Mechanisms regulating adipocyte inflammatory potential and consequent impact o

185 FN)/IFNalpha receptor (IFNAR) axis amplifies adipocyte inflammatory vigor and uncovers dormant gene e

186 It is essential to elucidate brain-adipocyte interactions in order to tackle obesity and it

187 ng-induced DICER-miR-203-3p up-regulation in adipocytes is a key adaptive response that coordinates s

188 that the intracellular TGF-beta signaling in adipocytes is inhibited by the transcriptional factor PP

189 Additionally, GIPR activity in adipocytes is partially responsible for muGIPR-Ab to pre

190 somal acid lipase (LAL), highly expressed in adipocytes, is unclear.

191 megamitochondria" with altered MAMs in brown adipocytes lacking the Sel1L-Hrd1 protein complex of ER-

192 is, as conditional deletion of Mpc1 in brown adipocytes leads to impaired cold adaptation.

193 The adipocyte-like morphology of clear cell renal cell carci

194 (epinephrine) infusion profoundly stimulated adipocyte lipolysis and simultaneously triggered insulin

195 d demonstrating an essential requirement for adipocyte lipolysis in promoting stress-induced insulin

196 Here, we identify an essential role for adipocyte lipolysis in regulating inflammation and repai

197 ndings demonstrate the central importance of adipocyte lipolysis in the metabolic response to injury.

198 We investigated the contributions of adipocyte lipolysis to the metabolic response to acute s

199 Mice with Kbtbd2 knockout in adipocytes, liver, and muscle all showed normal growth,

200 d throughout the body in distinct depots and adipocytes make up a minority of the cells within the ti

201 confirmed in humans, the oxidative state of adipocytes may be a therapeutic target in chronic renal

202 Furthermore, adipocyte mediated myofibroblast induction occurred thro

203 ycolytic beige fat, a subpopulation of beige adipocytes mediated by GABPalpha emerging in the absence

204 er or not p53 is directly involved in mature adipocyte metabolic regulation remains unclear.

205 sought to determine whether perturbation of adipocyte mitochondria influences energy metabolism duri

206 entifies the unique and critical impact that adipocyte mitochondrial dysfunction has on increasing be

207 In brown adipocytes, mTORC2 regulates glucose and lipid metabolis

208 t animals, peri-weaning development of beige adipocytes occurs in a temperature- and sympathetic nerv

209 This study examined the effects on adipocytes of administering a peptide that reduces oxida

210 erentiation into a myofibroblast, but not an adipocyte or neuronal phenotype, was also impaired.

211 ractions on the differentiation of MSCs into adipocytes or osteoblasts using single-cell RNA sequenci

212 of a western diet significantly worsened the adipocyte oxidant stress, but expression of NaKtide in a

213 lothobeta (FGFR1/KLB) complexes expressed in adipocytes, pancreatic acinar cells, and the nervous sys

214 ces oxidative stress and dramatically alters adipocyte phenotype in vitro.

215 e roles of cADORA(1) signaling in energy and adipocyte physiology.

216 selected non-HLA antibodies (against agrin, adipocyte plasma membrane-associated protein, Rho GDP-di

217 ase response and platelet activation (APMAP [adipocyte plasma membrane-associated protein], GPLD1 [ph

218 tal for adipocyte state loss which underlies adipocyte plasticity.

219 Oxidative stress in adipocyte plays a central role in the pathogenesis of ob

220 hat governs genome accessibility and renders adipocytes poised for thermogenic activation remains elu

221 s induce senescence and metabolic changes in adipocytes, potentially driving new therapeutic directio

222 ngle-cell RNA sequencing to identify a beige adipocyte precursor cell that gives rise to thermogenic

223 fferentiation of skin-derived REDD1 knockout adipocyte precursor cells as indicated by higher lipid a

224 dback loop of cellular senescence within the adipocyte precursor compartment, as demonstrated in norm

225 lls, however upon their differentiation into adipocyte precursors (AP), premature senescence emerged,

226 thus suggest that proliferative potential of adipocyte precursors is limited and can restrain the dev

227 , including UCP1, increased numbers of beige adipocyte precursors, and expanded UCP1-expressing cell

228 c roles of G(i)-type G proteins expressed by adipocytes, primarily due to the lack of suitable animal

229 In the absence of OSM, BM adipocytes produced less CXCL12, being arguably devoid o

230 Adipocyte progenitors (APs) express platelet-derived gro

231 Adipocyte progenitors can also migrate from the bone mar

232 However, the proliferative potential of adipocyte progenitors in vivo is unknown (Faust et al.,

233 d cytoskeletal genes and suppression of many adipocyte programs most notably those associated with mi

234 Thus, adipocytes regulate multiple aspects of repair and may b

235 (2020) reveal that dermal adipocytes regulate skin wound repair via release of fat

236 e effects of an MR antagonist (MRA) in human adipocytes remains very limited.

237 ls mediate estrogen-induced inflammation and adipocytes repopulation, estrogen-induced mammary cell d

238 by exacerbating inflammation, cell death and adipocytes repopulation.

239 Together, these data reveal that (a) adipocyte respiration is principally fueled from nongluc

240 The data demonstrate that the adipocyte responds to the HFD by adopting a fibroblast-l

241 n levels at PND1; however, at PND21 MFR male adipocytes showed an upward trend in the expression of t

242 sed in several studies as a marker for beige adipocytes, showed elevated levels of thermogenic marker

243 Inducing the loss of p53 in mature adipocytes significantly reprograms energy metabolism an

244 Adipocyte size and fibrosis were determined in biopsies

245 nsulin resistance, associated with a smaller adipocyte size and increased cristae formation.

246 We observed elevated fibrosis, adipocyte size, and adipogenic marker expression in SCAT

247 pose tissue, and is associated with enlarged adipocyte size, tissue inflammation, enhanced maternal g

248 nsulin signaling and action in human primary adipocytes, skeletal muscle, and liver cells.

249 Previously we reported that adipocyte SNAP23 (synaptosome-associated protein of 23 k

250 eny phenotype results from loss of KBTBD2 in adipocytes, some features are adipocyte-extrinsic.

251 adipose and liver pathogenesis, we generated adipocyte-specific Atg5 knockout (KO), adipocyte-specifi

252 Adipocyte-specific Atg5 KO mice had increased circulatin

253 Here, we report the surprising finding that adipocyte-specific deletion of P2Y(6)R protects mice fro

254 Then adipocyte-specific expression of the peptide was assesse

255 Here we show that mice with an adipocyte-specific knockout of Kbtbd2 accumulate p85alph

256 rated adipocyte-specific Atg5 knockout (KO), adipocyte-specific mTOR KO, adipocyte-specific Raptor KO

257 bated alcohol-induced steatosis, but neither adipocyte-specific mTOR nor adipocyte-specific tuberous

258 Adipocyte-specific MyD88 or IRAK2 deficiency reduced hig

259 Adipocyte-specific Raptor KO mice experienced exacerbate

260 5 knockout (KO), adipocyte-specific mTOR KO, adipocyte-specific Raptor KO, and adipocyte-specific tub

261 c mTOR KO, adipocyte-specific Raptor KO, and adipocyte-specific tuberous sclerosis complex 1 KO mice

262 sis, but neither adipocyte-specific mTOR nor adipocyte-specific tuberous sclerosis complex 1 KO mice

263 sion profiling established STAT1 deletion in adipocytes (STAT1 (a-KO) ) enhanced mitochondrial functi

264 In this study, we determine the dynamics of adipocyte state loss in response to the profibrotic cyto

265 However, TGF-beta can lead to adipocyte state loss when it is present simultaneously w

266 occurring in a specific order is pivotal for adipocyte state loss which underlies adipocyte plasticit

267 Mature adipocytes store fatty acids and are a common component

268 ricted to a subpopulation of MCT1-expressing adipocytes suggesting MCT1 as a marker of inducible beig

269 pressing adipogenesis and increasing gluteal adipocyte susceptibility to apoptosis.

270 ously uncharacterized subpopulation of brown adipocytes that display distinct characteristics from th

271 stress and an altered molecular phenotype of adipocytes that increased production of systemic inflamm

272 y JNK-regulated FGF21 autocrine signaling in adipocytes that promotes increased expression of the adi

273 ondria-enriched thermogenic fat cells (brown adipocytes) that play a crucial role in the regulation o

274 essed by cold and other stimulators of beige adipocyte thermogenesis.

275 ation regulates the activity of neighbouring adipocytes through acetate-mediated modulation of their

276 induces these phenotypic changes in primary adipocytes through the xanthine oxidoreductase-catalyzed

277 In human adipocytes, TL1A enhanced basal and impaired insulin-inh

278 ed a transcriptome analysis of isolated vWAT adipocytes to assess global pathway changes occurring in

279 that reprograms mitochondrial metabolism in adipocytes to exacerbate obesity.

280 mmunicate the intracellular energy status of adipocytes to other nonadipose tissues including liver,

281 ssue had ongoing lipolysis in the absence of adipocyte triglyceride lipase (ATGL).

282 We applied the Adipocyte U-Net to 4 cohorts with histology, genetic, an

283 method and the state-of-the-art approaches (Adipocyte U-net vs. CellProfiler: R2visceral = 0.94, P <

284 coupling protein-1 (UCP1) in brown and beige adipocytes uncouples fatty acid oxidation from ATP gener

285 l proteome, secretome and phosphoproteome of adipocytes under chronic inflammation condition, as well

286 accharides were toxic to macrophages but not adipocytes under high concentration or long time treatme

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

288 autonomous, light-sensing mechanism in brown adipocytes via Opn3-GPCR signaling that can regulate fue

289 ng-term viability and functionality of white adipocytes was confirmed by real-time monitoring of fatt

290 Similarly, the viability of mouse adipocytes was not affected by cottonseed extracts.

291 g primary rat adipocytes and cultured 3T3-L1 adipocytes, we observed that insulin increased respirati

292 Based on the developmental dynamics of brown adipocytes, we propose that the murine iBAT has two diff

293 The resulting adipocytes were also found to be senescent, with increas

294 Mice with ERAD deficiency in brown adipocytes were cold sensitive and exhibited mitochondri

295 s-specific RT-PCR array showed that male MFR adipocytes were programmed to exhibit stronger adipogeni

296 lin/flin) ) and ALMS1-silenced human primary adipocytes, whereas selective reactivation of ALMS1 gene

297 Treatment of adipocytes with conditioned media from RBP4-activated ma

298 e have shown that treatment of mature 3T3-L1 adipocytes with recombinant Lcn2 (rec-Lcn2) resulted in

299 Treatment of cultured human adipocytes with troglitazone increased PPARgamma binding

300 tenance of 3D tissues based on human primary adipocytes, with supporting nourishment provided through