ライフサイエンスコーパス: adipocyte

1 ature white adipocytes to convert into beige adipocytes.

2 levels, and this increase relies largely on adipocytes.

3 o a subset of preadipocytes and mature white adipocytes.

4 x to activate thermogenic gene expression in adipocytes.

5 esentative in vitro model of human white pre-adipocytes.

6 ative metabolism, and thermogenesis in brown adipocytes.

7 mote lipolysis and adipogenesis in mammalian adipocytes.

8 maintaining properties of preexisting beige adipocytes.

9 nergy storage capacity and browning of white adipocytes.

10 etal bovine skeletal muscle and induced into adipocytes.

11 functions as a major Ca(2+) entry channel in adipocytes.

12 d clathrin and promotes their association in adipocytes.

13 erol and TSHB were studied in isolated human adipocytes.

14 differentiation of preadipocytes into beige adipocytes.

15 ated UCP1 expression and lipolysis by 3T3-L1 adipocytes.

16 evant doses of EDCs on differentiated murine adipocytes.

17 nal knockdown of Arl15 in murine 3T3-L1 (pre)adipocytes.

18 e Adrb3-induced, but not cold-induced, beige adipocytes.

19 to them in cultured preadipocytes and mature adipocytes.

20 ssing white fat and muscle-specific genes in adipocytes.

21 ished with the depletion of alpha-catenin in adipocytes.

22 ar (Acta2+) cells to form cold-induced beige adipocytes.

23 ith teriparatide prevented the appearance of adipocytes.

24 d increase glycolytic metabolism in cultured adipocytes.

25 ed adiposity by promoting more, but smaller, adipocytes.

26 cholesterol up-regulated TSHB mRNA in human adipocytes.

27 d muscle tissues of mice and cultured 3T3-L1 adipocytes.

28 and primary human white subcutaneous (PHWSC) adipocytes.

29 xpression in pre-adipocytes and mature brown adipocytes.

30 ion and lipid droplet accumulation in 3T3-L1 adipocytes.

31 thylhexyl phthalate (MEHP) in differentiated adipocytes.

32 s a direct result of increased production by adipocytes.

33 expression and knockdown of Cx43 in cultured adipocytes.

34 ression and blocks differentiation to mature adipocytes.

35 -PGC-1alpha-expressing PGC-1alpha(-/-) brown adipocytes.

36 ent for de novo sphingolipid biosynthesis in adipocytes, a cell type with highly regulated lipid meta

37 Aging and obesity induce ectopic adipocyte accumulation in bone marrow cavities.

38 esident immune cells are thought to regulate adipocyte activity.

39 wever, whether the activation of thermogenic adipocytes affects the metabolism and anti-atherogenic p

40 educed Wt1 lineage cell differentiation into adipocytes after myocardial infarction.

41 Genetic deletion of Acly in cultured adipocytes also suppressed acetyl-CoA and histone acetyl

42 neuronal genes and provide new evidence for adipocyte and energy expenditure biology, widening the p

43 We show that ADSCs differentiated into adipocytes and accumulated lipids in the cytoplasm when

44 We used 3T3-L1 adipocytes and Brd4 heterozygous mice to investigate whe

45 ines may increase the release of leptin from adipocytes and by those means induce glucagon-like pepti

46 toylation, whereas DHHC7 knockdown in 3T3-L1 adipocytes and DHHC7 KO in adipose tissue and muscle dec

47 h the appearance of multilocular brown/beige adipocytes and elevated thermogenic gene expression.

48 NFalpha-mediated ERK 1/2 signaling in 3T3-L1 adipocytes and in adipose tissue of mice.

49 receptor alpha is highly enriched in mature adipocytes and is induced in response to differentiation

50 differentiation, and UCP1 expression in pre-adipocytes and mature brown adipocytes.

51 can affect the functioning of cells, such as adipocytes and pancreatic beta cells.

52 involved in regulating the phenotype of both adipocytes and peripheral macrophages and is required fo

53 ic metabolism within subpopulations of white adipocytes and preadipocytes.

54 sively examined key differences between SGBS adipocytes and primary human white subcutaneous (PHWSC)

55 Histological analysis revealed smaller adipocytes and qPCR analysis showed upregulated expressi

56 eoblasts, MMPs also give rise to bone marrow adipocytes and stromal cells in vivo.

57 a causal relationship between loss of CB1 in adipocytes and systemic metabolic changes.

58 Adiponectin is a hormone secreted from white adipocytes and takes part in the regulation of several m

59 tissue metabolism through direct effects on adipocytes and through signaling in the central nervous

60 Fibroblasts differentiated to adipocytes and treated with TIP39 also showed increased

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

62 s, from B cells to macrophages, myoblasts to adipocytes, and human fibroblasts to neurons, highlighti

63 r, CAST overexpression significantly reduced adipocyte apoptosis, adipose tissue collagen and macroph

64 Since osteoblasts and adipocytes are derived from the same precursor cells, ad

65 Uncoupling protein 1(+) beige adipocytes are dynamically regulated by environment in r

66 lipid accumulation and GLUT4 localization in adipocytes are present in 1.3% of European Americans and

67 rdm16 deletion strategies, demonstrated that adipocytes are required and are predominant source to ge

68 tion of pro-inflammatory mediators by 3T3-L1 adipocytes as well as in human sera.

69 EC and its acetylated form in HDAC-deficient adipocytes as well as the adipose tissue of obese animal

70 nd PDC subunits in murine and human cultured adipocytes, as well as in adipose tissue.

71 In this study adipocyte-autonomous roles for ARL15 were investigated u

72 sociated with diminished generation of beige adipocytes ('beige adipogenesis'), a thermogenic and ene

73 e the mechanisms by which these genes affect adipocyte biology and how their perturbations contribute

74 ncert to regulate key aspects of thermogenic adipocyte biology remains largely unknown.

75 roliferation, epithelial stem cell survival, adipocyte biology, and inflammatory skin responses.

76 mplications for our current understanding of adipocyte biology.

77 identifies the molecular signature of white adipocyte browning downstream of Egr1 deletion and highl

78 stablishes the properties that define mature adipocytes, but the contribution of posttranscriptional

79 Lsd1 maintains beige adipocytes by controlling the expression of peroxisome p

80 Beige adipocytes can form through de novo adipogenesis; howeve

81 In adipocytes, catecholamines target the beta-adrenergic (b

82 st is sufficient to rescue the loss of beige adipocytes caused by Lsd1 ablation.

83 sion of Prdm16, which determines beige/brown adipocyte cell fate.

84 he Simpson Golabi Behmel Syndrome (SGBS) pre-adipocyte cell strain is widely considered to be a repre

85 vo sphingolipid biosynthesis is required for adipocyte cell viability and normal metabolic function a

86 ls differentiate along diverse lineages into adipocytes, chondrocytes, osteoblasts, fibroblasts, and

87 Brown and beige adipocytes combust nutrients for thermogenesis and throu

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

89 bal transcriptomic analysis of FACS-isolated adipocytes confirmed the presence of distinct anabolic a

90 atography showed that isolated tibial marrow adipocytes contain the medium-chain fatty acids utilised

91 ic function of uncoupling protein 1(+) beige adipocytes contributed to metabolic fitness in adipocyte

92 Brown and beige adipocytes convert chemical energy into heat through unc

93 nes, such as uncoupling protein 1 (Ucp1), in adipocytes cultured with the conditioned media.

94 nthesis within adipocytes is associated with adipocyte death, adipose tissue remodeling, and metaboli

95 of adipose tissue accompanied by evidence of adipocyte death, increased macrophage infiltration, and

96 eople are following a diet, the volume of an adipocyte decreases by loss of triglycerides, which crea

97 utant larvae are transparent and have severe adipocyte defects caused by up-regulation of beta-cateni

98 nd thermoregulation in a mechanism involving adipocyte-dependent uridine biosynthesis and leptin sign

99 Some of these adipocytes derived from cells marked by Sox9-cre express

100 STAT5 proteins play a role in adipocyte development and function, but their specific f

101 Maternal resveratrol promotes beige adipocyte development in offspring white adipose tissue.

102 Finally, in brown adipocytes differentiated in culture, MLL4 identifies pr

103 ine kinase (SYK) is upregulated during brown adipocyte differentiation and activated by beta-adrenerg

104 We found that adipocyte differentiation and maturation required a puls

105 e role of glucose availability in regulating adipocyte differentiation and maturation.

106 gamma with high affinity without stimulating adipocyte differentiation and the expression of adipogen

107 Relevant human models for beige adipocyte differentiation are essential to implement suc

108 ing to identify small molecules that promote adipocyte differentiation by engaging the poorly charact

109 ific gene adiponectin (Adipoq) during 3T3-L1 adipocyte differentiation is closely associated with epi

110 igate whether the induction of Adipoq during adipocyte differentiation is regulated by histone acetyl

111 s are derived from the same precursor cells, adipocyte differentiation may occur at the expense of os

112 equence of cardiac disease and epicardium to adipocyte differentiation should be taken into account b

113 ts the conclusion that high glucose promotes adipocyte differentiation via distinct metabolic pathway

114 Adipocyte differentiation was not affected by the Sptlc1

115 evel to reciprocally regulate osteoblast and adipocyte differentiation, indicating that the polycysti

116 mary mouse adipose progenitor cells impaired adipocyte differentiation, suggesting physiological role

117 vity in Sirt7(-/-) mice blocks PPARgamma and adipocyte differentiation, thereby diminishing accumulat

118 ious in vitro assays are available to assess adipocyte differentiation, though little work has been d

119 understand the nutrient signals that promote adipocyte differentiation, we investigated the role of g

120 on in mesenchymal stem cells decreases beige adipocyte differentiation, while increasing extracellula

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

122 Transcriptional regulators are crucial in adipocyte differentiation.

123 but conversely with DeltaNp63 levels, during adipocyte differentiation.

124 reviously unrecognized molecules influencing adipocyte differentiation.

125 t deposits potentially mediated by increased adipocyte differentiation.

126 atty acid chaperone, which is induced during adipocyte differentiation.

127 Since adipocytes do not produce sclerostin, these findings sug

128 uthors show that PD-L1 is expressed on brown adipocytes, does not change upon BAT activation, and tha

129 echanisms is difficult in animals or primary adipocytes due to these intertwined dimorphisms.

130 We conclude that the GR in adipocytes exerts central but diverging roles in the reg

131 Isolated UCP1 KO brown adipocytes exhibited defective induction of uncoupled re

132 itric oxide are released after activation of adipocyte-expressed beta3 adrenoceptors by catecholamine

133 ls of TFAM expression, PGC-1alpha(-/-) brown adipocytes expressing NT-PGC-1alpha had higher expressio

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

135 ortant insight into epigenetic regulation of adipocyte fate and thermogenic gene expression.

136 xisting drugs, including icosapent ethyl and adipocyte fatty-acid-binding protein.

137 te alcohol intake on thermogenic brown/beige adipocyte formation and glucose and lipid homeostasis, a

138 eige adipocytes inhibited cold-induced beige adipocyte formation in adult mice.

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

140 ous knockout mice have defects in brown-like adipocyte formation in iWAT, and develop glucose intoler

141 ng the molecular mechanisms regulating beige adipocyte formation may lead to the development of new t

142 cohol intake induces thermogenic brown/beige adipocyte formation via elevating retinoic acid signalin

143 the BMP receptor in myofibroblasts prevented adipocyte formation.

144 Adipocytes formed from human keloid fibroblasts either w

145 In this study, we show that beige adipocytes formed postnatally in subcutaneous inguinal w

146 ound enlarged hypertrophied, dead, and dying adipocytes, forming crown-like structures.

147 ng protein 16, a key factor present in brown adipocytes found in depots.

148 protocol to generate functional human beige adipocytes from human induced pluripotent stem cells (hi

149 itro models of AML, we show that bone marrow adipocytes from the tumor microenvironment support the s

150 PDGFRalpha inhibited the formation of adipocytes from these precursors while favoring the form

151 Maternal obesity impairs offspring brown adipocyte function and correlates with obesity in offspr

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

153 lso controls other gene programs to regulate adipocyte function was unclear.

154 electrophysiological regulatory mechanism of adipocyte function.

155 d that development of fatty liver depends on adipocyte GH signaling.

156 Here, we demonstrate that adipocyte GR deficiency in mice significantly impacts sy

157 The adipocyte GR is indispensable for the feeding-fasting tr

158 CTRP6-overexpressing mice or CTRP6-treated adipocytes had reduced insulin-stimulated Akt phosphoryl

159 Transient brown adipocytes have been shown to be a critical regulator of

160 may partly explain the mechanism underlying adipocyte hyperplasia that occurs much later than adipoc

161 n during diet-induced obesity (DIO) promotes adipocyte hypertrophy and inflammation, thereby contribu

162 cyte hyperplasia that occurs much later than adipocyte hypertrophy in the development of obesity.

163 ut (DKO)) mice show HF diet-induced obesity, adipocyte hypertrophy, and present with non-alcoholic fa

164 de compelling evidence for a crosstalk among adipocytes, immune cells, and the sympathetic nervous sy

165 hat myofibroblasts can generate lipid-filled adipocytes in large skin wounds that regenerate hair fol

166 r results reveal an unexpected role of white adipocytes in maintaining properties of preexisting beig

167 Engraftment of hiPSC-derived adipocytes in mice produces well-organized and vasculari

168 precursor cells generate lipid-filled mature adipocytes in multiple tissues during a high-fat diet an

169 findings, DUSP5 mRNA expression increased in adipocytes in response to TNFalpha, parallel with ERK1/2

170 owed that ApoA-IV improved glucose uptake in adipocytes in the absence of insulin by upregulating GLU

171 ecursor fibroblasts differentiate into white adipocytes in the embryo.

172 so inhibited the formation of juvenile beige adipocytes in the inguinal fat pad.

173 olytic, whereas Tbx15(Low) preadipocytes and adipocytes in the same depot are more oxidative and less

174 stimulated genes (ISGs), including Stat1, in adipocytes in vitro and in vivo Ectopic activation of ty

175 activity restores adipogenesis in Sirt7(-/-) adipocytes in vitro and in vivo.

176 ated transition of beige adipocytes to white adipocytes in vivo, whereas loss of Lsd1 precipitates it

177 s, and suppresses their differentiation into adipocytes in vivo.

178 n BAT thermogenesis and programming of beige adipocytes in white adipose tissue (WAT).

179 ation of uncoupling protein 1-positive beige adipocytes in white adipose tissue, and increased thermo

180 ite adipose tissue and 3T3-L1 differentiated adipocytes; in the latter, Pep19 activates pERK1/2 and A

181 hdrawal of teriparatide therapy, bone marrow adipocytes increased dramatically in number.

182 Inhibition of Cx43 in cultured adipocytes increased the generation of reactive oxygen s

183 nterleukin (IL)-6-type cytokine signaling in adipocytes induces free fatty acid release from visceral

184 activation of type I IFN signaling in brown adipocytes induces mitochondrial dysfunction and reduces

185 Ablation of these postnatal beige adipocytes inhibited cold-induced beige adipocyte format

186 In adipocytes, insulin stimulated S6K1-dependent EPRS phosp

187 ced de novo sphingolipid biosynthesis within adipocytes is associated with adipocyte death, adipose t

188 on induced by Pep19 in 3T3-L1 differentiated adipocytes is blocked by AM251, a cannabinoid type 1 rec

189 ng mechanisms by which a population of beige adipocytes is increased in white adipose tissue (WAT) re

190 nt, and insulin-stimulated glucose uptake in adipocytes is suppressed.

191 comitant deletion of Jak2 in hepatocytes and adipocytes (JAK2LA) completely normalized insulin sensit

192 oothened (SmoM2) or Gli2 (DeltaNGli2) in the adipocyte lineage of postnatal mice, we show that target

193 Early suppression of adipocyte lipid turnover induces immunometabolic modulat

194 phages regulate the age-related reduction in adipocyte lipolysis in mice by lowering the bioavailabil

195 e Angptl4 domain responsible for stimulating adipocyte lipolysis is unknown.

196 ipocytes contributed to metabolic fitness in adipocyte liver kinase b1-deficient mice, our results re

197 de support to our view that earlier onset of adipocyte maturation arrest/insulin resistance during we

198 hesized that IL-6-type cytokine signaling in adipocytes may regulate insulin secretion.

199 dhesive interactions between macrophages and adipocytes mediated by the integrin alpha4 and its count

200 nce, are not likely to have a direct role in adipocyte metabolism or adaptive thermogenesis.

201 vestigate the role of NT-PGC-1alpha in brown adipocyte mitochondria.

202 or loci influencing insulin secretion and in adipocytes, monocytes, and hepatocytes for insulin actio

203 beige adipocytes progressively gain a white adipocyte morphology.

204 s cell population consisting of mature white adipocytes, multipotent mesenchymal stem cells, committe

205 e observed that PDC-E2 is present within the adipocyte nucleus where it associates with STAT5A.

206 Adipocyte numbers were decreased in both subcutaneous an

207 As seen in the brown adipocytes observed during HO in the mouse, these UCP1(+

208 l for studying thermogenic function in brown adipocytes of both murine and human origins.

209 Ex vivo, supernatant collected from isolated adipocytes of gp130 knockout mice blunted Pcsk1 expressi

210 untreated HemECs readily differentiated into adipocytes on adipogenic induction.

211 This is the first evidence of human infant adipocyte- or myocyte-related alterations in cellular me

212 ltiple cell lineages including chondrocytes, adipocytes, osteoblasts, and multiple neuronal cell type

213 bution of posttranscriptional factors to the adipocyte phenotype is poorly understood.

214 issue origin can shift towards a brown/beige adipocyte phenotype.

215 de important insights into the regulation of adipocyte physiology by CB1.

216 Dysregulated adipocyte physiology leads to imbalanced energy storage,

217 of TIMP3 blocked the conversion of FAPs into adipocytes, pointing to a strategy to combat fatty degen

218 e development, maintenance, and expansion of adipocyte pools in mice.

219 Adipocyte precursor cells generate lipid-filled mature a

220 Recent studies have identified distinct adipocyte precursor populations that are physiologically

221 sting cells and increased differentiation of adipocyte precursors (hyperplasia).

222 With new tools available, the properties of adipocyte precursors can now be defined, and the regulat

223 For decades, our knowledge of adipocyte precursors has relied on cellular models.

224 PDGFRalpha is a marker of adipocyte precursors, and increased PDGFRalpha activity

225 This adipocyte profile was paralleled by upregulated expressi

226 ular, with time, thermogenic-competent beige adipocytes progressively gain a white adipocyte morpholo

227 We conclude that adipocyte RBP4 is not a significant source of circulatin

228 Observations that adipocyte RBP4 mRNA increases in parallel with circulati

229 Loss of DPF3 in brown adipocytes reduced chromatin accessibility at EBF2-bound

230 nockdown or overexpression of MRAP in 3T3-L1 adipocytes reduced or increased ACTH-induced lipolysis,

231 ered in the mouse that during wound healing, adipocytes regenerate from myofibroblasts, a cell type t

232 cal interactions between cells in the MS and adipocytes regulate their immune and metabolic functions

233 protein complex disassembly are involved in adipocyte regulation.

234 ated transition of beige adipocytes to white adipocytes remain unclear.

235 metabolism depend on the GC receptor (GR) in adipocytes remains unclear.

236 g characteristics, a phenomenon termed beige adipocyte renaissance.

237 cose metabolism by targeting macrophages and adipocytes, respectively.

238 Leptin is an adipocyte-secreted hormone that is delivered via a speci

239 Adipocytes sense systemic nutrient status and systemical

240 Compared to PHWSC adipocytes, SGBS adipocytes showed not only greater indu

241 ctron microscopy revealed that tibial marrow adipocytes show prominent expression of the UAG-activati

242 Compared to PHWSC adipocytes, SGBS adipocytes showed not only greater induction of adipogen

243 lpha and PGC-1alpha in PGC-1alpha(-/-) brown adipocytes similarly induced expression of nuclear DNA-e

244 The smaller subcutaneous adipocyte size predicted better glycemic control in T2D.

245 However, the longitudinal contribution of adipocyte size reduction and fatty acid metabolic handli

246 re led to reduced adiponectin levels, larger adipocyte size, and reduced insulin sensitivity in WTs.

247 Adiponectin, together with adipocyte size, is the strongest factor associated with

248 ooth muscle cells, macrophages, hepatocytes, adipocytes, skeletal muscle, and finally, those from mic

249 hat focal sites of inflammation around dying adipocytes, so-called crown-like structures, exhibit a u

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

251 In cultured 3T3-L1 adipocytes, sortilin together with retromer rescues Glut

252 ects of Cx43 were evaluated using inducible, adipocyte-specific Cx43 knockout in mice (Gja1 (adipoq)

253 similar to S6K1-deficient mice and mice with adipocyte-specific deficiency of raptor, an mTORC1 const

254 lipid metabolism, we generated mice with an adipocyte-specific deletion of Sptlc1 Sptlc1 is an oblig

255 Mice with adipocyte-specific depletion of Hdac6 exhibited increase

256 We previously reported that induction of the adipocyte-specific gene adiponectin (Adipoq) during 3T3-

257 In conclusion, adipocyte-specific IL-6 signaling induces intestinal GLP

258 Accordingly, adipocyte-specific increase of Lsd1 expression is suffic

259 In this work, adipocyte-specific inducible deletion of the CB1 gene (A

260 The metabolic effects of adipocyte-specific knockout of Cx43 were assessed during

261 To this end, mice with adipocyte-specific knockout of gp130, the signal transdu

262 Necessity tests, using mature adipocyte-specific Prdm16 deletion strategies, demonstra

263 ial growth factor (VEGF)-C was driven by the adipocyte-specific promoter adiponectin (ADN), to determ

264 We studied mice with hepatocyte- or adipocyte-specific SREBP-1c overexpression as models of

265 onstrate that the Tbx15(Hi) preadipocyte and adipocyte subpopulations of cells are highly glycolytic,

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

267 nergy-dissipating function mediated by beige adipocytes that express the uncoupling protein UCP1.

268 a distinct property of activated beige/brite adipocytes that might be under epigenetic control.

269 e pups receiving low n-6/n-3 ratios had more adipocytes that were smaller in size; decreased Ppargamm

270 nduces free fatty acid release from visceral adipocytes, thereby promoting obesity-induced hepatic in

271 ctive oxygen species (ROS) signal to support adipocyte thermogenic identity and function.

272 Zfp423, a transcriptional suppressor of the adipocyte thermogenic program.

273 hen enables the transfer of fatty acids from adipocytes to AML blasts.

274 Daily exposure of differentiated adipocytes to blue light resulted in decreased lipid dro

275 st, Adrb3 activation stimulates mature white adipocytes to convert into beige adipocytes.

276 t description of AML programming bone marrow adipocytes to generate a protumoral microenvironment.

277 that AML blasts alter metabolic processes in adipocytes to induce phosphorylation of hormone-sensitiv

278 o rescue the age-related transition of beige adipocytes to white adipocytes in vivo, whereas loss of

279 trolling the age-related transition of beige adipocytes to white adipocytes remain unclear.

280 otein (BMP) signaling and then activation of adipocyte transcription factors expressed during develop

281 m controlling the age-related beige-to-white adipocyte transition and identify Lsd1 as a regulator of

282 -acyltransferase 1) and degrade LD via ATGL (adipocyte triglyceride lipase) after FA loading.

283 esity-induced inflammation upregulates brown adipocytes TRIP-Br2 expression via the ER stress pathway

284 tagonist chlorpheniramine potently inhibited adipocyte UCP1 mRNA induction by mast cell CM.

285 teraction between STAT5A and PDC subunits in adipocytes under physiological conditions.

286 decreased lipolytic capacity of GR-deficient adipocytes under postabsorptive and fasting conditions,

287 In line, leptin release from isolated adipocytes was reduced, and intestinal proprotein conver

288 n vivo By deleting GR in precursors of brown adipocytes, we found unexpectedly that GR is dispensable

289 Primary brown adipocytes were additionally examined for their bioenerg

290 eart rate; changes in the number and size of adipocytes were also observed.

291 atin to activate brown fat-specific genes in adipocytes were unknown.

292 obilization and oxidation in brown and beige adipocytes, where the harnessed energy is dissipated as

293 and humans; cold induces formation of beige adipocytes, whereas warm temperature and nutrient excess

294 ression unless activated to differentiate to adipocytes, whereupon these cells reduce expression of s

295 In conclusion, we confirmed that SGBS adipocytes, which are considered of white adipose tissue

296 KEGG pathways significantly enriched in SGBS adipocytes, which included positively enriched mitochond

297 ory effects on macrophages, hepatocytes, and adipocytes, which is distinct from the effect of STING a

298 he attenuation of thermogenic genes in brown adipocytes with impaired respiratory capacity, while ind

299 we combined existing data and models for rat adipocytes with new data collected for the signaling net

300 ed of normal-sized, UCP1-negative unilocular adipocytes, with mitochondrial network fragmentation, di