ライフサイエンスコーパス: white adipose tissue

1 nificantly higher mRNA expression of CysC in white adipose tissue.

2 tes beige adipocyte development in offspring white adipose tissue.

3 ivate brown adipose tissue and by 'browning' white adipose tissue.

4 induced obesity, and elicits the browning of white adipose tissue.

5 r expression of Tfe3, Tf3b, and Ppargamma in white adipose tissue.

6 x43 expression was higher in BAT compared to white adipose tissue.

7 turnover in all organs, except the brain and white adipose tissue.

8 s effects on Wnt signaling and metabolism in white adipose tissue.

9 mic alterations and inflammation in visceral white adipose tissue.

10 id pools in lung, spleen, muscle, liver, and white adipose tissue.

11 increased expression of UCP1 and browning of white adipose tissue.

12 a process often referred to as "browning" of white adipose tissue.

13 ost, but not Ucp1 or Ppargamma expression in white adipose tissue.

14 mmation- and metabolism-related processes in white adipose tissue.

15 ense and respond to external cues to remodel white adipose tissue.

16 tion consistent with cold climate, affecting white adipose tissue.

17 s the recruitment of beige adipocytes within white adipose tissue.

18 ranscriptome and metabolic pathways of human white adipose tissue.

19 ytes are mediated by the browning/beiging of white adipose tissue.

20 f the Ucp1 promoter in subcutaneous inguinal white adipose tissue.

21 nduced obesity and had significantly reduced white adipose tissue.

22 n within the same cells in classic brown and white adipose tissues.

23 1-dependent thermogenesis in mouse brown and white adipose tissues.

24 own adipose activity and browning program of white adipose tissues.

25 lso migrate from the bone marrow to populate white adipose tissue, a process that accelerates during

26 After infection, white adipose tissue accumulated large numbers of pathog

27 and relative expression of genes regulating white adipose tissue adipogenesis and Irx3.

28 ed UCP1-expressing cell clusters in inguinal white adipose tissue after chronic cold exposure.

29 act of CerS5-dependent ceramide synthesis in white adipose tissue after high fat diet feeding.

30 tively related to glucose uptake in visceral white adipose tissue, although glucose uptake in viscera

31 uced uncoupling protein 1 expression in both white adipose tissue and 3T3-L1 differentiated adipocyte

32 sufficient for the induction of lipolysis in white adipose tissue and are an efferent effector of lep

33 ons as a negative regulator of "browning" in white adipose tissue and call into question the use of t

34 Initially, dysfunction of white adipose tissue and circulating metabolites modulat

35 Inguinal subcutaneous white adipose tissue and dWAT in REDD1 knockouts were ex

36 Dermal adipose tissue (also known as dermal white adipose tissue and herein referred to as dWAT) has

37 ity associated with an increased browning of white adipose tissue and hypermetabolism.

38 hetic nervous system-dependent remodeling of white adipose tissue and increasing uncoupling protein 1

39 ntified extravascular fibrin deposits within white adipose tissue and liver as distinct features of m

40 18-hydroxyeicosapentaenoic acid (18-HEPE) in white adipose tissue and liver.

41 is up-regulated via Ppargamma activation in white adipose tissue and plasma following an acute treat

42 ociated immune cell responses predominate in white adipose tissue and protect against weight gain and

43 es uncoupling protein 1 (Ucp1) expression in white adipose tissue and protects mice from developing o

44 ted beta3-AR stimulation-induced browning of white adipose tissue and reduced mitochondrial activity

45 nce has been shown so far only indirectly in white adipose tissue and still continues to be a matter

46 ed lipolysis may be restricted to mesenteric white adipose tissue and that it contributes to hepatic

47 body energy expenditure, hyperplastic brown/white adipose tissues and larger hyperplastic hearts.

48 increasing glucose uptake in cardiac muscle, white adipose tissue, and brown adipose tissue through a

49 pling protein 1-positive beige adipocytes in white adipose tissue, and increased thermogenesis in mic

50 ion of body mass, total fat, size of gonadal white adipose tissue, and interscapular brown adipose ti

51 ls were significantly lower in iBAT, gonadal white adipose tissue, and livers of ppHF dams.

52 ner and impaired insulin signaling in liver, white adipose tissue, and skeletal muscle.

53 Here, we show that Grb14 knockdown in liver, white adipose tissues, and heart with an AAV-shRNA (Grb1

54 ut they show expansion of their subcutaneous white adipose tissue, as compared to wild-type (WT) mice

55 mation with reduced macrophage counts within white adipose tissue, as well as near-complete protectio

56 nd brown adipocytes, but also differences in white adipose tissue at the depot level and even heterog

57 In obesity, inflammation of white adipose tissue (AT) is associated with diminished

58 was to determine the importance of brown and white adipose tissue (BAT and WAT) NAD(+) metabolism in

59 ide exchange factor PDZ-RhoGEF (Arhgef11) in white adipose tissue biology.

60 cemic clamps (HECs), and skeletal muscle and white adipose tissue biopsies to assess insulin signalin

61 White adipose tissue bridges body organs and plays a fun

62 In contrast to white adipose tissue, brown adipose tissue (BAT) is know

63 reduced mitochondrial oxygen consumption in white adipose tissue, brown adipose tissue, and hepatocy

64 h Hlx as a powerful regulator for systematic white adipose tissue browning and offer molecular insigh

65 ted with enhanced brown adipose function and white adipose tissue browning in HFD+RES compared with H

66 Loss of glucagon signaling alters white adipose tissue browning.

67 , as a direct target gene of Rev-erbalpha in white adipose tissue but not liver.

68 fspring had lower thermogenesis in brown and white adipose tissues compared with CON offspring, which

69 that Lsd1 levels decrease in aging inguinal white adipose tissue concomitantly with beige fat cell d

70 Here, we have shown that at steady state, white adipose tissue contained abundant memory lymphocyt

71 It is unclear, however, how beige or white adipose tissue contributes to brown fat thermogeni

72 glucose uptake in visceral and subcutaneous white adipose tissue depots was unchanged upon cold accl

73 Expansion of white adipose tissue-derived epididymal BK(L1/L1) preadi

74 hydrogels to support the differentiation of white adipose tissue-derived multipotent stem cells (ADM

75 omal versus adipogenic cell expansion during white adipose tissue development, with PDGFRalpha activi

76 We found that Ct-1 mRNA expression in white adipose tissue directly involved PPARalpha and PPA

77 ody fat, plasma hormone levels, and visceral white adipose tissue DNA methylome and transcriptome col

78 (SSc) is accompanied by attrition of dermal white adipose tissue (dWAT) and reduced levels of circul

79 Dermal white adipose tissue (dWAT) expansion is associated with

80 ical of scleroderma is atrophy of the dermal white adipose tissue (DWAT).

81 difference in the growth of their epididymal white adipose tissue (epiWAT) but they show expansion of

82 Thus, white adipose tissue, even in a single depot, is compris

83 Such Treg activity lost in male epididymal white adipose tissue (eWAT) and female gonadal gWAT.

84 of these effects, we transplanted epididymal white adipose tissue (eWAT) from wild-type donors (B(1)

85 expressing Tnmd develop increased epididymal white adipose tissue (eWAT) mass, and preadipocytes deri

86 in cultured adipocytes and in the epididymal white adipose tissue (EWAT) of C57BL/6 mice.

87 In epididymal white adipose tissue (eWAT) of PDE3B KO mice on a SvJ129

88 resident macrophages from healthy epididymal white adipose tissue (eWAT) tightly associate with blood

89 protocol caused further increased epididymal white adipose tissue (eWAT) weight, preadipocyte prolife

90 nsulin singling in both liver and epididymal white adipose tissue (eWAT).

91 lysis of bioenergetics revealed thatNrf2(-/-)white adipose tissues exhibit greater oxygen consumption

92 ce with targeted deletion of EPO receptor in white adipose tissue exhibited sex-differential phenotyp

93 preadipocyte cilia in mice severely impairs white adipose tissue expansion.

94 Memory T cells in white adipose tissue expressed a distinct metabolic prof

95 Transient p53 inhibition sensitizes aged white adipose tissue for beige adipocyte recruitment by

96 White adipose tissue from MRTFA(-/-) mice contains more

97 stromal vascular fraction from periprostatic white adipose tissue from obese HiMyc mice at 6 months o

98 expressed a distinct metabolic profile, and white adipose tissue from previously infected mice was s

99 Consistent with this finding, white adipose tissue from S6K1-deficient mice exhibits n

100 ferential inflammatory cytokine responses in white adipose tissues from the prefrontal cortex in the

101 ut all are characterized by perturbations in white adipose tissue function and, in many instances, it

102 sitivity in Bscl2(-/-) mice by improving the white adipose tissue gene expression pattern.

103 STRA6 signaling in white adipose tissue has been shown to inhibit insulin r

104 Immune cells residing in white adipose tissue have been highlighted as important

105 ated UCP1 expression in BAT and subcutaneous white adipose tissue, have increased BAT mass and higher

106 Dissecting white adipose tissue heterogeneity revealed that the MCT

107 acrophages and dendritic cells (DCs) in lean white adipose tissue homeostasis have received little at

108 sis and oxidation in mouse brown, beige, and white adipose tissues; however, the cellular basis of th

109 brown adipocyte-specific gene expression in white adipose tissue in a murine model of obesity.

110 infiltration, except minimal infiltration in white adipose tissue in animals treated with the highest

111 progress in understanding the role of dermal white adipose tissue in immunity, both as an innate anti

112 tion attenuates exercise-induced browning of white adipose tissue in mice.

113 in hypoxia, a serious comorbidity affecting white adipose tissue in obese individuals, and corrected

114 A subset of UCP1+ adipocytes develops within white adipose tissue in response to physiological stimul

115 scriptomic analysis of subcutaneous inguinal white adipose tissue in the absence of Egr1 identifies t

116 t essential for exercise-induced browning of white adipose tissues in mice.

117 MI, MC progenitors originated primarily from white adipose tissue, infiltrated the heart, and differe

118 White adipose tissue inflammation (WATi) has been linked

119 intenance of glucose homeostasis and reduced white adipose tissue inflammation after high fat diet ch

120 These lead to systemic and visceral white adipose tissue inflammation in addition to altered

121 n features of this disorder, such as chronic white adipose tissue inflammation, adipocyte hypertrophy

122 White adipose tissue inflammation, in part via myeloid c

123 s did not increase proliferation in inguinal white adipose tissue (ingWAT), the percentage of BAs, de

124 Dermal white adipose tissue is a unique layer of adipocytes wit

125 tissues including skeletal muscle and liver, white adipose tissue is also an important physiological

126 ersely, inducible expression of PGC-1beta in white adipose tissue is sufficient to induce beige fat g

127 Hypertrophic remodeling of white adipose tissues is associated with overexposure of

128 Ip6k1 in murine inguinal and retroperitoneal white adipose tissue (IWAT and RWAT) depots.

129 ing of white adipocytes in vitro or inguinal white adipose tissue (iWAT) in vivo.

130 ic and postganglionic inputs to the inguinal white adipose tissue (iWAT) is limited.

131 gene and UCP1 protein expression in inguinal white adipose tissue (iWAT), a common site for emergent

132 express UCP1 in beige adipocytes in inguinal white adipose tissue (iWAT), suggesting a role of this p

133 brown adipose tissue (BAT) and subcutaneous white adipose tissue (iWAT).

134 of detached caveolae were found in brown and white adipose tissue lacking EHD2, and increased caveola

135 id production in liver and redistribution to white adipose tissue, leading to visceral obesity at 2 m

136 duction of a type 2 cellular response in the white adipose tissue leads to weight loss and improves g

137 increased insulin-stimulated suppression of white adipose tissue lipolysis and reduced inflammation.

138 formed postnatally in subcutaneous inguinal white adipose tissue lost thermogenic gene expression an

139 All three mutants showed increased white adipose tissue mass and adipocyte size.

140 overweight, mainly because of an increase in white adipose tissue mass and BAT whitening.

141 t the potential of GPAT inhibitors to rescue white adipose tissue mass in CGL2.

142 ancement of glucose uptake and catabolism in white adipose tissue may be a key contributor to the ant

143 postprandial insulin secretion and improves white adipose tissue metabolism and gut microbiome compo

144 6 weeks after which metabolism, behavior and white adipose tissue morphology were analyzed together w

145 of pro-inflammatory markers was decreased in white adipose tissue of Cpt1b(m-/-) mice.

146 White adipose tissue of HF/HC-fed ALR-deficient mice dev

147 White adipose tissue of HFD-fed Asxl2DeltaLysM mice also

148 Furthermore, the white adipose tissue of iePPARgammaKO CR mice showed low

149 fects of FGF21 were markedly enhanced in the white adipose tissue of mice lacking Rev-erbalpha.

150 immortalized clonal preadipocyte lines from white adipose tissue of mice.

151 White adipose tissue of NASH mice was characterized by i

152 idative catabolism in primary adipocytes and white adipose tissue of nitrate-treated rats.

153 MARCH1 expression is increased in white adipose tissue of obese humans, suggesting that MA

154 cumulation of neutrophils and macrophages in white adipose tissue of wt and AhRR Tg mice.

155 expression was lower in inguinal and gonadal white adipose tissues of ESR1 total body knockout female

156 White adipose tissues of undernourished rats transferred

157 hat PDGFRalpha activation inhibits embryonic white adipose tissue organogenesis in a tissue-autonomou

158 hat SGBS adipocytes, which are considered of white adipose tissue origin can shift towards a brown/be

159 tified lipid particle, adiponectin, abnormal white adipose tissue physiology and bone development and

160 ellular energy metabolism, but their role in white adipose tissue physiology remains incompletely und

161 White adipose tissue plays an important role in physiolo

162 ed in wild-type female mice, suggesting that white adipose tissue plays an integral role in mediating

163 bited changes in liver, skeletal muscle, and white adipose tissue PPARdelta protein levels that may,

164 Beige adipocyte differentiation within white adipose tissue, referred to as browning, is seen a

165 approximately 80% in the liver and by 70% in white adipose tissue relative to control ASO-treated mic

166 showed that genotypic and dietary effects on white adipose tissue remodeling resulted in profound inc

167 Our results suggest that white adipose tissue represents a memory T cell reservoi

168 We identify that white adipose tissue-resident multipotent stromal cells

169 White adipose tissue samples from P2-null mice contain l

170 application induced beiging in subcutaneous white adipose tissue (SC WAT) of humans independent of b

171 ates beige adipose formation in subcutaneous white adipose tissue (SC WAT), would induce other benefi

172 vements in glucose homeostasis, subcutaneous white adipose tissue (scWAT) from exercise-trained or se

173 Subcutaneous white adipose tissue (scWAT) is the major fat depot in h

174 ve energy balance reduces human subcutaneous white adipose tissue (scWAT) mass through the formation

175 White adipose tissue showed a >2-fold increase inUcp1gen

176 own adipocyte-specific genes and proteins in white adipose tissue, substantially increasing oxygen co

177 eased amounts of beige cells in subcutaneous white adipose tissue (sWAT) and increased thermogenic ge

178 nd mitochondrial dysfunction in subcutaneous white adipose tissue (sWAT).

179 5(+)Cd11b(+)Cd11c(+)MHCII(+) F4/80(-) DCs in white adipose tissue than did wild-type controls.

180 tion attenuates exercise-induced browning of white adipose tissue that is crucial for the metabolic b

181 pronounced cold-induced browning of inguinal white adipose tissue that is linked to induction of MC2R

182 In skeletal muscle and white adipose tissue, the abundance of GLUT4 protein, bu

183 s well as browning and lipid mobilization in white adipose tissue through stimulation of the sympathe

184 luation of MSCs from human bone marrow (BM), white adipose tissue, umbilical cord, and skin cultured

185 weight of various tissues but the brown and white adipose tissues underwent much more pronounced wei

186 Visceral white adipose tissue (vWAT) expands and undergoes extens

187 irect calorimetry was performed and visceral white adipose tissues (VWAT) were assessed for inflammat

188 Induction of recall responses within white adipose tissue was associated with the collapse of

189 r uncoupled respiration or "browning" of the white adipose tissue was found.

190 ereas sensitivity of the skeletal muscle and white adipose tissue was lower in HFHS than control dams

191 ncoupling protein 1 competent brite cells in white adipose tissue was not influenced by presence or a

192 White adipose tissue (WAT) - a key contributor in many m

193 dified mice to define the roles of Chi3l1 in white adipose tissue (WAT) accumulation and Th2 inflamma

194 gh-fat diet (HFD)-induced M1-M2 imbalance in white adipose tissue (WAT) and blocked HFD-induced obesi

195 IGFRKO) had a approximately 25% reduction in white adipose tissue (WAT) and brown adipose tissue (BAT

196 White adipose tissue (WAT) and brown adipose tissue (BAT

197 ore, palmitate oxidation was elevated in the white adipose tissue (WAT) and brown adipose tissue of A

198 nment normalized postnatal growth, decreased white adipose tissue (WAT) and hepatic fat, improved glu

199 ughout the study and biochemical analyses of white adipose tissue (WAT) and liver were performed.

200 Col5a2 knockdown also led to loss of dermal white adipose tissue (WAT) and markedly decreased abdomi

201 White adipose tissue (WAT) and the liver specifically ex

202 l model to investigate perivascular cells in white adipose tissue (WAT) and their potential to cause

203 hat endothelial production of PDGF-CC during white adipose tissue (WAT) angiogenesis regulates WAT br

204 ereas preferential expansion of subcutaneous white adipose tissue (WAT) appears protective.

205 on BA and the TGR5 receptor in subcutaneous white adipose tissue (WAT) are unknown.

206 nhanced Akt and AMPK signaling in muscle and white adipose tissue (WAT) as well as increased FoxO1 ph

207 We detected significant white adipose tissue (WAT) browning and improved systemi

208 fraction (SVF) under conditions that promote white adipose tissue (WAT) browning in mice.

209 endocrine factors contribute to cold-induced white adipose tissue (WAT) browning, but glucagon has la

210 White adipose tissue (WAT) can undergo a phenotypic swit

211 show that Sucnr1 is highly expressed in the white adipose tissue (WAT) compartment of mice and regul

212 ein-1 (Ucp1) regulates energy dissipation in white adipose tissue (WAT) depots.

213 White adipose tissue (WAT) dysfunction is generally thou

214 androgenemia, increased risk of obesity, and white adipose tissue (WAT) dysfunction.

215 The manner in which white adipose tissue (WAT) expands and remodels directly

216 a in developmental adipose lineage disrupted white adipose tissue (WAT) formation.

217 We determined that white adipose tissue (WAT) from CDK4-deficient mice exhi

218 esity results from an excessive expansion of white adipose tissue (WAT) from hypertrophy of preexisti

219 White adipose tissue (WAT) functions as an energy reserv

220 LSD1 interacts with PRDM16 to repress select white adipose tissue (WAT) genes but also represses hydr

221 Recently, browning of white adipose tissue (WAT) has gained attention as a the

222 ity, the physiological functions of Epac1 in white adipose tissue (WAT) has not been explored.

223 The recent discovery of browning of white adipose tissue (WAT) has raised great research int

224 that IEX-1 expression was highly induced in white adipose tissue (WAT) in both epidydmal and subcuta

225 Tbx15 is also differentially expressed among white adipose tissue (WAT) in different body depots.

226 istic events that facilitate the browning of white adipose tissue (WAT) in response to burns.

227 RK1/2 phosphatase, was induced in epididymal white adipose tissue (WAT) in response to diet-induced o

228 Human subcutaneous (SC) white adipose tissue (WAT) increases the expression of b

229 White adipose tissue (WAT) inflammation contributes to t

230 ajor risk factor for metabolic disease, with white adipose tissue (WAT) inflammation emerging as a ke

231 eleased Rosi promotes both transformation of white adipose tissue (WAT) into brown-like adipose tissu

232 White adipose tissue (WAT) is a complex organ with both

233 of lipid-burning pathways in the fat-storing white adipose tissue (WAT) is a promising strategy to im

234 Aging of white adipose tissue (WAT) is associated with reduced in

235 White adipose tissue (WAT) is essential for maintaining

236 e phenotype (CD45-CD34(+)) resident in human white adipose tissue (WAT) is known to promote the progr

237 The primary task of white adipose tissue (WAT) is the storage of lipids.

238 rmogenesis, though its effect on browning of white adipose tissue (WAT) is unclear.

239 es chronic macrophage-driven inflammation in white adipose tissue (WAT) leading to insulin resistance

240 ic acetyl CoA by suppression of lipolysis in white adipose tissue (WAT) leading to reductions in pyru

241 Subsequent macrophage infiltration into white adipose tissue (WAT) leads to increased lipolysis,

242 These derangements increase white adipose tissue (WAT) lipolysis and hepatic acetyl-

243 rown adipose tissue (BAT) thermogenesis, and white adipose tissue (WAT) lipolysis in vivo.

244 ng brown adipose tissue (BAT) thermogenesis, white adipose tissue (WAT) lipolysis, and insulin sensit

245 increased insulin-stimulated suppression of white adipose tissue (WAT) lipolysis.

246 as most significantly attenuated in visceral white adipose tissue (WAT) of DIO mice, and was coincide

247 s the recruitment of beige adipocytes in the white adipose tissue (WAT) of mice and humans, a process

248 we show that RIPK3 is over expressed in the white adipose tissue (WAT) of obese mice fed with a chol

249 White adipose tissue (WAT) overgrowth in obesity is link

250 White adipose tissue (WAT) primarily functions as an ene

251 programming; however, the effect of IUGR on white adipose tissue (WAT) progenitors is unknown.

252 Aifm2 in BAT and subcutaneous white adipose tissue (WAT) promotes oxygen consumption,

253 adipose tissue (BAT) function or browning of white adipose tissue (WAT) provides a defense against ob

254 ty lipoprotein-triglycerides (VLDL-TGs) into white adipose tissue (WAT) rather than oxidative tissues

255 pulation of beige adipocytes is increased in white adipose tissue (WAT) reflects a potential strategy

256 Maintenance of white adipose tissue (WAT) requires the proliferation an

257 ed 56% less body weight and 74% less gonadal white adipose tissue (WAT) than WT mice.

258 Obesity fosters low-grade inflammation in white adipose tissue (WAT) that may contribute to the in

259 Glucocorticoids promote lipolysis in white adipose tissue (WAT) to adapt to energy demands un

260 isomer in the adaptive metabolic response of white adipose tissue (WAT) to cold exposure (CE) in mice

261 of rapamycin complex 2 (mTORC2) functions in white adipose tissue (WAT) to control expression of the

262 pose tissue (BAT) and discriminating it from white adipose tissue (WAT) using cross-validation via PE

263 "brown-like" adipocytes within subcutaneous white adipose tissue (WAT) via a mechanism that stimulat

264 Sections of rat BAT and subcutaneous white adipose tissue (WAT) were stained for CB1 and unco

265 nses, and were recently identified in murine white adipose tissue (WAT) where they may act to limit t

266 lar brown tissue (iBAT) and those induced in white adipose tissue (WAT) with respect to their thermog

267 roduces a rapid and persistent remodeling of white adipose tissue (WAT), an increase in energy expend

268 In white adipose tissue (WAT), FGF21 regulates aspects of g

269 Activation of inflammation in white adipose tissue (WAT), includes infiltration/expans

270 have long been known to cause adaptations to white adipose tissue (WAT), including decreases in cell

271 s to inhibition of lipogenesis in epididymal white adipose tissue (WAT), induction of browning in ing

272 induced obesity because of browning of their white adipose tissue (WAT), leading to increased whole b

273 f acyl-CoAs and histone acetylation in mouse white adipose tissue (WAT), liver, and pancreas.

274 in the heart and skeletal muscle, but not in white adipose tissue (WAT), suggesting that lipasin supp

275 e tissue (BAT) thermogenesis and browning of white adipose tissue (WAT), which are both potential tar

276 n murine pregnancy, while there is a gain of white adipose tissue (WAT)-like features.

277 nesis and programming of beige adipocytes in white adipose tissue (WAT).

278 al co-activator Prdm16 regulates browning of white adipose tissue (WAT).

279 ar interest in thermogenesis and browning of white adipose tissue (WAT).

280 es in classic brown adipose tissue (BAT) and white adipose tissue (WAT).

281 triacylglycerol stored by adipocytes in the white adipose tissue (WAT).

282 nergy expenditure, partly due to browning of white adipose tissue (WAT).

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

284 ige/brite adipocytes (so-called browning) in white adipose tissue (WAT).

285 ty induces chronic low-grade inflammation in white adipose tissue (WAT).

286 ied by a decreased norepinephrine content in white adipose tissue (WAT).

287 hile enhancing thermogenesis and browning of white adipose tissue (WAT).

288 mportance of the enzyme for TG catabolism in white adipose tissue (WAT).

289 nsdifferentiation of BeAT into lipid-storing white adipose tissue (WAT).

290 exercise, brown fat cells also emerge in the white adipose tissue (WAT; also known as beige cells), a

291 Lipolysis in white adipose tissues (WAT) and lipolysis-induced blood

292 Beige/brite adipocytes are induced within white adipose tissues (WAT) and, when activated, consume

293 iver and visceral adipose tissue (epididymal white adipose tissue [WAT]), reduced WAT inflammation, e

294 rance of brown adipocytes (BAs) in brown and white adipose tissues (WATs) of adult mice.

295 n contrast, when LSD2-KO cells from inguinal white adipose tissues were subjected to beige induction,

296 White adipose tissue, where APN is produced and assemble

297 Here we report that FTO has a role in white adipose tissue which modifies its response to high

298 UCP1 (uncoupling-protein-1) in subcutaneous white adipose tissue which, together with classical brow

299 In contrast with white adipose tissue, which stores excess energy in the

300 hermoneutrality promotes the infiltration of white adipose tissue with mast cells that are highly enr