ライフサイエンスコーパス: WAT

1 WAT deposits were negative for (18)F-FMPEP-d2, consisten

2 WAT macrophages, however, differ in their origin, gene e

3 issue (WAT) and markedly decreased abdominal WAT that was characterized by miniadipocytes and increas

4 Brown adipose tissue (BAT) activity, WAT browning and energy expenditure were significantly h

5 or over 75% of fatty acids in white adipose (WAT) triacylglycerol (TAG).

6 syndrome through impairing BAT activity and WAT browning.

7 Caspase-8-dependent adipocyte apoptosis and WAT inflammation, associated with impaired insulin signa

8 ne with Gsalpha deficiency in mature BAT and WAT adipocytes (Ad-GsKO).

9 ation and cold-induced activation of BAT and WAT in lean young adults.

10 e the contribution of cold-activated BAT and WAT to daily DEE.

11 Both BAT and WAT undergo specific metabolic changes during acute cold

12 dynamic PET scans at the location of BAT and WAT.

13 ic responses during cold exposure in BAT and WAT.

14 chanism governing BAT fate determination and WAT plasticity.

15 ogated HFD-induced adipocyte hypertrophy and WAT inflammation.

16 ofiling of Rsl1-sensitive genes in liver and WAT indicates that RSL1 accentuates sex-biased gene expr

17 rake that inhibits fatty acid metabolism and WAT browning.Histone deacetylases, such as HDAC3, have b

18 ationship between the expression of Nck2 and WAT expansion was recapitulated in humans such that redu

19 noleic acid, which were present in serum and WAT after n-3 PUFA supplementation.

20 pression modulates MBH insulin signaling and WAT function in fasted mice.

21 Here we describe the relationship between WAT TAG composition in obese mouse models and obese huma

22 IGF1R has only a modest contribution to both WAT and BAT formation and function.

23 ost comparable with wild-type (WT) mice, but WAT content was greater.

24 These proteins were released by WAT progenitors in xenograft and transgenic breast cance

25 n in Insr(P1195L/+)/HFD liver was rescued by WAT transplantation, and the expression of Cyp7a1 was su

26 t regulatory mechanisms operate in different WAT depots.

27 DGFA target that is activated in ASCs during WAT hyperplasia and is functionally required for dermal

28 sed metabolism and measures of epididymal (e)WAT mitochondria and artery function in young (6.1 +/- 0

29 Enhanced WAT thermogenic potential, brown adipose tissue differen

30 uced weight loss was accompanied by enhanced WAT A20 expression, which is positively correlated with

31 Chronically enhancing WAT lipolysis could produce ectopic steatosis because of

32 ple levels, enhances lipolysis in epididymal WAT (eWAT) because of the upregulation of genes promotin

33 ipolysis and lipogenesis genes in epididymal WAT.

34 duced insulin signaling in liver, epididymal WAT and heart, and downregulation of oxidative enzymes i

35 cal brown fat (BAT) mass, but not white fat (WAT) mass.

36 ommon to both brown fat (BAT) and white fat (WAT), and the expression of BAT-selective genes.

37 rotic cells instead, which leads to fibrotic WAT in transplant experiments.

38 fferentiate into adipocytes ex vivo and form WAT when transplanted into recipient mice.

39 tection of human BAT and discrimination from WAT.

40 romal cells (ASCs) can become mobilized from WAT, recruited by tumours and promote cancer progression

41 ocytes and the resultant lipid overflow from WAT led to marked hepatosteatosis, dyslipidemia, and sys

42 ormin inhibited GM-CSF and MMP9 release from WAT progenitors in in vitro and xenograft models.

43 GM-CSF induced GM-CSF and MMP9 release from WAT progenitors, and GM-CSF knockdown in breast cancer c

44 els and increased adiponectin secretion from WAT explants in vitro, highlighting a potential anti-inf

45 0.0001) in supraclavicular BAT than gluteal WAT in all pediatric subjects.

46 Here we identify ILC2s in human WAT and demonstrate that decreased ILC2 responses in WAT

47 Furthermore, expression of Gq in human WAT inversely correlates with UCP1 expression.

48 pha(+) progenitor cells, as well as in human WAT-PDGFR-alpha(+) adipocytes, supporting the physiologi

49 atory role of this adipokine in hypertrophic WAT.

50 Taken together, these data identify WAT-derived hepatic acetyl CoA as the main regulator of

51 In WAT and the pancreas, HFD also impacted the levels of hi

52 In WAT, Id1 is mainly localized in the stromal vascular fra

53 rol regulatory element binding protein-1c in WAT accounted for the phenotype.

54 ased conversion of glucose to fatty acids in WAT but not liver.

55 r of adiponectin anti-inflammatory action in WAT and a potential target for mitigating obesity-relate

56 ator of energy homeostasis via its action in WAT.

57 ling protein 1 (UCP1)(+) beige adipocytes in WAT, a process known as beiging or browning that regulat

58 In contrast, cold up-regulates ANGPTL4 in WAT, abolishing a cold-induced increase in LPL activity.

59 adipose tissue and induction of browning in WAT and could be reversed by antagonism of beta3 adrener

60 dventitial cells and pericyte-like cells) in WAT, and Nestin-GFP specifically labels pericyte-like ce

61 tes were observed to significantly change in WAT depots up to 6 hours post exposure.

62 illic infiltration and subset composition in WAT.

63 ndrial function and mitochondrial content in WAT and found that MnSOD deletion increased mitochondria

64 s, an increase in beige adipocyte content in WAT browning would raise energy expenditure and reduce a

65 eased food intake, elevated lipid cycling in WAT and improved whole-body glucose metabolism and hepat

66 and increased M2-like Msmall ef, Cyrillic in WAT, while decreasing inflammatory monocytes.

67 obesity despite complete ATGL deficiency in WAT and normal adipocyte differentiation.

68 protectins and resolvins derived from DHA in WAT.

69 ChREBPbeta expression, which reduces DNL in WAT, and impairs hepatic insulin sensitivity.

70 further reveal that suppression of Epac1 in WAT decreases leptin mRNA expression and secretion by in

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

72 estigated EPO receptor (EPO-R) expression in WAT and characterized the role of its signaling during o

73 le for FSP27 in the storage of excess fat in WAT with minimizing ectopic fat accumulation that causes

74 n-1 in BAT, but neither protein was found in WAT.

75 These data suggest mTORC2 functions in WAT as part of an extra-hepatic nutrient-sensing mechani

76 d upregulation of anti-inflammatory genes in WAT, and peritoneal macrophages from KO mice displayed s

77 be critical for the maintenance of ILC2s in WAT and in limiting adiposity in mice by increasing calo

78 report that NNMT expression is increased in WAT and liver of obese and diabetic mice.

79 Browning is the result of the induction in WAT of a newly discovered type of adipocyte, the beige c

80 n led to adipocyte death and inflammation in WAT and a whitening of BAT.

81 ng machinery, while limiting inflammation in WAT, which together could restrict HFD-induced fat accum

82 ession in liver but greatly diminishes it in WAT.

83 Nnmt knockdown in WAT and liver protects against diet-induced obesity by a

84 sting induces Angptl4, which inhibits LPL in WAT to direct circulating TAG to cardiac and skeletal mu

85 h acetylation of specific histone lysines in WAT but not in the liver.

86 ts phosphodiesterase Pde1b in BAT but not in WAT.

87 Ablation of PDE3B in WAT prevents inflammasome activation by reducing express

88 However, the role SMAD3 plays in WAT browning is not clearly understood.

89 lar cells as fibro/adipogenic progenitors in WAT and show that PDGFRalpha targets progenitor cell pla

90 g and activated thermogenic genes program in WAT but not in BAT by promoting alternative activation o

91 le in macrophage chemotaxis, were reduced in WAT of PDE3B(-/-)mice.

92 only the IR (F-IRKO) had a 95% reduction in WAT, but a paradoxical 50% increase in BAT with accumula

93 demonstrate that decreased ILC2 responses in WAT are a conserved characteristic of obesity in humans

94 cold exposure decreased the (11)C-HED RI in WAT (0.44 +/- 0.22 vs. 0.41 +/- 0.18) as a consequence o

95 hese findings provide evidence that RIPK3 in WAT maintains tissue homeostasis and suppresses inflamma

96 Chi3l1 also played a critical role in WAT accumulation and lung Th2 inflammation.

97 minished angiopoietin-1 (Ang-1) secretion in WAT from obese subjects.

98 promoting leptin expression and secretion in WAT.

99 er but are dependent on insulin signaling in WAT, which becomes defective with inflammation.

100 is a major regulator of insulin signaling in WAT.

101 sociated with impaired insulin signalling in WAT as the basis for glucose intolerance.

102 ed to reduced lipid synthesis and storage in WAT of HFD-fed AKO/cTg mice.

103 uction in delivery to and retention of TG in WAT, fat mass was largely preserved by a compensatory in

104 ke and EE and activation of thermogenesis in WAT and brown adipose tissue were lost in Fgf21(-/-) mic

105 teins that were significantly upregulated in WAT-derived progenitors after coculture with breast canc

106 f proopiomelanocortin neurons also increased WAT browning and decreased adiposity.

107 fat storage without the predicted increased WAT inflammation or loss of insulin sensitivity.

108 prevented diet-induced obesity by increasing WAT browning and energy expenditure.

109 Macrophage-induced WAT lipolysis also stimulates hepatic gluconeogenesis, p

110 ipid storage and diminish macrophage-induced WAT lipolysis will reverse the root causes of type 2 dia

111 ted overexpression (Ad-FLD) not only induces WAT lipolysis in vivo but also reduces diet-induced obes

112 induced skeletal muscle hormone that induces WAT browning similar to that observed in SMAD3-deficient

113 in, but it increased FNDC5 content in SC Ing WAT.

114 ely, exercise induced browning of the SC Ing WAT.

115 nover is very different in iBAT and inguinal WAT (ingWAT); the former showed minimal changes in prote

116 /-) mice, particularly in heart and inguinal WAT.

117 sue (WAT), induction of browning in inguinal WAT and activation of adaptive thermogenesis in brown ad

118 nd oxidative and lipogenic genes in inguinal WAT.

119 ocular subcutaneous adipose tissue (inguinal WAT) with upregulated oxidative/thermogenic gene express

120 ro analyses in mice, EPO treatment inhibited WAT inflammation, normalized insulin sensitivity, and re

121 ly that the increased uptake of glucose into WAT explains the increased insulin sensitivity associate

122 excessive inflammatory cell recruitment into WAT and by supporting thermogenic activity of BAT.

123 hereas feeding increased VLDL-TG uptake into WAT eightfold in wild-type mice, no increase occurred in

124 Glucose uptake into WAT was increased 10-fold in KO mice, and tracer studies

125 d suggest that Nck2 is important in limiting WAT expansion and dysfunction in mice and humans.

126 s a browning signature programme that limits WAT expansion in transgenic mice for a period of up to 1

127 g monocyte-derived inflammatory macrophages, WAT-resident macrophages counteract inflammation and ins

128 The major WAT depots in the body are found in the visceral cavity

129 SREBP-1 is highly expressed in mature WAT and plays a critical role in promoting in vitro adip

130 responses, were modulated in PDE3B(-/-)mice WAT, including smad, NFAT, NFkB, and MAP kinases.

131 In several murine models, WAT cells and progenitors were found to have cooperative

132 of a beige phenotype in differentiated mouse WAT-PDGFR-alpha(+) progenitor cells, as well as in human

133 ipogenesis and lipolysis activities in mouse WAT as well as in stromal vascular fraction and 3T3-L1 p

134 ression is markedly increased in obese mouse WAT and is stimulated by tumor necrosis factor-alpha in

135 of the radiotracer to BAT sections (but not WAT) in vitro was high and displaceable by pretreatment

136 IGFRKO) showed an almost complete absence of WAT and BAT.

137 w to inhibit the tumor-promoting activity of WAT cells and progenitors.

138 s neutralized the protumorigenic activity of WAT progenitors in preclinical models.

139 on mitochondrial function, the "beiging" of WAT, regulation of adipokines, metabolic effects of trai

140 mediator Rbpj in mice results in browning of WAT and elevated expression of uncoupling protein 1 (Ucp

141 ad impaired BAT function, absent browning of WAT, and reduced lipolysis, and were therefore cold-into

142 /6J mice with LXA4, which showed browning of WAT, strongly suggests that LXA4 is responsible for the

143 The contribution of WAT to whole-body DEE was approximately 150 kcal/d at re

144 ulin and leptin, with the central control of WAT browning.

145 reatments with chemicals, specific depots of WAT undergo a browning process, characterized by highly

146 nd MMP9 promote the protumorigenic effect of WAT progenitors on local and metastatic breast cancer.

147 ue (WAT), includes infiltration/expansion of WAT macrophages, contributes pathogenesis of obesity, in

148 allergen challenge augment the expression of WAT and pulmonary Chi3l1.

149 Dysregulation of all of these functions of WAT, together with low-grade inflammation of the tissue

150 The level of WAT TGR5 gene expression decreased after surgery, but no

151 om caloric restriction, whereas the level of WAT TGR5 protein is unaffected.

152 ccompanied by increased levels of markers of WAT and lipid accumulation.

153 tify EPO-R signaling as a novel regulator of WAT inflammation, extending its nonerythroid activity to

154 Our results unveil HDAC3 as a regulator of WAT physiology, which acts as a molecular brake that inh

155 e effects of dietary MR on EE, remodeling of WAT, and increased insulin sensitivity but not of its ef

156 immune cell type in the beiging response of WAT.

157 3 in fat switches the metabolic signature of WAT by activating a futile cycle of de novo fatty acid s

158 The risks associated with the use of WAT cells for breast reconstructions should be better in

159 we discuss the recent increase in the use of WAT-derived progenitor cells in breast cancer patients t

160 Stimulating beige adipocyte development, or WAT browning, increases energy expenditure and holds pot

161 selective genes, but not common fat genes or WAT-selective genes, are demarcated by H3K27me3 in both

162 ynthesis and beta-oxidation that potentiates WAT oxidative capacity and ultimately supports browning.

163 together on hypothalamic neurons to promote WAT browning and weight loss.

164 didymal white adipose tissue [WAT]), reduced WAT inflammation, elevated adiponectin, mulitilocular su

165 In agreement with reduced WAT lipolysis, glucocorticoid- initiated hepatic steatos

166 adipose tissue (WAT) angiogenesis regulates WAT browning.

167 Here the authors show that HDAC3 regulates WAT metabolism by activating a futile cycle of fatty aci

168 that histone deacetylase 3 (HDAC3) regulates WAT metabolism and function.

169 d inflammatory responses in Reverbalpha(-/-) WAT depots were associated with tonic elevation of A20 p

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

171 Similar WAT expansion is achieved upon infection with an adeno-a

172 t methods, we show that even within a single WAT depot, high Tbx15 expression is restricted to a subs

173 In the small WAT of these mice, small adipocytes containing multilocu

174 energy expenditure, were lean with a smaller WAT compartment, and had improved glucose buffering.

175 Adrb1 activation stimulates WAT resident perivascular (Acta2+) cells to form cold-in

176 ted differences in visceral and subcutaneous WAT thermogenic metabolism and demonstrate the distinct

177 brown adipose tissue (BAT) and subcutaneous WAT.

178 e key transcriptional events in subcutaneous WAT of mice in response to mitoNEET overexpression and a

179 od flow and (18)F-FDG uptake in subcutaneous WAT, indicating that the physiologic response is to redu

180 xpression of UCP1 and Pref-1 in subcutaneous WAT.

181 ormation of beige adipocytes in subcutaneous WAT.

182 ic genes (Ucp1 and Ppargc1a) in subcutaneous WAT.

183 and mitochondrial biogenesis in subcutaneous WAT.

184 Therefore, browning of subcutaneous WAT likely exerted a compensatory effect and raised whol

185 y (2 hours) in both BAT and the subcutaneous WAT depots, with the most striking change being observed

186 xercise-induced browning of the subcutaneous WAT provides an alternative mechanism that reduces therm

187 Unlike subcutaneous WAT, visceral WAT is resistant to adopting a protective

188 acid synthesis and oxidation, which supports WAT browning.

189 ts of glucose metabolism, and in susceptible WAT depots, it can cause browning.

190 i.v. administration of these NPs can target WAT vasculature, stimulate the angiogenesis that is requ

191 is because of an overflow of lipids from the WAT to peripheral tissues; however, this did not occur w

192 cological blockade of PDGFR-alpha impair the WAT-beige transition.

193 reases beige gene and Ucp1 expression in the WAT in response to cold exposure.

194 the roles of Chi3l1 in white adipose tissue (WAT) accumulation and Th2 inflammation and blockers of s

195 ced M1-M2 imbalance in white adipose tissue (WAT) and blocked HFD-induced obesity, insulin resistance

196 ately 25% reduction in white adipose tissue (WAT) and brown adipose tissue (BAT), whereas mice lackin

197 on was elevated in the white adipose tissue (WAT) and brown adipose tissue of AdSod2 KO mice fed an H

198 eous inguinal (SC Ing) white adipose tissue (WAT) and how it affects whole-body energy expenditure in

199 us and intra-abdominal white adipose tissue (WAT) and interscapular brown adipose tissue (BAT), causi

200 iochemical analyses of white adipose tissue (WAT) and liver were performed.

201 led to loss of dermal white adipose tissue (WAT) and markedly decreased abdominal WAT that was chara

202 White adipose tissue (WAT) and the liver specifically expressed Fsp27alpha and

203 perivascular cells in white adipose tissue (WAT) and their potential to cause organ fibrosis.

204 tion of PDGF-CC during white adipose tissue (WAT) angiogenesis regulates WAT browning.

205 ansion of subcutaneous white adipose tissue (WAT) appears protective.

206 Beige adipocytes in white adipose tissue (WAT) are similar to classical brown adipocytes in that t

207 ceptor in subcutaneous white adipose tissue (WAT) are unknown.

208 ignaling in muscle and white adipose tissue (WAT) as well as increased FoxO1 phosphorylation and expr

209 e detected significant white adipose tissue (WAT) browning and improved systemic insulin sensitivity

210 onditions that promote white adipose tissue (WAT) browning in mice.

211 White adipose tissue (WAT) can undergo a phenotypic switch, known as browning,

212 we discuss the role of white adipose tissue (WAT) cells and of related soluble factors in the local a

213 ighly expressed in the white adipose tissue (WAT) compartment of mice and regulates adipose mass and

214 ion and secretion from white adipose tissue (WAT) depots, the induction of LCN2 varied among differen

215 ing gene expression in white adipose tissue (WAT) from adipose-specific Glut4-knockout or adipose-spe

216 We determined that white adipose tissue (WAT) from CDK4-deficient mice exhibits impaired lipogene

217 excessive expansion of white adipose tissue (WAT) from hypertrophy of preexisting adipocytes and enha

218 White adipose tissue (WAT) functions as an energy reservoir where excess circu

219 DM16 to repress select white adipose tissue (WAT) genes but also represses hydroxysteroid 11-beta-deh

220 functions of Epac1 in white adipose tissue (WAT) has not been explored.

221 scovery of browning of white adipose tissue (WAT) has raised great research interest because of its s

222 t immune activation in white adipose tissue (WAT) impairs insulin sensitivity and systemic metabolism

223 was highly induced in white adipose tissue (WAT) in both epidydmal and subcutaneous depots but not i

224 tially expressed among white adipose tissue (WAT) in different body depots.

225 induced in epididymal white adipose tissue (WAT) in response to diet-induced obesity.

226 uman subcutaneous (SC) white adipose tissue (WAT) increases the expression of beige adipocyte genes i

227 etabolic disease, with white adipose tissue (WAT) inflammation emerging as a key underlying pathology

228 both transformation of white adipose tissue (WAT) into brown-like adipose tissue and angiogenesis, wh

229 White adipose tissue (WAT) is a complex organ with both metabolic and endocrin

230 like transformation in white adipose tissue (WAT) is a promising strategy for combating obesity.

231 inflammation of human white adipose tissue (WAT) is associated with metabolic and vascular alteratio

232 White adipose tissue (WAT) is essential for maintaining metabolic function, es

233 (+)) resident in human white adipose tissue (WAT) is known to promote the progression of local and me

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

235 driven inflammation in white adipose tissue (WAT) leading to insulin resistance.

236 ession of lipolysis in white adipose tissue (WAT) leading to reductions in pyruvate carboxylase flux.

237 hage infiltration into white adipose tissue (WAT) leads to increased lipolysis, which further increas

238 and that key liver and white adipose tissue (WAT) metabolic genes are altered in both Rsl1(-/-) sexes

239 attenuated in visceral white adipose tissue (WAT) of DIO mice, and was coincident with elevated tissu

240 decreased by 50-90% in white adipose tissue (WAT) of Mif(-/-) mice.

241 over expressed in the white adipose tissue (WAT) of obese mice fed with a choline-deficient high-fat

242 tical influence of the white adipose tissue (WAT) on metabolism is well-appreciated in obesity, but a

243 White adipose tissue (WAT) overgrowth in obesity is linked with increased aggr

244 White adipose tissue (WAT) primarily functions as an energy reservoir, while b

245 erides (VLDL-TGs) into white adipose tissue (WAT) rather than oxidative tissues (skeletal muscle, hea

246 ocytes is increased in white adipose tissue (WAT) reflects a potential strategy in the fight against

247 White adipose tissue (WAT) releases fatty acids from stored triacylglycerol fo

248 Maintenance of white adipose tissue (WAT) requires the proliferation and differentiation of a

249 t and 74% less gonadal white adipose tissue (WAT) than WT mice.

250 s promote lipolysis in white adipose tissue (WAT) to adapt to energy demands under stress, whereas su

251 (mTORC2) functions in white adipose tissue (WAT) to control expression of the lipogenic transcriptio

252 discriminating it from white adipose tissue (WAT) using cross-validation via PET.

253 es within subcutaneous white adipose tissue (WAT) via a mechanism that stimulates UCP-1 expression.

254 t BAT and subcutaneous white adipose tissue (WAT) were stained for CB1 and uncoupling protein-1 by im

255 y identified in murine white adipose tissue (WAT) where they may act to limit the development of obes

256 ) and those induced in white adipose tissue (WAT) with respect to their thermogenic capacity, we exam

257 rsistent remodeling of white adipose tissue (WAT), an increase in energy expenditure (EE), and enhanc

258 y leukocyte content in white adipose tissue (WAT), despite comparable food intake.

259 upon overexpression in white adipose tissue (WAT), exerts a positive impact on tissue expansion and w

260 In white adipose tissue (WAT), FGF21 regulates aspects of glucose metabolism, and

261 ion of inflammation in white adipose tissue (WAT), includes infiltration/expansion of WAT macrophages

262 o cause adaptations to white adipose tissue (WAT), including decreases in cell size and lipid content

263 ogenesis in epididymal white adipose tissue (WAT), induction of browning in inguinal WAT and activati

264 e of browning of their white adipose tissue (WAT), leading to increased whole body energy expenditure

265 e acetylation in mouse white adipose tissue (WAT), liver, and pancreas.

266 tal muscle, but not in white adipose tissue (WAT), suggesting that lipasin suppresses the activity of

267 enesis and browning of white adipose tissue (WAT), which are both potential targets for treating obes

268 ile there is a gain of white adipose tissue (WAT)-like features.

269 wn-like/beige cells in white adipose tissue (WAT).

270 so-called browning) in white adipose tissue (WAT).

271 epinephrine content in white adipose tissue (WAT).

272 enesis and browning of white adipose tissue (WAT).

273 e for TG catabolism in white adipose tissue (WAT).

274 of beige adipocytes in white adipose tissue (WAT).

275 regulates browning of white adipose tissue (WAT).

276 enesis and browning of white adipose tissue (WAT).

277 ipose tissue (BAT) and white adipose tissue (WAT).

278 d by adipocytes in the white adipose tissue (WAT).

279 tly due to browning of white adipose tissue (WAT).

280 lls also emerge in the white adipose tissue (WAT; also known as beige cells), a process known as brow

281 ose tissue (epididymal white adipose tissue [WAT]), reduced WAT inflammation, elevated adiponectin, m

282 Lipolysis in white adipose tissues (WAT) and lipolysis-induced blood glucose rise were incre

283 es are induced within white adipose tissues (WAT) and, when activated, consume glucose and fatty acid

284 Thus, the profound changes to WAT in response to exercise training may be part of the

285 ion, suggesting alpha2(V) to be important to WAT development/maintenance.

286 ing restrains sympathetic nervous outflow to WAT in fasted mice.

287 keletal muscles to direct circulating TAG to WAT for storage; conversely, fasting induces Angptl4, wh

288 s circulating fatty acids are transported to WAT, converted to triglycerides, and stored as unilocula

289 nsformation of adipose tissue, and transform WAT into brown-like adipose tissue, by the up-regulation

290 in Insr(P1195L/+)/HFD mice, while wild-type WAT transplantation ameliorated the hyperglycemia and th

291 ession of TBX15 in subcutaneous and visceral WAT is positively correlated with markers of glycolytic

292 rmogenic genes in interscapular and visceral WAT.

293 These data indicate that beneficial visceral WAT browning can be engineered by directing visceral whi

294 Endothelial cells from visceral WAT (VAT-ECs) exhibit a proinflammatory and senescent ph

295 k2 protein and mRNA levels in human visceral WAT significantly correlate with the degree of obesity.

296 Similarly to mice, in visceral WAT of obese humans, RIPK3 is overexpressed and correlat

297 cal consequences of browning murine visceral WAT by selective genetic ablation of Zfp423, a transcrip

298 Thermogenic visceral WAT improves cold tolerance and prevents and reverses in

299 Unlike subcutaneous WAT, visceral WAT is resistant to adopting a protective thermogenic ph

300 heterogeneity of cellular metabolism within WAT that has potential impact in the understanding of hu