ライフサイエンスコーパス: WAT

1 WAT aging in mice impairs cold-induced beige adipocyte r

2 WAT and blood samples were collected from patients admit

3 WAT and serum collected were analyzed for browning marke

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

5 Adiponectin, a WAT-derived hormone that has antidiabetic and antiinflam

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

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

8 responses of skeletal muscle, white adipose (WAT), and brown adipose (BAT) tissues.

9 ially required for WAT development and adult WAT homeostasis.

10 gfra in adult adipose lineage did not affect WAT homeostasis.

11 f young mice yet increased autophagy in aged WAT.

12 geted to improve insulin sensitivity in aged WAT.

13 syndrome through impairing BAT activity and WAT browning.

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

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

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

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

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

19 e of brown and white adipose tissue (BAT and WAT) NAD(+) metabolism in regulating whole-body thermoge

20 ANKO mice, which lack NAMPT in both BAT and WAT, had impaired gene programs involved in thermogenesi

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

22 ic responses during cold exposure in BAT and WAT.

23 ojections to muscle + WAT, muscle + BAT, and WAT + BAT.

24 HFD dams decreased the body weight gain and WAT mass as well as lowered the serum levels of insulin

25 ogated HFD-induced adipocyte hypertrophy and WAT inflammation.

26 proinflammatory gene expression in liver and WAT and increased thermogenic gene expression in brown a

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

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

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

30 ese fatty acids alleviate obesity-associated WAT inflammation, improve energy metabolism, and increas

31 Cold exposure decreased p53 in beiging WAT of young mice but not in aged mice.

32 cold exposure repressed autophagy in beiging WAT of young mice yet increased autophagy in aged WAT.

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

34 s reveal a permissive mechanism that bridges WAT inflammation to whole-body insulin sensitivity.

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

36 er flow cytometry analysis in blood and s.c. WAT (SAT).

37 Ucp1 expression in canine WAT was increased at sites implanted with thermogenic vs

38 e tissue-resident multipotent stromal cells (WAT-MSCs) can act as a reservoir for IL-33, especially a

39 rrested state commensurate with conventional WAT measurements.

40 tional potential aimed to reduce deleterious WAT depots in humans and pets.

41 ly-used experimental techniques to determine WAT, none provides unambiguous molecular-level informati

42 t regulatory mechanisms operate in different WAT depots.

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

44 Enhanced WAT thermogenic potential, brown adipose tissue differen

45 Chronically enhancing WAT lipolysis could produce ectopic steatosis because of

46 ipolysis and lipogenesis genes in epididymal WAT.

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

48 gene itself are differentially required for WAT development and adult WAT homeostasis.

49 analyses revealed that BMAT is distinct from WAT and BAT, with altered glucose metabolism and decreas

50 Thus, BMAT is functionally distinct from WAT and BAT.

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

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

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

54 3 feed back to induce eotaxin secretion from WAT-MSCs, supporting eosinophil recruitment.

55 Healthy WAT expansion, observed in the "metabolically healthy" o

56 e has been established, it is less clear how WAT inflammation is initiated.

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

58 th innate and adaptive immune cells in human WAT under conditions of obesity and calorie restriction

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

60 nd cardioprotective effects, can also impact WAT and BAT function.

61 s can also modulate gut microbiota impacting WAT function and adiposity.

62 hite adipocytes is causative of age-impaired WAT beiging remains unknown.

63 d mitophagy in aged white adipocytes impedes WAT beiging and may be therapeutically targeted to impro

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

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

66 ator of energy homeostasis via its action in WAT.

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

68 e to the inhibition of beige adipogenesis in WAT, and also promotes age-related and diet-induced fat

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

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

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

72 ng and dissociating specific coregulators in WAT, driving the expression of PPARalpha target genes su

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

74 cylglycerol (TAG)/fatty acid (FA) cycling in WAT through impacting lipogenesis and lipolysis.

75 protectins and resolvins derived from DHA in WAT.

76 PAHSAs inhibited lipolysis directly in WAT explants and enhanced the action of insulin to suppr

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

78 C2 to sustain a type-2 immune environment in WAT.

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

80 rvoir of TAG-bound PAHSAs (TAG estolides) in WAT.

81 STAT1 expression in WAT inversely correlated with fasting plasma glucose in

82 of uncoupling protein 1 (UCP1) expression in WAT, which correlates with smoking status.

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

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

85 r suppressor p53 has also been implicated in WAT aging.

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

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

88 In addition, the absence of NAMPT in WAT markedly reduced adrenergic-mediated lipolytic activ

89 moted local production of 5- and 9-PAHSAs in WAT.

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

91 of tissue-resident progenitor populations in WAT made possible through single-cell RNA sequencing ana

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

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

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

95 nce due to oestradiol-mediated reductions in WAT inflammation, leading to improved insulin-mediated s

96 radiol also displayed striking reductions in WAT inflammation, represented by reductions in plasma an

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

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

99 promoting leptin expression and secretion in WAT.

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

101 is a major regulator of insulin signaling in WAT.

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

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

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

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

106 ferentiated adipocytes restored cold-induced WAT beiging and augmented whole-body energy expenditure

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

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

109 ynthesis pathway, alleviated obesity-induced WAT inflammation and insulin resistance.

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

111 ated with elevated BAT activity and inguinal WAT thermogenic program.

112 ted thermogenic function in BAT and inguinal WAT through the upregulation of UCP1 and other thermogen

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

114 nd oxidative and lipogenic genes in inguinal WAT.

115 ntrols, we examined the response of inguinal WAT (iWAT) and interscapular brown adipose tissue (BAT)

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

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

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

119 Despite its significance, many WAT-related pathophysiogical mechanisms in humans are st

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

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

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

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

124 % of CGRP cells dually projected to muscle + WAT and muscle + BAT.

125 rainstem showed dual projections to muscle + WAT, muscle + BAT, and WAT + BAT.

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

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

128 atients (eg, burns, cancer), the browning of WAT has presented substantial clinical challenges relate

129 e show that nicotine induces the browning of WAT through a central mechanism and that this effect is

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

131 ignaling blunts the cold-induced browning of WAT, possibly due, in part, to impaired adrenergic signa

132 /6J mice with LXA4, which showed browning of WAT, strongly suggests that LXA4 is responsible for the

133 mogenic markers resulting in the browning of WAT.

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

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

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

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

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

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

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

141 that central nicotine-induced modulation of WAT browning may be a target against human obesity.

142 mined sex-specific adipogenic programming of WAT progenitors isolated from pups on the postnatal day

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

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

145 ging applications in mechanistic research of WAT-related biology, in studying of pathophysiological m

146 immune cell type in the beiging response of WAT.

147 3 in fat switches the metabolic signature of WAT by activating a futile cycle of de novo fatty acid s

148 to improved insulin-mediated suppression of WAT lipolysis and reduced ectopic lipid content in liver

149 agon was required for the effects of cold on WAT browning.

150 SD) exerts synergistic functional effects on WAT, leading to increased lipid accumulation in visceral

151 Moreover, pathologic WAT remodeling, typically characterized by adipocyte hyp

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

153 In summary, IUGR programs WAT preadipocytes to greater adipogenic potential in mal

154 ce with mild hyperbilirubinemia have reduced WAT size and an increased number of mitochondria, associ

155 STAT1 (a-KO) reduced WAT inflammation, but insulin resistance persisted in ob

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

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

158 adipose tissue (WAT) angiogenesis regulates WAT browning.

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

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

161 he PPARalpha coregulator profile, remodeling WAT to improve metabolic function, and reducing fat accu

162 whether transient p53 inhibition can rescue WAT beiging.

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

164 Mast cells increased in number in SC WAT in lean subjects, and there was an increase in the n

165 n subjects and mast cell degranulation in SC WAT of all research participants independent of baseline

166 ted positively with the change in UCP1 in SC WAT, leading to the hypothesis that mast cells promote S

167 In SC WAT, mirabegron treatment stimulated lipolysis, reduced

168 We quantified mast cell recruitment into SC WAT and degranulation.

169 Subjects with the most SC WAT beiging showed the greatest improvement in beta cell

170 s, these data suggest that the beiging of SC WAT by mirabegron reduces adipose tissue dysfunction, wh

171 to the hypothesis that mast cells promote SC WAT beiging in response to cold.

172 arkers, cytokines, and chemokines) on the SC WAT from lean subjects.

173 ing in subcutaneous white adipose tissue (SC WAT) of humans independent of body mass index.

174 ion in subcutaneous white adipose tissue (SC WAT), would induce other beneficial changes in fat and m

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

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

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

178 tries among skeletal muscle and subcutaneous WAT and BAT.

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

180 brown adipose tissue (BAT) and subcutaneous WAT.

181 se into male rat gastrocnemius, subcutaneous WAT and interscapular BAT, coupled with neurochemical ch

182 d with reduced fat cell size in subcutaneous WAT depots.

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

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

185 and mitochondrial biogenesis in subcutaneous WAT.

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

187 greater than in axial bones or subcutaneous WAT and can be greater than that in skeletal muscle, und

188 ages recruited to burn-stressed subcutaneous WAT (sWAT) undergo alternative activation to induce tyro

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

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

191 for insulin resistance, whereas subcutaneous WAT expansion is protective.

192 acid synthesis and oxidation, which supports WAT browning.

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

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

195 Wax appearance temperature (WAT), defined as the temperature at which the first soli

196 Indeed, we demonstrate that WAT-MSCs also support ICAM-1-mediated proliferation and

197 We hypothesized that WAT, BAT, and skeletal muscle may share an integrated re

198 The WAT-on-a-chip is a multilayer device that features tissu

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

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

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

202 White adipose tissue (WAT) - a key contributor in many metabolic diseases - co

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

204 White adipose tissue (WAT) and brown adipose tissue (BAT) are involved in whol

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

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

207 atal growth, decreased white adipose tissue (WAT) and hepatic fat, improved glucose and insulin toler

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

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

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

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

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

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

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

215 ribute to cold-induced white adipose tissue (WAT) browning, but glucagon has largely been ignored.

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

217 energy dissipation in white adipose tissue (WAT) depots.

218 White adipose tissue (WAT) dysfunction is generally thought to promote the dev

219 d risk of obesity, and white adipose tissue (WAT) dysfunction.

220 The manner in which white adipose tissue (WAT) expands and remodels directly impacts the risk of d

221 pose lineage disrupted white adipose tissue (WAT) formation.

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

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

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

225 Recently, browning of white adipose tissue (WAT) has gained attention as a therapeutic strategy to c

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

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

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

229 litate the browning of white adipose tissue (WAT) in response to burns.

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

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

232 White adipose tissue (WAT) inflammation contributes to the development of insu

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

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

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

236 ays in the fat-storing white adipose tissue (WAT) is a promising strategy to improve metabolic health

237 Aging of white adipose tissue (WAT) is associated with reduced insulin sensitivity, whi

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

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

240 effect on browning of white adipose tissue (WAT) is unclear.

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

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

243 derangements increase white adipose tissue (WAT) lipolysis and hepatic acetyl-CoA content, rates of

244 AT) thermogenesis, and white adipose tissue (WAT) lipolysis in vivo.

245 e (BAT) thermogenesis, white adipose tissue (WAT) lipolysis, and insulin sensitivity.METHODSWe treate

246 mulated suppression of white adipose tissue (WAT) lipolysis.

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

248 eige adipocytes in the white adipose tissue (WAT) of mice and humans, a process that has been extensi

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

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

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

252 the effect of IUGR on white adipose tissue (WAT) progenitors is unknown.

253 n BAT and subcutaneous white adipose tissue (WAT) promotes oxygen consumption, uncoupled respiration,

254 unction or browning of white adipose tissue (WAT) provides a defense against obesity.

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

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

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

258 -grade inflammation in white adipose tissue (WAT) that may contribute to the insulin resistance that

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

260 metabolic response of white adipose tissue (WAT) to cold exposure (CE) in mice, exploring the cross

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

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

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

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

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

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

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

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

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

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

271 eAT into lipid-storing white adipose tissue (WAT).

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

273 regulates browning of white adipose tissue (WAT).

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

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

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

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

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

279 -grade inflammation in white adipose tissue (WAT).

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

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

282 , yet unlike white or brown adipose tissues (WAT or BAT) its metabolic functions remain unclear.

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

284 arly, 31-68% of CGRP cells projected both to WAT + BAT.

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

286 her in vivo studies showed that, compared to WAT, BMAT resists insulin-stimulated Akt phosphorylation

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

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

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

290 rmogenic genes in interscapular and visceral WAT.

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

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

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

294 -genome transcriptional response in visceral WAT to T and WSD, alone and in combination.

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

296 Preferential accumulation of visceral WAT is associated with increased risk for insulin resist

297 -genome DNA methylation analysis of visceral WAT.

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