ライフサイエンスコーパス: thermogenesis

1 icing program that suppresses adipose tissue thermogenesis.

2 ical controller of brown and beige adipocyte thermogenesis.

3 reased energy expenditure and adipose tissue thermogenesis.

4 on and treatment of obesity by enhancing BAT thermogenesis.

5 sis, which may have contributed to increased thermogenesis.

6 ble to achieve weight loss through increased thermogenesis.

7 sure and whether they are both necessary for thermogenesis.

8 tent with increased fatty acid oxidation and thermogenesis.

9 re in mice, highlighting a potential role in thermogenesis.

10 o prioritize translation of key proteins for thermogenesis.

11 ate and activate beige adipocytes, producing thermogenesis.

12 metabolism, physical activity, and adaptive thermogenesis.

13 e to the LPS-induced suppression of adaptive thermogenesis.

14 nses are key regulators to suppress adaptive thermogenesis.

15 ted and/or multiple redundant control of BAT thermogenesis.

16 an important role in cold- and diet-induced thermogenesis.

17 es strongly implicated in the control of BAT thermogenesis.

18 ing fatty acids to BAT to fuel non-shivering thermogenesis.

19 brown adipose tissue and thus non-shivering thermogenesis.

20 iture by shifting nutrient oxidation towards thermogenesis.

21 4) as a dominant transcriptional effector of thermogenesis.

22 th increased energy expenditure and adaptive thermogenesis.

23 oupling protein 1 (Ucp1), a key regulator of thermogenesis.

24 ipose cell fate, and hormonal control of BAT thermogenesis.

25 ion and uncoupling protein 1 (UCP1)-mediated thermogenesis.

26 rated by the respiratory chain and increases thermogenesis.

27 eration substituted for brown adipose tissue thermogenesis.

28 onidine-evoked inhibition of BAT SNA and BAT thermogenesis.

29 ator of mitochondrial function and brown fat thermogenesis.

30 mmunity is an outcome of cold stress-induced thermogenesis.

31 hypotheses on the role of thyroid hormone in thermogenesis.

32 tabolic rate caused by impaired nonshivering thermogenesis.

33 sults from variation in brown adipose tissue thermogenesis.

34 long been implicated in feeding behavior and thermogenesis.

35 ld-induced hypothermia was due to suppressed thermogenesis.

36 blood flow to deliver glucose and oxygen for thermogenesis.

37 BAT sympathetic nerve activity (SNA) and BAT thermogenesis.

38 critical organs from hypothermia by adaptive thermogenesis.

39 small mammals and neonates through adaptive thermogenesis.

40 PGDPs reduces body weight and increases iBAT thermogenesis.

41 viously unappreciated pathway that regulates thermogenesis.

42 ficantly compromises the beige phenotype and thermogenesis.

43 ) BAT, suggesting that loss of Id1 increases thermogenesis.

44 odenal lipid-induced activation of brown fat thermogenesis.

45 (Serca) pump, is necessary for muscle-based thermogenesis.

46 onal coregulator of oxidative metabolism and thermogenesis.

47 XM requires GLP-1R activation to induce iBAT thermogenesis.

48 ave recently been shown to control brown fat thermogenesis.

49 physiological relevance of this E3 ligase in thermogenesis.

50 in-brown adipose tissue neuraxis to regulate thermogenesis.

51 ature, created by captured sunlight or plant thermogenesis.

52 pothalamus receptors to control appetite and thermogenesis.

53 with specialized roles in energy storage and thermogenesis.

54 ect role in adipocyte metabolism or adaptive thermogenesis.

55 activates brown adipose tissue and enhances thermogenesis.

56 nergy expenditure, a process called adaptive thermogenesis.

57 pated as heat in a process known as adaptive thermogenesis.

58 issue (BAT) provides a means of nonshivering thermogenesis.

59 nic program by PRDM16, a master regulator of thermogenesis.

60 -Br2 significantly inhibits brown adipocytes thermogenesis.

61 , suggesting increased reliance on BAT-based thermogenesis.

62 as a built-in rheostat negatively regulating thermogenesis.

63 d mediator of brown adipose tissue-dependent thermogenesis.

64 ty acids (PUFA) promote brown adipose tissue thermogenesis.

65 equently, IEX-1(-/-) mice exhibited enhanced thermogenesis (24 +/- 0.1 versus 22 +/- 0.1 kcal/hour/kg

66 nd interscapular brown adipose tissue (iBAT) thermogenesis accompanied by reduced fat mass and improv

67 Thyroid hormone is a major regulator of thermogenesis, acting both in peripheral organs and on c

68 Awake and fed thermogenesis (AFT) is the energy expenditure (EE) of th

69 AdKO-induced increases in thermogenesis also protected mice from cold-induced decr

70 ent, and, when disrupted, leads to defective thermogenesis and a paradoxical increase in basal metabo

71 n mice stimulates brown adipose tissue (BAT) thermogenesis and adipocyte browning independent of nutr

72 nt to blunt both central liraglutide-induced thermogenesis and adipocyte browning.

73 GF21 induction was associated with decreased thermogenesis and adiponectin, an observation that direc

74 xpression of genes associated with beige fat thermogenesis and anti-inflammatory cytokines.

75 em stimulation of brown adipose tissue (BAT) thermogenesis and browning of white adipose tissue (WAT)

76 hepatic glucose production, while enhancing thermogenesis and browning of white adipose tissue (WAT)

77 energy balance, with particular interest in thermogenesis and browning of white adipose tissue (WAT)

78 Brown adipose tissue is the primary site for thermogenesis and can consume, in addition to free fatty

79 a potent driver of brown fat development and thermogenesis and cold-induced beige fat formation.

80 physiological level drives a full program of thermogenesis and converts iWAT to brown-like fat, which

81 ipose tissue (BAT) is essential for adaptive thermogenesis and dissipation of caloric excess through

82 upplementation of pregnant mice on offspring thermogenesis and energy expenditure.

83 et-induced obesity by enhancing diet-induced thermogenesis and FAO.

84 regulation of FGF21-target genes involved in thermogenesis and fatty acid oxidation in brown fat.

85 ategy for treatment of obesity by increasing thermogenesis and fatty acid oxidation, while inhibition

86 ergy expenditure due in part by induction of thermogenesis and fatty acid oxidation.

87 s the coordinated control of energy balance, thermogenesis and glucose homoeostasis.

88 reliance on carbohydrate to provide fuel for thermogenesis and had increased expression of genes regu

89 t mice demonstrated increased adipose tissue thermogenesis and improved glycemia.

90 ed increased expression of genes involved in thermogenesis and increased norepinephrine-stimulated gl

91 se mice with the IP6K inhibitor TNP enhanced thermogenesis and inhibited progression of DIO.

92 adrenergic mechanism by which Lcn2 regulates thermogenesis and lipid metabolism.

93 amma/p38/ERRgamma pathway that regulates BAT thermogenesis and may enable new approaches for the stim

94 eases oxygen consumption in part by inducing thermogenesis and mitochondrial biogenesis in BAT along

95 y expenditure because of increased adipocyte thermogenesis and oxidative metabolism caused by upregul

96 hrough simultaneous regulation of lipolysis, thermogenesis and oxidative metabolism.

97 ition in vivo represses beta-agonist-induced thermogenesis and oxygen consumption.

98 e demonstrate a novel function of Id1 in BAT thermogenesis and programming of beige adipocytes in whi

99 Bmp8b(-/-) mice exhibit impaired thermogenesis and reduced metabolic rate, causing weight

100 ecifically in brown adipose tissue increases thermogenesis and reduces weight gain.

101 The offspring thermogenesis and related regulatory factors in adipose

102 P3 as an important mediator of physiological thermogenesis and support a renewed focus on targeting U

103 CP1 and SLN are required to maintain optimal thermogenesis and that loss of both systems compromises

104 ve found two separate sites: one that drives thermogenesis and the other, previously unknown, that dr

105 n and beige adipocytes combust nutrients for thermogenesis and through their metabolic activity decre

106 or GPR50 plays an important role in adaptive thermogenesis and torpor.

107 ) has been associated with activation of BAT thermogenesis and weight loss in mice and rats.

108 as a mechanism that supports UCP1-dependent thermogenesis and whole-body energy expenditure, which o

109 pling protein 1 (UCP1) mediates nonshivering thermogenesis and, upon cold exposure, is induced in bro

110 dipocytes (BAs) are specialized for adaptive thermogenesis and, upon sympathetic stimulation, activat

111 dicating impaired brown adipose tissue (BAT) thermogenesis and/or inability to oxidize the fat excess

112 s CLA's linkage with lipogenesis, lipolysis, thermogenesis, and browning of white and brown adipose t

113 hysical activity thermogenesis, diet-induced thermogenesis, and energy intake) were measured under fr

114 rticularly the linkage between inflammation, thermogenesis, and energy metabolism, is unclear.

115 regulation of cellular stress responses and thermogenesis, and how O2 deficiency leads to metabolic

116 s surveys energy availability to engage iBAT thermogenesis, and identify AGRP neurons as a neuronal s

117 increased aerobic mitochondrial capacity and thermogenesis, and improved glucose and insulin profiles

118 undance of uncoupling proteins that mediates thermogenesis, and it normalized the molecular signature

119 ent, causes browning of white fat, increases thermogenesis, and leads to substantial and sustained we

120 s for mitochondrial fatty acid oxidation and thermogenesis, and overall energy expenditure.

121 contribute to leptin's stimulatory effect on thermogenesis, and protect against diet-induced obesity.

122 nal sympathectomy compromises adipose tissue thermogenesis, and renders mice susceptible to obesity.

123 c insulin sensitivity and increased adaptive thermogenesis, and Them2-/- mice are also resistant to d

124 Weight loss results in adaptive thermogenesis, and there is no indication for a change i

125 gnaling pathways that promote adipose tissue thermogenesis are well characterized, but the limiters o

126 id hormone receptor alpha1 display increased thermogenesis as a consequence of high sympathetic brown

127 Remarkably, this process supports in vivo thermogenesis, as pharmacological depletion of mitochond

128 hand, brain UGN induces brown adipose tissue thermogenesis, as well as browning and lipid mobilizatio

129 ose tissue (BAT), due to its direct roles in thermogenesis, as well as through additional mechanisms.

130 Adaptive thermogenesis (AT) is the fat-free mass (FFM)-independen

131 ficantly rescue LPS, but not sympathomimetic thermogenesis blunted in UCP3KO mice.

132 Beyond thermogenesis, brown and beige fats engage other metabol

133 ompletely abrogated lipopolysaccharide (LPS) thermogenesis, but a normal response to noradrenaline.

134 mphetamine and fully inhibited noradrenaline thermogenesis, but an increased febrile response to LPS.

135 Leptin's ability to stimulate thermogenesis, but not to reduce feeding, is markedly at

136 ated with increased adiposity and diminished thermogenesis, but the critical transcription factors in

137 dipocytes, with a reduction in mitochondrial thermogenesis by a factor of 5, as well as an increase i

138 ate a potent inhibition of BAT and shivering thermogenesis by alpha2-AR activation in the rRPa, and s

139 rat brown adipose tissue (BAT) and shivering thermogenesis by alpha2-AR agonists.

140 Id1 suppresses BAT thermogenesis by binding to and suppressing PGC1alpha tr

141 ndividuals, which has been linked to greater thermogenesis by brown fat.

142 beta-ARs) promote brown adipose tissue (BAT) thermogenesis by mobilizing fatty acids and inducing the

143 lays important roles in feeding behavior and thermogenesis by modulating neuronal functions within th

144 suggest that SLN could play a role in muscle thermogenesis by promoting uncoupling of the SERCA pump,

145 tor 1alpha (PGC1alpha) controls BAT-mediated thermogenesis by regulating the expression of Ucp1 Inhib

146 N terminal (NT)-PGC-1alpha regulate adaptive thermogenesis by transcriptional induction of thermogeni

147 on (by huddling in groups) with the costs of thermogenesis (by contributing heat).

148 Induction of nonshivering thermogenesis can be used to influence energy balance to

149 issue (BAT) regulates cold- and diet-induced thermogenesis (CIT; DIT).

150 e (resting metabolic rate, physical activity thermogenesis, diet-induced thermogenesis, and energy in

151 consistent effect on 24-h physical activity thermogenesis (difference: 272 kcal/d; 95% CI: -254, 798

152 s were performed to investigate diet-induced-thermogenesis (DIT) and appetite sensation.

153 ctivity (SPA), postintervention diet-induced thermogenesis (DIT), appetite sensations, ad libitum ene

154 ation was found between BAT and diet-induced thermogenesis (DIT).

155 y, and in the bi-directional control of iBAT thermogenesis during nutrient deficiency and excess.

156 akfast resulted in greater physical activity thermogenesis during the morning than when fasting durin

157 unction as a developmental switch to license thermogenesis during the perinatal period.

158 ) inhibited shivering EMGs, BAT SNA, and BAT thermogenesis, effects that were reversed by nanoinjecti

159 e (resting metabolic rate, physical activity thermogenesis, energy intake) and 24-h glycemic response

160 skeletal muscle is also an important site of thermogenesis especially when brown adipose tissue funct

161 BAT thermogenesis explains the essential part played by thyr

162 as an alternative way to target nonshivering thermogenesis for treatment of obesity and metabolic dis

163 Thermogenesis from these adipocytes can combat obesity a

164 ctivated receptor-gamma and genes regulating thermogenesis, gluconeogenesis, and carnitine biosynthes

165 Cold thermogenesis had the highest representation in the dors

166 This phenomenon of BAT-mediated diet-induced thermogenesis has been observed in rodents and suggests

167 own adipose tissue as a site of nonshivering thermogenesis has been well documented.

168 o norepinephrine (NE)-mediated regulation of thermogenesis have been a topic of debate.

169 energy-dissipating pathways that facilitate thermogenesis have been extensively described, yet littl

170 In addition to this nonshivering thermogenesis, human BAT may also combat weight gain by

171 duced weight loss is accompanied by adaptive thermogenesis, ie, a disproportional or greater than exp

172 primary cells demonstrated that p62 controls thermogenesis in a cell-autonomous manner, independently

173 ociated with obesity represses mitochondrial thermogenesis in adipocyte precursor cells in a tissue-a

174 tor relative, LR11/SorLA (sLR11), suppresses thermogenesis in adipose tissue in a cell-autonomous man

175 )-androgenic receptor activation to adaptive thermogenesis in adipose tissue.

176 meostasis of retinoids and retinoid-mediated thermogenesis in adipose tissue.

177 driving the expression of genes involved in thermogenesis in adipose tissues.

178 be to develop strategies for activating BAT thermogenesis in adult humans to increase whole-body ene

179 itive fluorescent dye, ERthermAC, to monitor thermogenesis in BAs derived from murine brown fat precu

180 Mild cold-induced thermogenesis in BAT accounts for 15-25 kcal/d in subjec

181 R stress-induced inhibition of lipolysis and thermogenesis in BAT.

182 -stimulated chromatin dynamics that modulate thermogenesis in BATs.

183 A2b-RyR2 pathway stimulates UCP1-independent thermogenesis in beige adipocytes.

184 ysiological and pharmaceutical activators of thermogenesis in both tissues.

185 ty acid oxidation, oxidative metabolism, and thermogenesis in brown adipocytes.

186 Thermogenesis in brown adipose tissue (BAT) is an import

187 Thermogenesis in brown adipose tissue (BAT) is fundament

188 t of increased locomotor activity, increased thermogenesis in brown adipose tissue (BAT), and alterat

189 g in inguinal WAT and activation of adaptive thermogenesis in brown adipose tissue (BAT).

190 entral transcriptional regulator of adaptive thermogenesis in brown adipose tissue (BAT).

191 ein 1 (UCP1) is responsible for nonshivering thermogenesis in brown adipose tissue (BAT).

192 so increases expression of genes involved in thermogenesis in brown adipose tissue including Dio2, Pg

193 Here we show that acutely activated thermogenesis in brown adipose tissue is defined by a su

194 program to maintain a critical capacity for thermogenesis in brown adipose tissue that can be rapidl

195 ressed lipogenesis in the liver and enhanced thermogenesis in brown adipose tissue which was coincide

196 the long noncoding RNA Blnc1 as a driver of thermogenesis in brown and beige adipocytes.

197 At weaning, HFD offspring had lower thermogenesis in brown and white adipose tissues compare

198 (UCP1) plays a central role in nonshivering thermogenesis in brown fat; however, its role in beige f

199 reviously unrecognized molecular pathway for thermogenesis in fat cells.

200 is dispensable for cold-induced nonshivering thermogenesis in FL-PGC-1alpha(-/-) mice, since a slight

201 lipopolysaccharide-evoked (10 mug/kg, i.p.) thermogenesis in free-behaving rats.

202 Decreased thermogenesis in Gpr50(-/-) mice is not due to a deficit

203 f SERCA2b impairs UCP1-independent beige fat thermogenesis in humans and mice as well as in pigs, a s

204 BAT contributes to cold-induced nonshivering thermogenesis in humans has not been proven.

205 identified as a facilitator of cold-induced thermogenesis in humans.

206 MRO2 indicates that BAT is a minor source of thermogenesis in humans.

207 causally linked to higher physical activity thermogenesis in lean adults, with greater overall dieta

208 al GPR50 to be a novel component of adaptive thermogenesis in mammals.

209 e tissue, the principal site of nonshivering thermogenesis in mice [8].

210 cytes in white adipose tissue, and increased thermogenesis in mice, which is associated with decrease

211 ion leads to angiogenesis and UCP1-dependent thermogenesis in mouse brown and white adipose tissues.

212 sms responsible for the compromised adaptive thermogenesis in obese subjects have not yet been elucid

213 actation promoted white adipose browning and thermogenesis in offspring at weaning accompanied by per

214 p fever autonomically: they did not increase thermogenesis in response to a low, pyrogenic dose of LP

215 Because of the dominant role of BAT-mediated thermogenesis in rodents, the role of muscle-based NST i

216 The effect of resveratrol on thermogenesis in skeletal muscle and interscapular brown

217 regulator of energy metabolism and adaptive thermogenesis in the brown fat cell.

218 dings suggest that UCP1 contributes to local thermogenesis in the squirrel brain, and thus supports n

219 We also built maps for cold-induced thermogenesis in unanesthetized rats and found the dorsa

220 se in energy intake and EE and activation of thermogenesis in WAT and brown adipose tissue were lost

221 The increase in thermogenesis in WT mice correlates with increased expre

222 capable of augmenting uncoupled respiration (thermogenesis) in brown adipocytes.

223 y adrenergic signaling and required for iBAT thermogenesis, including PGC1a and UCP-1.

224 markable physiological adaptations including thermogenesis, increased intake of dietary energy, and e

225 m participants with the risk allele restored thermogenesis, increasing it by a factor of 7, and overe

226 d browning expression programs, and restored thermogenesis, increasing it by a factor of 7.

227 apted to mild cold up-regulated muscle-based thermogenesis, indicated by increases in muscle succinat

228 A decrease in adaptive thermogenesis is a contributing factor to obesity.

229 These results further confirm that SLN-based thermogenesis is a key player in muscle non-shivering th

230 Brown adipose tissue (BAT)-induced thermogenesis is a promising therapeutic target to treat

231 e compensatorily induced when UCP1-dependent thermogenesis is ablated, and creatine reduction in Ucp1

232 is study was to determine to what extent BAT thermogenesis is activated in adults during cold stress

233 Adaptive thermogenesis is an energy-demanding process that is med

234 gh interscapular brown adipose tissue (iBAT) thermogenesis is an important contributor to adaptive en

235 Thermogenesis is an important homeostatic mechanism esse

236 ategy, as the capacity for sustained aerobic thermogenesis is critical for survival during periods of

237 This nonshivering thermogenesis is crucial for mammals as a defense agains

238 around glucose and fatty acid metabolism and thermogenesis is found to decline with age and is implic

239 is study was to investigate whether adaptive thermogenesis is sustained during weight maintenance aft

240 Adaptive thermogenesis is the cellular process transforming chemi

241 Adaptive thermogenesis is the process of heat generation in respo

242 eukin-33 acts perinatally to ensure adaptive thermogenesis lifelong.

243 n response to pharmacological stimulation of thermogenesis linked to increased HDL levels in APOE*3-L

244 80, Mcp1 and Tnfalpha, which are involved in thermogenesis, lipogenesis and chronic inflammation in t

245 drenergic signaling axis that acts to dampen thermogenesis, maintain tissue homeostasis, and reveal a

246 Our data suggest that the increase in BAT thermogenesis may be an additional mechanism whereby pha

247 To explore a role in thermogenesis, mice were exposed to ambient temperatures

248 esis is a key player in muscle non-shivering thermogenesis (NST) and can compensate for loss of BAT a

249 has been suggested as a site of nonshivering thermogenesis (NST) besides brown adipose tissue (BAT).

250 The role of skeletal muscle in nonshivering thermogenesis (NST) is not well understood.

251 in parallel with an increase in nonshivering thermogenesis (NST).

252 a marked reduction of BAT-mediated adaptive thermogenesis, obesity and systemic insulin resistance.

253 ltered insulin response/glucose handling and thermogenesis occurred prior to any functional decline i

254 Recent studies suggest that thermogenesis of adipose tissues is involved in energy w

255 Adaptive thermogenesis of BAT was impaired in HFD offspring at we

256 ral raphe pallidus (rRPa) neurons influences thermogenesis of brown adipose tissue (BAT) independent

257 of sympathetic premotor neurons controlling thermogenesis of brown adipose tissue (BAT).

258 now enable the capture of physical activity thermogenesis on a minute-by-minute basis and over a sus

259 ) to investigate the effects of diet-induced thermogenesis on HFD-induced obesity.

260 uate the potential of mustard AITC to induce thermogenesis (primary outcome) and alter body temperatu

261 keletal muscle (i.e. sarcolipin (SLN)-based) thermogenesis processes play important roles in temperat

262 levates energy expenditure through increased thermogenesis, producing weight loss, improved insulin s

263 ut energy status and are reported to promote thermogenesis, raising the possibility that they interac

264 Our results point to a pathway for adipocyte thermogenesis regulation involving ARID5B, rs1421085, IR

265 he distinct demands, such as ATP production, thermogenesis, regulation of reactive oxygen species (RO

266 Lipopolysaccharide thermogenesis requires skeletal muscle UCP3 but not UCP1

267 ate early and late phases of sympathomimetic thermogenesis, respectively.

268 rons that control brown adipose tissue (BAT) thermogenesis, suggesting an additional role in energy h

269 -null background fully restored muscle-based thermogenesis, suggesting that Sln is the basis for Serc

270 de insight into the physiological control of thermogenesis that could inform future therapy.

271 bition of brown adipose tissue and shivering thermogenesis that is mediated by neurons in the nucleus

272 We show that, during stimulation of BAT thermogenesis, the lipophilic gas xenon preferentially a

273 NE enhances thermogenesis through beta3-adrenergic receptors to acti

274 ate dehydrogenase activity for ATP-dependent thermogenesis through the SERCA2b pathway; beige fat the

275 m, tail-skin vasoconstriction, and brown fat thermogenesis), thus suggesting that TRPM8 is a universa

276 in AgRP neurons is essential for suppressing thermogenesis to conserve energy in response to fasting.

277 s cause mild chronic cold stress, activating thermogenesis to maintain normal body temperature.

278 to postnatal life requires the activation of thermogenesis to maintain their core temperature.

279 g the role of mitochondrial ROS signaling in thermogenesis together with testable hypotheses for unde

280 e heat, relying on the principal effector of thermogenesis: uncoupling protein 1 (UCP1).

281 suggest that selection to sustain prolonged thermogenesis under hypoxia promotes a shift in metaboli

282 rplay between skeletal muscle- and BAT-based thermogenesis under mild versus severe cold adaptation b

283 re is no indication for a change in adaptive thermogenesis up to 1 y, when weight loss is maintained.

284 brown adipose tissue (BAT) consumes fuel for thermogenesis using tissue-specific uncoupling protein 1

285 rived cytokine in the regulation of adaptive thermogenesis via a non-adrenergic pathway.

286 Treatment of adipocytes with sLR11 inhibits thermogenesis via the bone morphogenetic protein/TGFbeta

287 he association between miR-30b/378 and brown thermogenesis was also confirmed in fish oil-fed C57/BL6

288 Rather, physical activity thermogenesis was markedly higher with breakfast than wi

289 ncreasing visceral adiposity and in reducing thermogenesis, we assessed the existence of a possible l

290 243 treatments, oxygen consumption, and BAT thermogenesis were diminished in UCP1 KO mice, but BAT (

291 PGC1alpha, and other markers of browning and thermogenesis were elevated in IWAT and RWAT of AdKO mic

292 In contrast, changes in thermogenesis were uninvolved in the attenuation of the

293 sed at 30 degrees C (to minimize facultative thermogenesis) were treated with 800 mg/liter DNP in dri

294 ipose tissue (BAT) is an important source of thermogenesis which is nearly exclusively dependent on i

295 enon uptake by BAT during stimulation of BAT thermogenesis, which enables us to acquire background-fr

296 minants of adipocyte plasticity and adaptive thermogenesis, which may have potential therapeutic impl

297 ed to investigate brown adipose tissue (BAT) thermogenesis, which requires mitochondrial uncoupling p

298 s metabolic rate to accommodate diet-induced thermogenesis while simultaneously coping with the stres

299 UCP1 Cys253 is sulfenylated during thermogenesis, while mutation of this site desensitizes

300 in mice decreases PGC-1alpha expression and thermogenesis, while overexpressing SCF systemically or