ライフサイエンスコーパス: fat cell

1 th BMI and adipose morphology (few but large fat cells).

2 lism and adaptive thermogenesis in the brown fat cell.

3 the expression of genes selective for white fat cells.

4 switch between skeletal myoblasts and brown fat cells.

5 d promoted preadipocyte differentiation into fat cells.

6 urified native PRDM16 protein complexes from fat cells.

7 mitted fibroblasts to be differentiated into fat cells.

8 sts induces their differentiation into brown fat cells.

9 , and ability to differentiate into bone and fat cells.

10 ke, all of which are modulated by insulin in fat cells.

11 PDK4 expression was hormonally regulated in fat cells.

12 de have revealed the endocrine properties of fat cells.

13 pecifically in the nucleus of differentiated fat cells.

14 d IRAP in the perinuclear region of cultured fat cells.

15 hanisms regulating cholesterol metabolism in fat cells.

16 imulation of glucose transport in muscle and fat cells.

17 ding total energy stored as triglycerides in fat cells.

18 an important determinant of GS activation in fat cells.

19 orter 4 to the plasma membrane in muscle and fat cells.

20 d stimulation of GT by insulin in muscle and fat cells.

21 ated with decreased IRS-1 and GLUT4 in these fat cells.

22 ite decreased glucose uptake into muscle and fat cells.

23 placement of Ewing sarcoma cells with benign fat cells.

24 Resistin is a hormone produced by fat cells.

25 UT4 and its insulin-induced translocation in fat cells.

26 n influences the degradation of PPARgamma in fat cells.

27 s receptor were present in mature unilocular fat cells.

28 e in differentiation-dependent activation in fat cells.

29 present the mechanism of glucose toxicity in fat cells.

30 ed with increased production of TNF-alpha by fat cells.

31 leptin is synthesized and released by fetal fat cells.

32 et tissues such as human skeletal muscle and fat cells.

33 reduced catecholamine action on lipolysis in fat cells.

34 of both classical brown and inducible beige fat cells.

35 nized molecular pathway for thermogenesis in fat cells.

36 mmunoprecipitation assays performed in human fat cells.

37 dipokine leptin, is released from Drosophila fat cells.

38 rons; and smooth muscle, bone, cartilage and fat cells.

39 k between constitutive and recruitable brown fat cells.

40 expressed only by sebocytes and subcutaneous fat cells.

41 t upstream of the leptin (LEP) gene in human fat cells.

42 d lipid metabolism were studied in FRic(-/-) fat cells.

43 r for omega-3 fatty acids on macrophages and fat cells.

44 egulation of glucose and lipid metabolism in fat cells.

45 Ccz1-Mon1-Rab7 module in starved Drosophila fat cells.

46 e switch from myoblastic precursors to brown fat cells.

47 s the ability to affect insulin signaling in fat cells.

48 prevent intermixing of arterial- and venous-fated cells.

49 sors and transdifferentiation of parathyroid-fated cells.

50 adipocytes, including the discovery of beige fat cells, a new thermogenic cell type.

51 he mechanisms controlling the development of fat cells (adipocytes).

52 In addition to these distinct properties of fat cells, adipocytes exist within adipose tissue, where

53 In response to cold or exercise, brown fat cells also emerge in the white adipose tissue (WAT;

54 earch in the last few decades has shown that fat cells also play a critical role in sensing and respo

55 ed to function in a cell-fate choice between fat cell and somatic gonadal precursors.

56 efforts to understand the formation of these fat cells and critically review genetic models and other

57 at, the protein is also found in bone marrow fat cells and has an inhibitory effect on adipocyte diff

58 isms regulating signaling pathways in mature fat cells and indicate that EBF1 functions as a key inte

59 he mesoderm induces the formation of ectopic fat cells and prevents the migration and coalescence of

60 The appearance of new fat cells and the increase in fat mass were depot specif

61 rmine how expression of Lcn2 is regulated in fat cells and to ascertain whether Lcn2 could be involve

62 Leptin is a 16-kDa protein secreted by fat cells and transported into the brain where it decrea

63 n of insulin-stimulated glucose transport in fat cells, and likely contributes to PRL-induced insulin

64 pid by hormones is a fundamental function of fat cells, and there is strong evidence that perilipin (

65 sion analysis indicated that the BMP-derived fat cells are bona fide adipocytes but differ from conve

66 These brown fat cells are subject to further up-regulation of UCP1 a

67 Furthermore, rictor-null fat cells are unable to suppress lipolysis in response t

68 Adipose (fat) cells are specialized for the storage of energy in

69 f the hormone resistin, which is secreted by fat cells, are proposed to cause insulin resistance and

70 vivo fate mapping that brown, but not white, fat cells arise from precursors that express Myf5, a gen

71 Recent data suggests that brown fat cells arise in vivo from a Myf5-positive, myoblastic

72 The fat cell as an endocrine organ, in addition to contribut

73 of adipoQ is observed exclusively in mature fat cells as the stromal-vascular fraction of fat tissue

74 and act as agonists in the insulin-dependent fat cell assay, suggesting that Site 1 marks the hotspot

75 ct as antagonists in the phosphorylation and fat cell assays.

76 formation of this specialized compartment in fat cells, based on the general mechanism described in C

77 insulin, glucose, or lipids that occur when fat cells become full and insulin-insensitive, and lose

78 taglandins may have an important impact upon fat cell biology and may help to explain some of the obs

79 ever, it is normally targeted only to fusion-fated cell borders via mutual interaction between EFF-1-

80 ve enhanced glucose transport, especially in fat cells, but the compounds do not stimulate GLUT4 tran

81 ular ATP levels and affect insulin action in fat cells by mechanisms independent of increased intrace

82 arise from hyperproliferation of the primary fat-cell clusters but they do associate with the endogen

83 suggest the existence of two types of brown fat cells: constitutive BAT (cBAT), which is of embryoni

84 embrane compartment that sequesters GLUT4 in fat cells contains long chain acyl-CoA synthetase-1 and

85 hite adipose tissue concomitantly with beige fat cell decline.

86 e intact PGC-1 coactivator expression, brown fat cells deficient for LRP130 exhibit attenuated expres

87 stem cells can differentiate into muscle or fat cells, depending on the exposure to growth factors.

88 Muscle and fat cells develop insulin resistance when cultured under

89 Muscles and fat cells develop insulin resistance when exposed to hig

90 transgenic overexpression of this enzyme in fat cells develop visceral obesity with insulin resistan

91 These data implicate LRP130 in brown fat cell development and differentiation.

92 actor that has been demonstrated to regulate fat cell development and glucose homeostasis.

93 PPAR gamma is required for fat cell development and is the molecular target of anti

94 ion and involvement of microRNAs (miRNAs) in fat cell development and obesity.

95 Notably, brown fat cell development common to both PGC-1 coactivators i

96 PPARgamma participate in a single pathway of fat cell development with PPARgamma being the proximal e

97 onal mechanisms that control brown and beige fat cell development.

98 ting to the transcriptional control of brown fat cell development.

99 Rgamma) is a nuclear receptor that regulates fat-cell development and glucose homeostasis and is the

100 rine brown fat precursors and in human brown fat cells differentiated from human neck brown preadipoc

101 found that knockout (KO) of DBC1 facilitated fat cell differentiation and lipid accumulation and incr

102 nous PPARgamma causes a dramatic increase in fat cell differentiation at both the morphological and m

103 Several growth factors that inhibit fat cell differentiation caused mitogen-activated protei

104 and the Gene Ontology (GO) biologic process fat cell differentiation human, which includes the trans

105 one receptor PPAR gamma, is known to promote fat cell differentiation in vitro.

106 Fat cell differentiation is a critical aspect of obesity

107 Our current understanding of fat cell differentiation is centered on the transcriptio

108 Further, fat cell differentiation is inhibited by cyclosporin A,

109 reover, its expression levels correlate with fat cell differentiation potential in humans.

110 s are present in 3T3-L1 adipocytes and, upon fat cell differentiation, bind to and transactivate the

111 rement for ligand activation of PPARgamma in fat cell differentiation, taking advantage of a natural

112 PPARgamma is a dominant regulator of fat cell differentiation.

113 e tissue upon cold exposure and during brown fat cell differentiation.

114 rms (-alpha and -delta) induces little or no fat cell differentiation.

115 B1 as a central transcriptional component of fat cell differentiation.

116 ctor gene serpent is necessary for embryonic fat-cell differentiation in Drosophila and has been prop

117 n, insulin resistance, body composition, and fat-cell differentiation in SAT were differentially regu

118 The ectopic fat cells do not arise from hyperproliferation of the pr

119 pond to cool temperatures, but classic brown fat cells do not.

120 e the opposite effects are observed in brown fat cells ectopically expressing wild-type RNF34 but not

121 Underlying this protection are smaller fat cells, elevated serum adiponectin, and reduced free

122 In addition to fat cells, endothelial cells were immunopositive for the

123 ation of IR and IRS-1 caused by TNF-alpha in fat cells, even at relatively high doses (25 ng/ml).

124 e end of the differentiation protocol, these fat cells exhibited decreased AKT2 phosphorylation after

125 and ACS5, the isoforms present in liver and fat cells, expressed the isoforms as ACS-Flag fusion pro

126 tion and developmental cues specifying brown-fat cell fate remain poorly understood.

127 fat cells or from cells that have acquired a fat-cell fate.

128 onverting these fibroblasts into lipid-laden fat cells following hormonal stimulation.

129 ising extra- and intracellular inhibitors of fat cell formation have been identified, but the modulat

130 Recombinant adiponectin blocked fat cell formation in long-term bone marrow cultures and

131 tracellular and intracellular stimulators of fat cell formation or adipogenesis.

132 s and their metabolites and is essential for fat cell formation.

133 tanding of the transcriptional regulation of fat cell formation.

134 As the master regulator of fat-cell formation, PPARgamma is required for the accumu

135 Epididymal white fat cells from cavin-1-null mice were small and insensit

136 n isolated fat cells, potentially regulating fat cell functions and (ii) either formation of IRS-1/PI

137 However, how caveolae participate in fat cell functions is poorly understood.

138 ndicate that ADD1 plays an important role in fat cell gene expression and differentiation, and sugges

139 a), a dominant regulator of adipogenesis and fat cell gene expression, at serine 273.

140 Furthermore, adiponectin failed to block fat cell generation when bone marrow cells were derived

141 In nutrient-rich fat cells, GRASP clusters in close proximity to the apic

142 Adiponectin, primarily produced by fat cells, has been implicated in the pathophysiology of

143 an insulin-sensitizing and anti-inflammatory fat cell hormone that has immense potential as a therape

144 lthy mice that have constitutively activated fat-cell HSL.

145 , lower-body fat responded to overfeeding by fat-cell hyperplasia, with adipocyte number increasing b

146 ression of the ob gene serves as a sensor of fat cell hypertrophy, independent of any effects on food

147 s offer a new perspective on the role of the fat cell in hematopoiesis.

148 Beige cells resemble white fat cells in having extremely low basal expression of UC

149 Indeed, the number of UCP1-positive brown fat cells in intermuscular fat in 129 mice is >700-fold

150 Our results indicate that fat cells in the head express sex-specific effectors, th

151 d found that all are expressed mainly in the fat cells in the head.

152 Lcn2 is highly expressed by fat cells in vivo and in vitro.

153 d the ability of CT-1 to induce signaling in fat cells in vivo.

154 for Dies1 in nutritional response of mature fat cells in vivo.

155 sion, suppress RNF34 expression in the brown fat cell, indicating a physiological relevance of this E

156 ncluded lymphocytes, mesendoderm, liver- and fat-cells, indicating that cell types outside the brain

157 To enhance glucose uptake into muscle and fat cells, insulin stimulates the translocation of GLUT4

158 cide' to differentiate into fully functional fat cells is critical to our understanding of diseases r

159 about site-related gene expression in human fat cells is limited.

160 Elevation of intracellular cAMP in fat cells is shown to increase PTP1B activity, whereas e

161 It is produced in fat cells, is stimulated by cytokines, and its levels in

162 In brown fat cells, knockdown of RNF34 increases the endogenous P

163 The signaling defects in FRic(-/-) fat cells lead to impaired insulin-stimulated GLUT4 tran

164 ting kinase, lysosome-mediated clearance and fat cell lipid accumulation; it demonstrates obesity-rel

165 eciprocal regulation of caveolae density and fat cell lipid droplet storage.

166 control adipocytes, inversely correlated to fat cell lipids.

167 peptides (NP) are major activators of human fat cell lipolysis and have recently been shown to contr

168 fat (adipocyte FABP null) exhibit diminished fat cell lipolysis, whereas transgenic mice with increas

169 on and identify Lsd1 as a regulator of beige fat cell maintenance.

170 ipid accumulation and elevated expression of fat cell marker proteins.

171 igand GIP augmented the expression of aP2, a fat cell marker.

172 n Drosophila include expansion of the insect fat cell mass both by increasing the adipocyte number an

173 ed adiposity is due to a marked reduction in fat cell mass without a decrease in adipocyte number.

174 s a major hormonal regulator of appetite and fat cell mass.

175 and their relationship to various stages of fat cell maturation have not been characterized as yet.

176 To establish the role of endogenous BKs in fat cell maturation, storage of excess dietary fat, and

177 is expressed in adipocytes, suggesting that fat cells may be targets of MCH or an MCH-like peptide u

178 n mice due to specific changes in energy and fat cell metabolism.

179 or PGC-1alpha and negatively regulates brown fat cell metabolism.

180 We suggest that the ectopic fat cells might originate from cells that have the poten

181 s associated with the function of the mature fat cell, most notably C/EBPalpha, adiponectin, perilipi

182 ssue renewal and obesity-driven expansion of fat cell number are dependent on proliferation and diffe

183 of different fat depots to overfeeding, and fat-cell number increases in certain depots in adults af

184 , which may result in long-term increases in fat cell numbers.

185 nd SB-415286 both inhibit GSK3 in muscle and fat cells, only Li stimulated GT.

186 d a number of potential molecular targets in fat cells or adipocytes.

187 ssary for regulation of glucose transport in fat cells or an additional signaling pathway is required

188 ial, but do not normally, differentiate into fat cells or from cells that have acquired a fat-cell fa

189 In each instance, MTB were localized in fat cells or oil drops during initiation of caseating gr

190 rtant factor is the generation of additional fat cells, or adipocytes, in response to excess feeding

191 Rictor/mTORC2 in fat cells plays an important role in whole-body energy h

192 rosine kinase signaling pathways in isolated fat cells, potentially regulating fat cell functions and

193 During development, fat cell precursors (i.e., preadipocytes) undergo a hype

194 Loss of rictor in fat cells prevents insulin-stimulated phosphorylation of

195 Our studies implicate a role for HMGIC in fat-cell proliferation, indicating that it may be an adi

196 The activities of brown and beige fat cells reduce metabolic disease, including obesity, i

197 ciated with a delay in alveolar collapse and fat cell repopulation.

198 White and beige fat cells respond to cool temperatures, but classic brow

199 fetuin-A, RSF and kidney, human renal sinus fat cells (RSFC) were isolated and cocultured with human

200 White fat cells secrete important hormone-like molecules such

201 The results of our studies suggest that fat cells secrete substances that inhibit apoptosis in c

202 Adiponectin is a fat cell-secreted protein that has been reported to incr

203 linked to fat distribution can be linked to fat cell size and number (morphology) and/or adipose tis

204 ally recovered proportional to the extent of fat cell size reduction.

205 Inasmuch as fat cell size, but not number, was increased in a previo

206 of lower-body fat is attributed to a reduced fat cell size, but not number, which may result in long-

207 esistance, but not increased body weight and fat cell size, were significantly decreased in adiponect

208 naling and action in fat cells, we developed fat cell-specific rictor knockout (FRic(-/-)) mice.

209 These include the fat-cell-specific cytokines adipsin, resistin, and adipo

210 r results, we discuss the role of serpent in fat-cell specification and in cell fate choices.

211 However, experiments in cultured fat cells stably expressing TNF-alpha demonstrated a sig

212 Increased oxygen consumption in inguinal fat cell suspensions and the up-regulation of genes of m

213 there are two distinct types of thermogenic fat cells, termed brown and beige adipocytes.

214 a distinct and inducible type of thermogenic fat cell that express the mitochondrial uncoupling prote

215 s from lack of leptin, a hormone released by fat cells that acts in the brain to suppress feeding and

216 tanding of the relationship between bone and fat cells that arise from the same progenitor within the

217 Thermogenic fat cells that convert chemical energy into heat are pre

218 Leptin is an adipokine produced by fat cells that regulates food consumption and metabolic

219 However, in rat fat cell the vast majority of Akt-1 is cytosolic and sho

220 ed the cloning and characterization of beige fat cells, the thermogenic "brown-like" cells that can d

221 preadipocytes, but is undetectable in mature fat cells; this down-regulation is required for adipocyt

222 whether Spry1 can modify the development of fat cells through its activity in regulating growth fact

223 s can be the result of the production of new fat cells through the process of adipogenesis and/or the

224 rs but they do associate with the endogenous fat cells to form a fat body that is expanded in both th

225 Exposure of fat cells to lipolytic agents or external FFA results is

226 ) channels affect the metabolic responses of fat cells to nutrients.

227 tiated cells, such as motor neurons or brown fat cells, to control the expression of genes that are s

228 Translocations of 12q13-15 in lipomas (fat cell tumors) disrupt HMGI-C and fuse its DNA-binding

229 of mesenchymal tumour cell types, including fat-cell tumours (lipomas).

230 se mechanism to prevent the formation of new fat cells upon overfeeding with dietary cholesterol.

231 In differentiated fat cells, upregulation of Sirt1 triggers lipolysis and

232 In primary mouse white fat cells, we detected expression of both ET(A) and ET(B

233 or/mTORC2 in insulin signaling and action in fat cells, we developed fat cell-specific rictor knockou

234 ther investigate the effects of IFN-gamma on fat cells, we examined the effects of this cytokine on t

235 order to investigate the effects of CNTF on fat cells, we examined the expression of CNTF receptor c

236 Pseudomonas aeruginosa form chains of short, fat cells when grown in low osmotic strength media.

237 Leptin is a 16 kDa protein secreted by fat cells which regulates body weight and thermogenesis

238 ant serum protein, secreted exclusively from fat cells, which is implicated in energy homeostasis and

239 tion led to accelerated differentiation into fat cells, which was confirmed by the earlier and increa

240 before and after differentiation into mature fat cells, while IRS-3 transcript was not detectable in

241 antly reduced H-Ras occurred in subcutaneous fat cells, while the reduced PI3K and PCNA took place on

242 at are selectively activated by treatment of fat cells with the PPARgamma ligand, troglitazone.