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1  OoC that integrates functional mature human white adipocytes.
2 s with mitochondrial fatty acid oxidation in white adipocytes.
3 eous (SC) or intra-abdominal epididymal (EP) white adipocytes.
4  in determining the switch between brown and white adipocytes.
5 wn adipocytes stimulates their conversion to white adipocytes.
6 f a latent leptin-stimulated caloric sump in white adipocytes.
7 ion in mammals; that is, fat mobilization in white adipocytes.
8 by up-regulating fatty acid oxidation within white adipocytes.
9 on cold-induced and enriched in brown versus white adipocytes.
10 mption required the presence of beta3-ARs in white adipocytes.
11 family receptors and BMP4 expression only in white adipocytes.
12 al function are increased in Park2 deficient white adipocytes.
13 BMP4 and BMP9 signalling in mature brown and white adipocytes.
14  mitochondrial respiration in both brown and white adipocytes.
15 vels of the TBX1 gene than subcutaneous neck white adipocytes.
16 eficient cells across phyla including murine white adipocytes.
17 Acox1-LKO mice promotes browning in cultured white adipocytes.
18 aling and insulin-mediated glucose uptake in white adipocytes.
19 nd thorax, and is comprised predominantly of white adipocytes.
20 uppression of critical metabolic pathways in white adipocytes.
21 n mouse brown adipocytes and human brown and white adipocytes.
22 ered energy storage capacity and browning of white adipocytes.
23 cted to a subset of preadipocytes and mature white adipocytes.
24 liver kinase b1 and histone deacetylase 4 in white adipocytes.
25 (LD) growth and triglyceride (TG) storage in white adipocytes.
26 osteoblast functions and promote browning of white adipocytes.
27 thetic nerve fibers that directly "envelope" white adipocytes.
28 o increase the brown-like characteristics in white adipocytes.
29 nesis pathway, in mature brown as well as in white adipocytes.
30 he differentiation and function of brown and white adipocytes.
31 glucose uptake in skeletal muscle but not in white adipocytes.
32 nduces, Ppargc1a and Prdm16 transcription in white adipocytes.
33 t least two distinct classes of subcutaneous white adipocytes.
34 metabolic rate and attenuated hypertrophy of white adipocytes.
35 chymal cells and inhibits differentiation of white adipocytes.
36 e ability for efficient differentiation into white adipocytes.
37 ochondrial depolarization in human and mouse white adipocytes.
38 apular brown adipose tissue and subcutaneous white adipocytes, a cell autonomous effect.
39 other maneuvers that increase cAMP levels in white adipocytes acutely induces mitochondrial uncouplin
40 ly little is known about mechanisms by which white adipocytes adapt to temperatures below 37 C.
41 we sought to determine how STAT1 activity in white adipocytes affects insulin sensitivity.
42 roplets in brown adipose tissue, and smaller white adipocytes after a high fat diet feeding or in age
43 e receptor, as a marker gene for a subset of white adipocytes and an aging-upregulated gene in adipoc
44 t fat tissues in vivo, i.e. inguinal fat for white adipocytes and brite cells, interscapular brown ad
45 s, beige adipocytes sporadically reside with white adipocytes and emerge in response to certain envir
46 red the relationship between the gains in BM white adipocytes and invasive Ly6C(high) monocytes by in
47  circulating hormone released primarily from white adipocytes and is crucial for regulating satiety a
48 duce a brown adipocyte-specific phenotype in white adipocytes and mitochondrial oxidative energy meta
49 ycolytic metabolism within subpopulations of white adipocytes and preadipocytes.
50 rphogenetic protein 4 (BMP4) is expressed in white adipocytes and remodels white adipose tissue, whil
51       Adiponectin is a hormone secreted from white adipocytes and takes part in the regulation of sev
52 he significance of fat-storing properties of white adipocytes and the role of local FSP27 in whole-bo
53 r understanding of both the heterogeneity of white adipocytes and their link to normal metabolism and
54 tty acids and expressed widely, including in white adipocytes and various immune and enteroendocrine
55 pressed in skeletal muscle, heart, brown and white adipocytes, and testes.
56 by three distinct cell types: energy-storing white adipocytes, and thermogenic beige and brown adipoc
57                 It is generally assumed that white adipocytes arise from resident adipose tissue mese
58 ody metabolism is regulated by lipid-storing white adipocytes as well as "brown" and "brite/beige" ad
59 with induction of brown fat-like features in white adipocytes, as demonstrated by increases in brown
60 rentiation and/or function of both brown and white adipocytes, as its absence in these cells leads to
61 rose non-fermenting-related kinase (SNRK) in white adipocyte biology was investigated.
62 n and immunity, chemerin is also involved in white adipocyte biology.
63 f Egr1 identifies the molecular signature of white adipocyte browning downstream of Egr1 deletion and
64 ented uncoupled respiration predominantly in white adipocytes (browning), whereas streptomycin antago
65 cellular LC-acyl-CoAs and activating AMPK in white adipocytes by pharmacological activation of ABHD5
66  protein-1 (Ucp1) mRNA and protein levels in white adipocytes by selectively activating the retinoic
67  our study shows that NTS-NTSR2 signaling in white adipocytes can regulate food intake via its direct
68 unction as epigenetic factors that stabilize white adipocyte cell identity, thereby modulating the ra
69 dies on MTIF3-deficient differentiated human white adipocyte cell line (hWAs-iCas9), generated throug
70 kout mice fed on a normal diet had increased white adipocyte cell sizes, increased numbers of inflamm
71 brown adipocytes to enforce brown and oppose white adipocyte cellular identity.
72 nt mice not producing brown fat suggest that white adipocytes convert into fat-oxidizing cells when b
73 tivator-3 (SRC-3) is a critical regulator of white adipocyte development.
74                       This fraction promoted white adipocyte differentiation and browning, maintained
75 has been described as an essential player in white adipocyte differentiation in mice.
76                  Furthermore, both brown and white adipocyte differentiation is markedly impaired in
77 f bone morphogenetic proteins (BMPs) support white adipocyte differentiation, BMP7 singularly promote
78 d biological pathways included regulation of white adipocyte differentiation, PPARalpha activation of
79 mic reticulum membrane protein essential for white adipocyte differentiation.
80 erall, results demonstrate that lipolysis in white adipocytes directly results in allosteric activati
81 higher in HIB1B brown adipocytes than 3T3-L1 white adipocytes during differentiation.
82 tioned media from BM adipocytes or bona fide white adipocytes favoured Ly6C(high) monocyte prepondera
83 ipocytes, and ear mesenchymal stem cells for white adipocytes from adult mice.
84           Fragmentation of lipid droplets in white adipocytes from FSP27-KO mice caused both increase
85        Additionally, we found that brown and white adipocytes from IIA+ mice have increased expressio
86                                    Moreover, white adipocytes from IIA+ mice were much more prone to
87 levance of these effects in vivo, we studied white adipocytes from ob/ob mice during the development
88                            Inhibition of the white adipocyte genes also depends on the expression of
89  unilocular lipid droplets and expression of white adipocyte genes suggest conversion of brown adipos
90 recursors or through reprogramming of mature white adipocytes has been a topic of intense discussion.
91                          Leptin, secreted by white adipocytes, has profound feeding, metabolic, and n
92                                              White adipocytes have a unique structure in which nearly
93 d microphysiological system (MPS) containing white adipocytes, hepatocytes and proinflammatory macrop
94 educed mitochondrial respiratory capacity in white adipocytes, impaired lipolytic signaling, represse
95 s suggest that p53-induced mitophagy in aged white adipocytes impedes WAT beiging and may be therapeu
96 , and fat-associated macrophages reside with white adipocytes in adipose tissue.
97  both the de novo development of a subset of white adipocytes in adults and a previously uncharacteri
98                                              White adipocytes in adults are typically derived from ti
99 ce, our results reveal an unexpected role of white adipocytes in maintaining properties of preexistin
100 ia-inducible factor 1alpha (HIF-1alpha) than white adipocytes in response to low O(2) but induced hig
101 ing precursor fibroblasts differentiate into white adipocytes in the embryo.
102          Furthermore, we also confirmed that white adipocytes in visceral fat of metabolically unheal
103 e essential for the browning of subcutaneous white adipocytes in vitro and in vivo.
104 ies suggest that CAP induces the browning of white adipocytes in vitro or inguinal white adipose tiss
105 thetic agonists induces a brown phenotype in white adipocytes in vivo and in vitro.
106 ge-related transition of beige adipocytes to white adipocytes in vivo, whereas loss of Lsd1 precipita
107 XL enhance thermogenic capacity of brown and white adipocytes, in vitro and in vivo.
108 n profiles on SDS gels of CPT I in brown and white adipocytes, indicate that the muscle form of the e
109                                          The white adipocyte is at the center of dysfunctional regula
110 ed that alternative lineage specification of white adipocytes is also present in human adipose tissue
111 whether p53-related cellular aging in mature white adipocytes is causative of age-impaired WAT beigin
112  Glucose transporter 4 (GLUT4) expression on white adipocytes is critical for facilitating cellular u
113 r in cultured brown preadipocytes promoted a white adipocyte-like phenotype and reduced expression of
114                                 In brown and white adipocytes, lysine myristoylation of gravin-alpha
115                               Energy-storing white adipocytes maintain their identity by suppressing
116 either brown (e.g. uncoupling protein 1) nor white adipocyte markers.
117  oxidative stress by limitingNrf2function in white adipocytes may be a novel means to modulate energy
118 ary human subcutaneous adipocytes as a human white adipocyte model, guiding the selection of appropri
119 petent beige adipocytes progressively gain a white adipocyte morphology.
120 geneous cell population consisting of mature white adipocytes, multipotent mesenchymal stem cells, co
121 OCS-3), was compared in the hypothalamus and white adipocytes of young and old rats before and after
122  suggest both BMP4 and BMP9 as regulators of white adipocyte plasticity with potential therapeutic im
123 filed the transcriptome of primary brown and white adipocytes, preadipocytes, and cultured adipocytes
124 A-2 and GATA-3 are specifically expressed in white adipocyte precursors and that their down-regulatio
125 ning can be engineered by directing visceral white adipocyte precursors to a thermogenic adipocyte fa
126                                    Brown and white adipocyte precursors were differentiated into adip
127             Knockdown of PPARgamma in mature white adipocytes prevented the usual robust induction of
128 sms by which beta3-AR agonist stimulation of white adipocytes produces these responses are unknown bu
129  homeostasis, at least partly by controlling white adipocyte profile and adiponectin secretion.
130 asculature, but the identity and location of white adipocyte progenitor cells in vivo are unknown.
131 ion factor KLF15 is required for maintaining white adipocyte properties selectively within the subcut
132  a pathway for depot-specific maintenance of white adipocyte properties that could enable the develop
133 or, is selectively expressed in subcutaneous white adipocytes relative to other white fat depots in m
134 ge-related transition of beige adipocytes to white adipocytes remain unclear.
135  However, it is not clear why differentiated white adipocytes require enhanced respiratory chain acti
136       Thermogenic activation of subcutaneous white adipocytes requires glycogen synthesis and turnove
137  These data demonstrate that the response of white adipocytes requires HIF-1alpha but also depends on
138                                        Human white adipocytes respond to direct blue light stimulatio
139 ilocular lipid droplet structure within each white adipocyte (see the related article beginning on pa
140 cose tolerance and inflammatory markers in a white-adipocyte selective and GPR116-dependent manner.
141 ore muscular than controls, have 62% smaller white adipocytes, show elevated basal lipolysis that is
142 KO adipocytes show reduced H3K27ac levels at white adipocyte-specific enhancers but elevated H3K27ac
143                                        While white adipocytes store excess calories as fat (triglycer
144 lysis of these clones reveals at least three white adipocyte subpopulations.
145 c1alpha-mediated mitochondrial biogenesis in white adipocytes, suggesting a potential therapeutic tar
146 d-coating protein highly expressed in mature white adipocytes that contributes to unilocular lipid dr
147 hich is typically expressed in brown but not white adipocytes, that RIP140 is essential for both DNA
148                           In contrast to the white adipocyte, the brown adipocyte is characterized by
149 sulin regulates metabolism in both brown and white adipocytes, the role of these tissues in energy st
150 ipogenesis and the metabolic state of mature white adipocytes through a common mechanism that is link
151 1alpha) reduced hepatic and plasma FGF21 and white adipocyte tissue-specific GLUT4 expression and rai
152                                  Exposure of white adipocytes to a peroxisome proliferator-activated
153 contrast, Adrb3 activation stimulates mature white adipocytes to convert into beige adipocytes.
154  to adipose tissues to convert lipid-storing white adipocytes to energy-catabolizing beige adipocytes
155                              The response of white adipocytes to hypoxia required HIF-1alpha, but its
156 sults suggest that NPs promote "browning" of white adipocytes to increase energy expenditure, definin
157 ds are higher in brown/beige adipocytes than white adipocytes to maintain the thermogenic mitochondri
158 AMT), a strategy that genetically reprograms white adipocytes to outcompete tumors for key nutrients.
159 chanism controlling the age-related beige-to-white adipocyte transition and identify Lsd1 as a regula
160 orphology, glucose homeostasis, and beige-to-white adipocyte transition were unaffected in vivo In ke
161 ion analysis of BAFF-stimulated subcutaneous white adipocytes unveils upregulation of lipid metabolis
162             Mobilization of fatty acids from white adipocytes upon fasting is compromised in Sirt1+/-
163 er, beige adipocytes quickly transition into white adipocytes upon removing stimuli.
164 udy, we found that the depletion of Ntsr2 in white adipocytes upregulated food intake, while the loca
165 romotes mitochondrial proteostasis in mature white adipocytes via the mitochondrial protease LONP1.
166               The presence of NPC2 in mature white adipocytes was also necessary for their maintenanc
167 ain long-term viability and functionality of white adipocytes was confirmed by real-time monitoring o
168 S), and (5) to show that parasymNs innervate white adipocytes (WATs) during development and promote W
169 terestingly, approximately 50% of the mutant white adipocytes were multilocular.
170                                   The mutant white adipocytes were smaller with a larger volume of cy
171 pargamma mutant induces a brown phenotype in white adipocytes, whereas an acetylated mimetic fails to
172 eceptors, noradrenaline induces lipolysis in white adipocytes, whereas it stimulates the expression o
173                 Here we demonstrate that the white adipocytes, which share a common precursor with th
174 ssion of thermogenic genes in both brown and white adipocytes, which was largely abolished by inhibit
175 induced pre-adipocyte differentiation toward white adipocytes while directly elevating uncoupling pro
176 strategies to enhance the brown phenotype in white adipocytes while reducing secretion of stress-rela
177 irected pre-adipocyte differentiation toward white adipocytes while suppressing differentiation into
178 and generation of reactive oxygen species in white adipocytes, while increasing these measures in bro
179 ss beta3-AR mRNA abundantly in brown but not white adipocytes, while rodents express beta3-AR mRNA ab
180 , is comprised of distinct subpopulations of white adipocytes with different physiological phenotypes
181 at dermal adipocytes are a distinct class of white adipocytes with high plasticity.
182 g beige (brite) adipocytes to energy-storing white adipocytes, with a reduction in mitochondrial ther
183 nment of a brown adipocyte cell phenotype in white adipocytes, with their abundant mitochondria and i
184 at the depot level and even heterogeneity of white adipocytes within a single depot.

 
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