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1 tiation, thereby diminishing accumulation of white fat.
2 ontained fat-laden cells resembling immature white fat.
3 responsive) in muscle and kidney, but not in white fat.
4 in the hypothalamus suppress the browning of white fat.
5 tream PGC1alpha levels leading to beiging of white fat.
6 ood glucose and increases Ucp1 expression in white fat.
7 th cells isolated from mesenteric or omental white fat.
8 erature, and diminished browning of inguinal white fat.
9 vated mutant of MLL3 have significantly less white fat.
10 ise to brown fat and skeletal muscle but not white fat.
11 epinephrine ([(3)H]NE) turnover in brown and white fat.
12 n the adipose vasculature caused ablation of white fat.
13 an increase the brown adipocyte character of white fat.
14 CP1)-independent respiration in subcutaneous white fat, 3) change the gut microbiota composition, and
15 nergy expenditure and promotion of beige and white fat activation.
16 man preadipocytes isolated from subcutaneous white fat also exhibit the greatest inducible capacity t
17 ith increased basal lipolysis, 'browning' of white fat and a healthy metabolic profile, whereas a pat
18 erance and insulin sensitivity and decreased white fat and adipocyte size in lean mice, obese leptin-
19 rt in abstract has also suggested effects on white fat and body weight.
20                    Although the functions of white fat and brown fat are increasingly well understood
21 pocyte function, including energy storage in white fat and energy dissipation in brown fat, a compreh
22 uction of beige cells causes the browning of white fat and improves energy metabolism.
23 es brown fat-specific genes while repressing white fat and muscle-specific genes in adipocytes.
24 e as a natural stimulus for OEA formation in white fat and suggest a role for the sympathetic nervous
25 dipocytes are required for the "browning" of white fat and the healthful effects of subcutaneous adip
26 iet selectively regulates UCP2 expression in white fat and UCP1 expression in brown fat and that resi
27 ell as in thymus, salivary gland, intestine, white fat, and brown fat.
28 n index of thermogenic capacity in brown and white fat, and increase in fat-associated anti-inflammat
29 sed glucose uptake in brown fat, browning of white fat, and overall increased energy expenditure.
30 cells, ScaPCs) residing in murine brown fat, white fat, and skeletal muscle.
31 imulates mitochondrial activity in brown and white fat; and improves CMS, without significantly alter
32  cells from skeletal muscle and subcutaneous white fat are highly inducible to differentiate into bro
33 of human and mouse subcutaneous and visceral white fat at single-cell resolution across a range of bo
34 e population induced by weight loss promotes white fat beiging to limit weight regain.
35 e tissue that acts in the brain, stimulating white fat breakdown.
36 d that midage Foxa3-null mice have increased white fat browning and thermogenic capacity, decreased a
37                              ASO-T3 enhances white fat browning, decreases genes for fatty acid synth
38 le tolerance to cold partly by promoting the white fat browning, leading to increased energy expendit
39  enhanced hepatic cholesterol metabolism and white fat browning.
40 ese mice are unique in that they do not have white fat but do develop type 2 diabetes.
41  staging platform for the emergence of adult white fat but that it has properties to serve the unique
42 e Myf5 lineage in brown fat and subcutaneous white fat, but exhibits gender-linked divergence in visc
43  via activation of brown fat and browning of white fat, but intact liver insulin action is required f
44                                   Epididymal white fat cells from cavin-1-null mice were small and in
45                         Beige cells resemble white fat cells in having extremely low basal expression
46                                              White fat cells secrete important hormone-like molecules
47                             In primary mouse white fat cells, we detected expression of both ET(A) an
48 essing the expression of genes selective for white fat cells.
49  by in vivo fate mapping that brown, but not white, fat cells arise from precursors that express Myf5
50                                          All white fat depots and brown fat pads were severely reduce
51             Induction of brown adipocytes in white fat depots by adrenergic stimulation is a complex
52     Whereas MMP14 promotes the generation of white fat depots crucial for energy storage, MMP15 diffe
53 es that control brown adipocyte induction in white fat depots in mice.
54 cutaneous white adipocytes relative to other white fat depots in mice.
55  macrophage polarization in the subcutaneous white fat depots of microbiota-depleted animals.
56 ice were considerably leaner and the size of white fat depots was markedly decreased compared with wi
57 iled to differentiate fully, and the size of white fat depots was markedly decreased.
58 lectively up-regulated in brown and inguinal white fat depots, and that midage Foxa3-null mice have i
59  cycling associated with brown adipocytes in white fat depots, are induced in UCP1-deficient mice by
60 hosphorylated form in inguinal fat and other white fat depots, but no induction was apparent in muscl
61 enditure and oxygen consumption in beige and white fat depots.
62 ereby promoting the formation of rBAT within white fat depots.
63 genic "brown-like" cells that can develop in white fat depots.
64 er and activity of "brown adipocytes" within white fat depots.
65 ly expressed in subcutaneous versus visceral white fat depots.
66 t the isolation of "beige" cells from murine white fat depots.
67 s a crucial role in the control of brown and white fat development, and, when disrupted, leads to def
68 olism has been expanded from inflammation in white fat during obesity development to immune cell func
69            Deep sequencing of the epididymal white fat (Epi WAT) transcriptome supported Dido1 contro
70                                              White fat failed to differentiate fully, and the size of
71    Thus, loss of IR is sufficient to disrupt white fat formation, but not brown fat formation and/or
72 neage and UCP1-positive cells that emerge in white fat from a non-myf-5 lineage.
73 n is characterized by repression of a set of white fat genes ("visceral white"), including the resist
74 ction selectively mediates the repression of white fat genes.
75  to induce brown fat in areas of traditional white fat had no impact on the ability to gain weight in
76  innervation of thermogenic fat, compared to white fat, has remained unknown.
77   Direct blue-light exposure to subcutaneous white fat improves high-fat diet-induced metabolic abnor
78 ltisynaptic pathways to liver and epididymal white fat in mice using pseudorabies virus strains expre
79 modeling and increased energy expenditure in white fat in response to rosiglitazone treatment in vivo
80 cytes, also known as beige cells, develop in white fat in response to various activators.
81 lic syndrome, highlighting the importance of white fat in the "safe" storage of surplus energy.
82 t likely due to significantly less brown and white fat in the absence of myostatin, and postweaning m
83  cerebellum, striatum, liver, brown fat, and white fat) in mouse models harboring CNVs of the synteni
84 and the browning marker UCP1 in all types of white fat, including visceral fat, and promoted addition
85 ose tissue (BAT) content, causes browning of white fat, increases thermogenesis, and leads to substan
86  discovered regulatory hormone that converts white fat into the more thermogenic beige fat.
87 level is lower in mouse brown fat (BAT) than white fat, is suppressed in mouse BAT during cold exposu
88                     Browning of subcutaneous white fat (iWAT) involves several reprograming events, b
89 etic neurites in mouse inguinal subcutaneous white fat (iWAT), little is known about when and how thi
90 t energy metabolism (skeletal muscle, heart, white fat, liver, and kidney).
91  by aP2-Cre, led to premature death, lack of white fat, low blood pressure, compensatory erythrocytos
92 ase in energy expenditure and an increase in white fat mass and adipocyte number.
93 rmates, Sf1Gck(-/-) mice displayed increased white fat mass and adipocyte size, reduced lean mass, im
94 te, reproductive function, body temperature, white fat mass, hepatic glucose output, and response to
95  in a significant increase in brown, but not white, fat mass and leads to an increase in energy expen
96    Hence, our results suggest that brown and white fat may be targets of specific amino acids to cont
97  mesoderm-specific transcript gene (Mest) in white fat of C57BL/6J (B6) mice fed an obesogenic diet i
98 nce, inducing thermogenic differentiation of white fat offers an attractive way to enhance whole-body
99 d significantly increased body mass and some white fat pad masses, markedly reduced Arc Nissl and neu
100 ed in a decrease in abdominal and epididymal white fat pad weights, while interscapular brown adipose
101                                     Relative white fat-pad mass of Il18(-/-) mice was approximately 2
102  demonstrated recombination in the brown and white fat pads.
103 nce that elicits apoptosis of endothelium in white fat potently reduced body weight.
104 ty for Ucp1 and brown adipocyte induction in white fat preferentially lost body weight following adre
105                        Loss of PGC-1alpha in white fat resulted in reduced expression of the thermoge
106 atic activity associated with fat storage in white fat, resulting in a more obese animal.
107                      This mouse model has no white fat, resulting in abnormal levels of glucose, insu
108 BP proteins on PRDM16 controls the brown and white fat-selective gene programs.
109 ociates with PRDM16 to repress expression of white fat-selective genes.
110  by loss of intra-abdominal and subcutaneous white fat, severe insulin resistance, and enlargement an
111  a PRDM16/CtBP complex onto the promoters of white fat-specific genes such as resistin, and is abolis
112                   In addition, some sites of white fat storage in the body are more closely linked th
113                                              White fat stores excess energy, whereas brown and beige
114 ss relaxation was observed in an artery with white fat (superior mesenteric artery) and in aorta from
115  is also expressed in blood vessels of human white fat, this work may lead to the development of targ
116 ted in specific deposits or can emerge among white fat through the so-called browning process.
117 P, but not 1866, treated cells isolated from white fat tissue (stromal vesicular fraction) produced t
118  subunit TAF7, is enriched in adipocytes and white fat tissue (WAT) in mouse.
119  The physiological consequences of having no white fat tissue are profound.
120 ated a cell-autonomous function for Foxa3 in white fat tissue browning.
121    Interestingly, Ebf2-expressing cells from white fat tissue in adult animals differentiated into br
122 We have generated a transgenic mouse with no white fat tissue throughout life.
123 lar brown fat, large differences occurred in white fat tissues, particularly in retroperitoneal fat.
124 rolling the induction of brown adipocytes in white fat tissues.
125          Hemizygotes exhibit major brown and white fat transcriptomic dysregulation, indicating poten
126 ide motif (sequence CKGGRAKDC) that homes to white fat vasculature.
127 In both KsJ and A/J mice, UCP2 expression in white fat was increased approximately 2-fold in response
128 ases classical brown fat (BAT) mass, but not white fat (WAT) mass.
129 nic genes common to both brown fat (BAT) and white fat (WAT), and the expression of BAT-selective gen
130 he molecular level, the lipolytic defects in white fat were caused by impaired perilipin phosphorylat
131 xhibits gender-linked divergence in visceral white fat while the MyoD1 lineage does not give rise to

 
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