ライフサイエンスコーパス: white fat

1 erature, and diminished browning of inguinal 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 tiation, thereby diminishing accumulation of white fat.

6 ood glucose and increases Ucp1 expression in white fat.

7 th cells isolated from mesenteric or omental white fat.

8 vated mutant of MLL3 have significantly less white fat.

9 ise to brown fat and skeletal muscle but not white fat.

10 epinephrine ([(3)H]NE) turnover in brown and white fat.

11 n the adipose vasculature caused ablation of white fat.

12 an increase the brown adipocyte character of white fat.

13 nergy expenditure and promotion of beige and white fat activation.

14 man preadipocytes isolated from subcutaneous white fat also exhibit the greatest inducible capacity t

15 ith increased basal lipolysis, 'browning' of white fat and a healthy metabolic profile, whereas a pat

16 erance and insulin sensitivity and decreased white fat and adipocyte size in lean mice, obese leptin-

17 rt in abstract has also suggested effects on white fat and body weight.

18 Although the functions of white fat and brown fat are increasingly well understood

19 uction of beige cells causes the browning of white fat and improves energy metabolism.

20 es brown fat-specific genes while repressing white fat and muscle-specific genes in adipocytes.

21 e as a natural stimulus for OEA formation in white fat and suggest a role for the sympathetic nervous

22 dipocytes are required for the "browning" of white fat and the healthful effects of subcutaneous adip

23 iet selectively regulates UCP2 expression in white fat and UCP1 expression in brown fat and that resi

24 ell as in thymus, salivary gland, intestine, white fat, and brown fat.

25 sed glucose uptake in brown fat, browning of white fat, and overall increased energy expenditure.

26 cells, ScaPCs) residing in murine brown fat, white fat, and skeletal muscle.

27 cells from skeletal muscle and subcutaneous white fat are highly inducible to differentiate into bro

28 e tissue that acts in the brain, stimulating white fat breakdown.

29 d that midage Foxa3-null mice have increased white fat browning and thermogenic capacity, decreased a

30 ASO-T3 enhances white fat browning, decreases genes for fatty acid synth

31 le tolerance to cold partly by promoting the white fat browning, leading to increased energy expendit

32 enhanced hepatic cholesterol metabolism and white fat browning.

33 ese mice are unique in that they do not have white fat but do develop type 2 diabetes.

34 staging platform for the emergence of adult white fat but that it has properties to serve the unique

35 e Myf5 lineage in brown fat and subcutaneous white fat, but exhibits gender-linked divergence in visc

36 via activation of brown fat and browning of white fat, but intact liver insulin action is required f

37 Epididymal white fat cells from cavin-1-null mice were small and in

38 Beige cells resemble white fat cells in having extremely low basal expression

39 White fat cells secrete important hormone-like molecules

40 In primary mouse white fat cells, we detected expression of both ET(A) an

41 essing the expression of genes selective for white fat cells.

42 by in vivo fate mapping that brown, but not white, fat cells arise from precursors that express Myf5

43 All white fat depots and brown fat pads were severely reduce

44 Induction of brown adipocytes in white fat depots by adrenergic stimulation is a complex

45 Whereas MMP14 promotes the generation of white fat depots crucial for energy storage, MMP15 diffe

46 cutaneous white adipocytes relative to other white fat depots in mice.

47 es that control brown adipocyte induction in white fat depots in mice.

48 macrophage polarization in the subcutaneous white fat depots of microbiota-depleted animals.

49 ice were considerably leaner and the size of white fat depots was markedly decreased compared with wi

50 iled to differentiate fully, and the size of white fat depots was markedly decreased.

51 lectively up-regulated in brown and inguinal white fat depots, and that midage Foxa3-null mice have i

52 cycling associated with brown adipocytes in white fat depots, are induced in UCP1-deficient mice by

53 hosphorylated form in inguinal fat and other white fat depots, but no induction was apparent in muscl

54 enditure and oxygen consumption in beige and white fat depots.

55 ereby promoting the formation of rBAT within white fat depots.

56 genic "brown-like" cells that can develop in white fat depots.

57 er and activity of "brown adipocytes" within white fat depots.

58 ly expressed in subcutaneous versus visceral white fat depots.

59 t the isolation of "beige" cells from murine white fat depots.

60 s a crucial role in the control of brown and white fat development, and, when disrupted, leads to def

61 White fat failed to differentiate fully, and the size of

62 Thus, loss of IR is sufficient to disrupt white fat formation, but not brown fat formation and/or

63 neage and UCP1-positive cells that emerge in white fat from a non-myf-5 lineage.

64 n is characterized by repression of a set of white fat genes ("visceral white"), including the resist

65 ction selectively mediates the repression of white fat genes.

66 to induce brown fat in areas of traditional white fat had no impact on the ability to gain weight in

67 ltisynaptic pathways to liver and epididymal white fat in mice using pseudorabies virus strains expre

68 modeling and increased energy expenditure in white fat in response to rosiglitazone treatment in vivo

69 cytes, also known as beige cells, develop in white fat in response to various activators.

70 t likely due to significantly less brown and white fat in the absence of myostatin, and postweaning m

71 and the browning marker UCP1 in all types of white fat, including visceral fat, and promoted addition

72 ose tissue (BAT) content, causes browning of white fat, increases thermogenesis, and leads to substan

73 discovered regulatory hormone that converts white fat into the more thermogenic beige fat.

74 level is lower in mouse brown fat (BAT) than white fat, is suppressed in mouse BAT during cold exposu

75 Browning of subcutaneous white fat (iWAT) involves several reprograming events, b

76 t energy metabolism (skeletal muscle, heart, white fat, liver, and kidney).

77 by aP2-Cre, led to premature death, lack of white fat, low blood pressure, compensatory erythrocytos

78 ase in energy expenditure and an increase in white fat mass and adipocyte number.

79 rmates, Sf1Gck(-/-) mice displayed increased white fat mass and adipocyte size, reduced lean mass, im

80 te, reproductive function, body temperature, white fat mass, hepatic glucose output, and response to

81 in a significant increase in brown, but not white, fat mass and leads to an increase in energy expen

82 mesoderm-specific transcript gene (Mest) in white fat of C57BL/6J (B6) mice fed an obesogenic diet i

83 d significantly increased body mass and some white fat pad masses, markedly reduced Arc Nissl and neu

84 ed in a decrease in abdominal and epididymal white fat pad weights, while interscapular brown adipose

85 Relative white fat-pad mass of Il18(-/-) mice was approximately 2

86 demonstrated recombination in the brown and white fat pads.

87 nce that elicits apoptosis of endothelium in white fat potently reduced body weight.

88 ty for Ucp1 and brown adipocyte induction in white fat preferentially lost body weight following adre

89 Loss of PGC-1alpha in white fat resulted in reduced expression of the thermoge

90 atic activity associated with fat storage in white fat, resulting in a more obese animal.

91 This mouse model has no white fat, resulting in abnormal levels of glucose, insu

92 BP proteins on PRDM16 controls the brown and white fat-selective gene programs.

93 ociates with PRDM16 to repress expression of white fat-selective genes.

94 by loss of intra-abdominal and subcutaneous white fat, severe insulin resistance, and enlargement an

95 a PRDM16/CtBP complex onto the promoters of white fat-specific genes such as resistin, and is abolis

96 In addition, some sites of white fat storage in the body are more closely linked th

97 is also expressed in blood vessels of human white fat, this work may lead to the development of targ

98 ted in specific deposits or can emerge among white fat through the so-called browning process.

99 subunit TAF7, is enriched in adipocytes and white fat tissue (WAT) in mouse.

100 The physiological consequences of having no white fat tissue are profound.

101 ated a cell-autonomous function for Foxa3 in white fat tissue browning.

102 Interestingly, Ebf2-expressing cells from white fat tissue in adult animals differentiated into br

103 We have generated a transgenic mouse with no white fat tissue throughout life.

104 lar brown fat, large differences occurred in white fat tissues, particularly in retroperitoneal fat.

105 rolling the induction of brown adipocytes in white fat tissues.

106 ide motif (sequence CKGGRAKDC) that homes to white fat vasculature.

107 In both KsJ and A/J mice, UCP2 expression in white fat was increased approximately 2-fold in response

108 ases classical brown fat (BAT) mass, but not white fat (WAT) mass.

109 nic genes common to both brown fat (BAT) and white fat (WAT), and the expression of BAT-selective gen

110 he molecular level, the lipolytic defects in white fat were caused by impaired perilipin phosphorylat

111 xhibits gender-linked divergence in visceral white fat while the MyoD1 lineage does not give rise to