ライフサイエンスコーパス: liver steatosis

1 racterized by the accumulation of fat in the liver (steatosis).

2 significant disease outcomes, such as fatty liver (steatosis).

3 e deposition of fat (triacylglycerol) in the liver (steatosis).

4 atty acid beta-oxidation plays a key role in liver steatosis.

5 itochondrial beta-oxidation, contributing to liver steatosis.

6 the formation of triacylglycerols leading to liver steatosis.

7 sociated obesity, adipocyte hypertrophy, and liver steatosis.

8 e for screening patients with a suspicion of liver steatosis.

9 rexpression of kappaOR in this area promoted liver steatosis.

10 triglyceride metabolism and protects against liver steatosis.

11 educed melanin concentrating hormone-induced liver steatosis.

12 d acylcarnitine profile and the reduction of liver steatosis.

13 sis, hyperinsulinemia, and early symptoms of liver steatosis.

14 is under both physiological and pathological liver steatosis.

15 s well as in the pathogenesis of obesity and liver steatosis.

16 g and as a contributor to obesity-associated liver steatosis.

17 al hepatectomy (PH) in mice with and without liver steatosis.

18 eased flux from PE to PC, but do not develop liver steatosis.

19 insulin sensitivity, plasma lipid levels and liver steatosis.

20 plays a protective role in alcohol-mediated liver steatosis.

21 iated with obesity, such as dyslipidemia and liver steatosis.

22 Forty patients had liver steatosis.

23 increased adiposity, insulin resistance, and liver steatosis.

24 in the management of obesity, diabetes, and liver steatosis.

25 w target for therapies aimed at nonalcoholic liver steatosis.

26 s an in vivo regulator of SIRT1 activity and liver steatosis.

27 zation showed that the diabetic rats develop liver steatosis, abdominal fat accumulation, nephropathy

28 5(-/-) mice were protected from diet-induced liver steatosis accompanied by decreased protein levels

29 e to high-fat diet (HFD)-induced obesity and liver steatosis, accompanied by improved insulin sensiti

30 n cholesterol synthesis underpins persistent liver steatosis after weaning off PN.

31 ay be used as biomarkers for the presence of liver steatosis and appear to be superior to BMI.

32 imals exhibit facial alopecia, have moderate liver steatosis and are slightly smaller than heterozygo

33 ompanied by the side effects of weight gain, liver steatosis and bone loss associated with current in

34 tative therapeutic targets in the context of liver steatosis and cancer.

35 gest that a leaky gut barrier is linked with liver steatosis and could be a new target for future ste

36 n contrast, knockdown of hepatic CES2 causes liver steatosis and damage in chow- or Western diet-fed

37 ) mice trade reduced adiposity for increased liver steatosis and develop aggravated systemic insulin

38 levels of alanine aminotransferase (ALT) and liver steatosis and fibrosis, compared with mice given i

39 romoted fatty acid oxidation and ameliorated liver steatosis and glucose intolerance in diet-induced

40 d fatty acid beta-oxidation; and ameliorated liver steatosis and glucose intolerance.

41 ive effects on weight loss, fat composition, liver steatosis and glucose tolerance; however, in the l

42 treated Tiparp(-/-) mice exhibited increased liver steatosis and hepatotoxicity.

43 ver-specific knockdown of TRAP80 ameliorated liver steatosis and hypertriglyceridemia induced by LXR

44 w-density lipoprotein secretion and promotes liver steatosis and hypolipidemia in an HNF4alpha-depend

45 t Zbtb20 ablation protects from diet-induced liver steatosis and improves hepatic insulin resistance.

46 Liver steatosis and inflammation were assessed.

47 ficient mice were protected from HFD-induced liver steatosis and inflammation, despite the developmen

48 these mice, GFT505 also prevented WD-induced liver steatosis and inflammation, indicating a contribut

49 eration of BHMT is associated with alcoholic liver steatosis and injury.

50 agy by rapamycin attenuates EtOH-LPS-induced liver steatosis and injury.

51 n db/db or HFD-fed mice markedly ameliorates liver steatosis and insulin resistance.

52 Sevelamer treatment significantly reduced liver steatosis and lobular inflammation.

53 on of B7.1/B7.2 deteriorates obesity-related liver steatosis and metabolic dysregulation, likely a re

54 ly mitigates their hyperphagia, obesity, and liver steatosis and normalizes deficits in glucose homeo

55 Ethanol feeding significantly increased liver steatosis and oxidative damage, compared with wild

56 In these mice, as observed in humans, liver steatosis and oxidative stress promoted NASH devel

57 and irrespective of the diet, they developed liver steatosis and progressive insulin resistance.

58 This was accompanied by reduced liver steatosis and reduced hepatic expression of marker

59 n-alcoholic fatty liver disease, we examined liver steatosis and related clinical and molecular trait

60 taneous inactivation of Hif-1beta suppressed liver steatosis and rescued the mice from death.

61 The association of lnc18q22.2 to liver steatosis and steatohepatitis was replicated in 44

62 se in serum alanine aminotransferase levels, liver steatosis and triglyceride levels suggesting liver

63 Alcohol-induced liver steatosis and triglyceride were attenuated in alco

64 d with control diet developed hyperglycemia, liver steatosis, and adipocyte hypertrophy, conditions d

65 uding metabolic syndrome, diabetes, obesity, liver steatosis, and Alzheimer disease.

66 resistant to high-fat diet-induced obesity, liver steatosis, and diabetes.

67 common metabolic disorders, such as obesity, liver steatosis, and for ageing.

68 , were protected against atherosclerosis and liver steatosis, and lived longer.

69 e epidemics of metabolic diseases, including liver steatosis, are associated with an increased freque

70 syndrome and increased with the severity of liver steatosis at ultrasound.

71 on was found with the histological degree of liver steatosis (beta, 0.15; standard error: 0.06; P = 0

72 ere resistant to high-fat diet (HFD)-induced liver steatosis, both of which were reproduced by liver-

73 associated with liver function tests or with liver steatosis by magnetic resonance spectroscopy.

74 meostatic model assessment index (HOMA), and liver steatosis by sonography and the fatty liver index

75 SIRT1-mediated activation of FGF21 prevents liver steatosis caused by fasting.

76 low in ob/ob mice and alcohol-fed mice with liver steatosis, compared with controls.

77 Histopathologic liver steatosis correlated well with liver SI loss on op

78 TGH deficiency did not further increase liver steatosis despite lowering plasma lipids, mainly d

79 n and whether obese patients with or without liver steatosis differ in this function.

80 14% (P < 0.001), and a marked improvement in liver steatosis (from 88% to 8%), inflammation (from 23%

81 IRT1 and for the development of experimental liver steatosis, genetic deletion of Dbc1 in mice led to

82 sity and obesity-related disorders including liver steatosis, glucose intolerance, or elevated serum

83 Body weight, body fat and lean mass, liver steatosis, glucose tolerance and pancreatic beta c

84 In liver steatosis (i.e. fatty liver), hepatocytes accumula

85 For the evaluation of liver steatosis in children CAP performs better than US,

86 lipid and cholesterol levels and attenuated liver steatosis in diet-induced and genetically obese mi

87 effect of GSH deficiency on alcohol-induced liver steatosis in Gclm knockout (KO) mice that constitu

88 is superior to CAP in detecting and grading liver steatosis in human NAFLD.

89 PI3K p110-alpha, and not p110-beta, promotes liver steatosis in mice fed an HFD.

90 ble NOX2-derived peptide and the severity of liver steatosis in subjects with non-alcoholic fatty liv

91 g of hepatic Fsp27 abolishes fasting-induced liver steatosis in the absence of changes in plasma lipi

92 indicate that the reduced adiposity, reduced liver steatosis, increased energy expenditure, and incre

93 supplemented (MCS) diet feeding evidenced by liver steatosis, increased triglycerides, inflammatory c

94 from the observation that BCMO1 mice develop liver steatosis independent of the vitamin A content of

95 was performed using a dietary mouse model of liver steatosis, induced by a high fat diet (HFD).

96 uired for the development of alcohol-induced liver steatosis, inflammation, and injury.

97 g exacerbated the HFD-induced NASH such that liver steatosis, inflammation, fibrosis, oxidative stres

98 is a heterogeneous disorder characterized by liver steatosis; inflammation and fibrosis are features

99 Liver steatosis is a common health problem associated wi

100 Severe liver steatosis is a known risk factor for increased isc

101 Donor liver steatosis is frequently encountered and often asso

102 indicator of increased fibrosis in diseased liver; steatosis may influence some perfusion parameters

103 ver, this trend did not translate into worse liver steatosis, necroinflammation or fibrosis.

104 In the liver, steatosis often proceeds cancer formation; howeve

105 is, and new factors possibly contributing to liver steatosis or fibrosis under ER stress (e.g., major

106 VSL#3 failed to prevent MCD-induced liver steatosis or inflammation.

107 n genetically obese mice indeed results from liver steatosis rather than the disruption of leptin sig

108 e >2-fold higher in patients with persistent liver steatosis than in those without steatosis or contr

109 ificant improvement of glucose tolerance and liver steatosis than the restrictive procedure.

110 Alcohol consumption induces liver steatosis; therefore, this study investigated the

111 fat diet-induced NAFLD with progression from liver steatosis to histological features compatible with

112 bility in obese individuals with and without liver steatosis undergoing a weight-reduction program to

113 plicate a novel mechanism protecting against liver steatosis via an oxidative stress adaptive respons

114 ): 43.7 +/- 5.2; 78% with moderate or severe liver steatosis] were included in the follow-up interven

115 exhibited reduced body weight, fat mass, and liver steatosis when fed with a high fat diet (HFD).

116 orrelate with increasing adiposity and fatty liver (steatosis), while with weight loss VA levels and

117 resistant to diet-induced hyperinsulinemia, liver steatosis, white adipose tissue (WAT) inflammation

118 A cutoff value of CAP of 249 dB/m rules in liver steatosis with a very high specificity.

119 n), these factors could increase the risk of liver steatosis with necroinflammatory lesions and fibro