ライフサイエンスコーパス: lipotoxicity

1 can lead to functional impairments known as "lipotoxicity".

2 ed with elevated islet triglyceride content (lipotoxicity).

3 sues when hepatocytes are injured by lipids (lipotoxicity).

4 gradation of membranous organelles, reducing lipotoxicity.

5 R(-/-)) displayed reduced palmitate-mediated lipotoxicity.

6 survival, yet their overaccumulation causes lipotoxicity.

7 ulated lipogenic program may protect against lipotoxicity.

8 t of pathological conditions associated with lipotoxicity.

9 logical basis for ectopic fat deposition and lipotoxicity.

10 ribute to organ failure, a phenomenon termed lipotoxicity.

11 may represent a protective mechanism against lipotoxicity.

12 of phosphatidylethanolamine as modifiers of lipotoxicity.

13 although they remain susceptible to hepatic lipotoxicity.

14 role of the lysosomal-mitochondrial axis on lipotoxicity.

15 acid oxidation, inflammation, and eventually lipotoxicity.

16 ing a receptor-mediated event and not simple lipotoxicity.

17 e deposition, features suggestive of cardiac lipotoxicity.

18 similar to those found in an animal model of lipotoxicity.

19 ed in free fatty acid (FFA)-mediated hepatic lipotoxicity.

20 usly been attributed to glucose toxicity and lipotoxicity.

21 evel hyperleptinemia protects the heart from lipotoxicity.

22 aired triglyceride synthesis, oleate induces lipotoxicity.

23 n non-adipose tissues, a phenomenon known as lipotoxicity.

24 :1, mol/mol) and does not induce significant lipotoxicity.

25 in nonadipocytes, thus protecting them from lipotoxicity.

26 in beta-cells of so-called glucotoxicity and lipotoxicity.

27 redict which patients with NAFL will develop lipotoxicity.

28 ROS production on the development of cardiac lipotoxicity.

29 s an important mediator of glucotoxicity and lipotoxicity.

30 FL differ in their ability to defend against lipotoxicity.

31 ssociated with in vivo cardiac steatosis and lipotoxicity.

32 on of autophagy and beta-cell function under lipotoxicity.

33 lytic subunit-2 (G6PC2) levels contribute to lipotoxicity.

34 mice consuming a diet that promotes hepatic lipotoxicity.

35 herapeutic target for insulin resistance and lipotoxicity.

36 pendent manner and reduced palmitate-induced lipotoxicity.

37 ic flux and lysosome function contributed to lipotoxicity.

38 hat NHE1 functions as a metabolic sensor for lipotoxicity.

39 ikely by limiting macrophage survival during lipotoxicity.

40 turated fatty acid pools resulting in severe lipotoxicity.

41 Chop(-/-) macrophages were resistant to its lipotoxicity.

42 o IS during IL infusion, indicative of acute lipotoxicity.

43 nctional adaptations of clonal beta-cells to lipotoxicity.

44 oes not display features of acute myocardial lipotoxicity.

45 In animal models of lipotoxicity, accumulation of triglycerides within cardi

46 During hepatocyte lipotoxicity, activated MLK3 induces the release of CXCL

47 olved a reduction in cardiac hypertrophy and lipotoxicity, adipose inflammation, and an upregulation

48 f hepatocyte nuclear factor 4 (Hnf4)-induced lipotoxicity and accumulation of free fatty acids as the

49 ER stress can be elicited by lipotoxicity and an increased demand for insulin in diab

50 adipose tissue unable to expand, leading to lipotoxicity and conditions such as diabetes and cardiov

51 epresent a novel transcriptional mediator of lipotoxicity and cytokine-induced beta-cell death.

52 Lipotoxicity and ectopic fat deposition reduce insulin s

53 acellular compartmentation of DAG in causing lipotoxicity and hepatic insulin resistance.

54 ects on developmental programming of hepatic lipotoxicity and inflammation in obese mice.

55 stribution of lipids in the liver, producing lipotoxicity and inflammation.

56 ., liver, skeletal muscle, pancreas) through lipotoxicity and inflammatory signaling networks.

57 to be important for the prevention of tissue lipotoxicity and insulin resistance.

58 s that reduce the risk of developing hepatic lipotoxicity and insulin resistance.

59 The liver injury is propagated by lipotoxicity and is associated with improved blood gluco

60 utic strategy in protection of cells against lipotoxicity and lipid-related metabolic diseases.

61 r Diabetic Fatty rats involves prevention of lipotoxicity and lipoapoptosis of beta cells, as well as

62 s and heart, and cause nitric oxide-mediated lipotoxicity and lipoapoptosis.

63 mprove insulin sensitivity by preventing ATM lipotoxicity and M1 polarization.

64 induced developmental programming of hepatic lipotoxicity and may help slow the advancing epidemic of

65 Inflammation, lipotoxicity and mitochondrial dysfunction have been imp

66 to the pathogenesis of obesity-induced renal lipotoxicity and nephropathy by regulating the liver kin

67 certain species of these lipids with cardiac lipotoxicity and subsequent myocardial dysfunction.

68 evels are thought to contribute to beta-cell lipotoxicity and the development of diabetes mellitus.

69 suggest that LMP is a key early mediator of lipotoxicity and underscore the value of interventions t

70 earoyl-PA (18:0/18:0-PA) mediate SFA-induced lipotoxicity and vascular calcification.

71 Effects of 11-DHC could be prevented by lipotoxicity and were associated with paracrine regulati

72 by excess insulin-stimulated lipogenesis and lipotoxicity and, if so, whether the damage can be preve

73 nking myocardial lipid accumulation (cardiac lipotoxicity) and peroxidation to congestive heart failu

74 in nonadipose tissues, causing dysfunction (lipotoxicity) and possible cell death (lipoapoptosis).

75 putative mediator of insulin resistance and lipotoxicity, and accumulation of ceramides within tissu

76 ced increases in intramyocardial TAG levels, lipotoxicity, and cardiac dysfunction.

77 ciency displayed increased TAG accumulation, lipotoxicity, and diastolic dysfunction comparable to wi

78 ating activin A, preserved fat mass, reduced lipotoxicity, and increased insulin sensitivity in 22-mo

79 interplay between mitochondrial performance, lipotoxicity, and insulin action is more complex than pr

80 nadipose tissues with generalized steatosis, lipotoxicity, and lipoapoptosis.

81 ion of AMPK, increased cardiac steatosis and lipotoxicity, and myocardial insulin resistance, which w

82 ) initiation by triggering oxidative stress, lipotoxicity, and subsequent activation of hepatic infla

83 link of ER stress, inflammation, and hepatic lipotoxicity, and that increased expression of CHOP repr

84 ther such alterations could be the result of lipotoxicity, and whether altered IGFBP-3 could affect p

85 FA) concentrations have been associated with lipotoxicity, apoptosis, and risk of diabetes mellitus a

86 Apoptosis and free fatty acid (FFA)-induced lipotoxicity are important features of NASH pathogenesis

87 tance (IR), supporting the current theory of lipotoxicity as a driver of IHTG accumulation.

88 timulated insulin secretion and the role of 'lipotoxicity' as a probable cause of hepatic and muscle

89 her found that the Nlrp3 inflammasome senses lipotoxicity-associated increases in intracellular ceram

90 toward TAG storage in LDs, thereby blunting lipotoxicity-associated insulin resistance.

91 resistance develops in bone as the result of lipotoxicity-associated loss of insulin receptors.

92 centration in hepatocytes during obesity and lipotoxicity attenuates autophagic flux by preventing th

93 In conclusion, a lipotoxicity-based genetic screen in a model microorgani

94 , hepatic insulin resistance originates from lipotoxicity but not from lower mitochondrial capacity,

95 lipid to adipose tissue to reduce peripheral lipotoxicity, but we found no evidence for this.

96 to protect nonadipocytes from steatosis and lipotoxicity by preventing the up-regulation of lipogene

97 Treatments that rescue the liver from lipotoxicity by restoring adipose tissue insulin sensiti

98 OP is responsible for HIV PI-induced hepatic lipotoxicity, C57BL/6J wild-type (WT) or CHOP knockout (

99 -6 PUFA represent a novel pathway of cardiac lipotoxicity caused by high n-6 PUFA diets.

100 and insulin-resistant adipocytes results in lipotoxicity, caused by the accumulation of triglyceride

101 To prevent lipotoxicity, cells store excess FAs as triglycerides (T

102 RATIONALE: Cardiac lipotoxicity, characterized by increased uptake, oxidati

103 y play a role in the ectopic lipogenesis and lipotoxicity complicating obesity in Zucker diabetic fat

104 Diabetes-associated glucotoxicity/lipotoxicity contribute to impaired beta-cell function a

105 herapies for common human disorders in which lipotoxicity contributes to pathogenesis.

106 t saturated fatty acid-induced (SFA-induced) lipotoxicity contributes to the pathogenesis of cardiova

107 ental studies have suggested atherogenic and lipotoxicity effects of long-chain and very-long-chain M

108 engages the core apoptotic machinery during lipotoxicity, especially activation of BH3-only proteins

109 ricle (RV) dysfunction is associated with RV lipotoxicity; however, the underlying mechanism for lipi

110 The results are consistent with the lipotoxicity hypothesis for adipogenic diabetes.

111 Our findings support the lipotoxicity hypothesis that the deposition of triglycer

112 To test the "lipotoxicity hypothesis," which attributes the beta cell

113 targets for therapeutic intervention against lipotoxicity in beta-cells.

114 t there is activation of the UPR with lethal lipotoxicity in conditional intestinal apoB100 Mttp-IKO

115 ary, we introduce an unexpected mechanism of lipotoxicity in endothelial cells and provide several no

116 ated insulin secretion that is reduced under lipotoxicity in INS1 cells and mouse islets.

117 to demonstrate that free fatty acid induced lipotoxicity in islets eliminates pulsatile insulin secr

118 ide (100 nmol/L) prevented palmitate-induced lipotoxicity in isolated mouse cardiomyocytes and primar

119 fat, mediated by the LPIN1 gene, may prevent lipotoxicity in muscle, leading to improved insulin sens

120 ASH, suggesting a new potential mechanism of lipotoxicity in NAFLD.

121 However, that lipotoxicity in nonadipose tissues of congenitally unlep

122 Lipotoxicity in pancreatic beta-cells, arising from exce

123 adiponectin is sufficient to mitigate local lipotoxicity in pancreatic islets, and it promotes recon

124 ngs suggest important features leading to RV lipotoxicity in pulmonary arterial hypertension and may

125 We conclude that lipotoxicity in Schwann cells results in cellular dysfun

126 , implicating SREBP1c induction in beta-cell lipotoxicity in some forms of type 2 diabetes.

127 ed the protective effect against cholesterol lipotoxicity in Sort1 knock-out mice.

128 CPT1b deficiency can cause lipotoxicity in the heart under pathological stress, lea

129 n adaptive mechanism that is able to prevent lipotoxicity in the ischemic myocardium.

130 This 'lipotoxicity' in liver, muscle, islets, and elsewhere ma

131 otein-1 (MuRF1) protected against gluco- and lipotoxicity-induced apoptosis.

132 F and metformin protected against gluco- and lipotoxicity-induced osteoblast apoptosis, and depletion

133 onic exposure to high levels of fatty acids (lipotoxicity) inhibits autophagic flux and concomitantly

134 ar changes in PKA signaling, suggesting that lipotoxicity is a contributor to diabetes-induced beta-a

135 Lipotoxicity is a presumed pathogenetic process whereby

136 HIV PI-induced hepatic lipotoxicity is closely linked to the up-regulation of C

137 Lipotoxicity is emerging as a significant contributor to

138 Lipid overload resulting in lipotoxicity is prominent in a number of chronic disease

139 Since the hallmark of lipotoxicity is the accumulation of fatty acids and thei

140 Because the role of TXNIP in lipotoxicity is unknown, the goal of the present study w

141 Further study of how BMPR2 mediates RV lipotoxicity is warranted.

142 Although NAFLD represents a form of lipotoxicity, its pathogenesis remains poorly understood

143 lation of liver free fatty acids and hepatic lipotoxicity marked by an elevation in the amount of pla

144 Murine data suggest that lipotoxicity may arise from reduction in FA oxidation.

145 isk of developing type 2 diabetes, beta-cell lipotoxicity may play an important role in the progressi

146 Lipotoxicity of pancreatic beta-cells, myocardium, and s

147 a (glucotoxicity) or chronic hyperlipidemia (lipotoxicity) on beta-cell function and is often accompa

148 ND Using a transgenic mouse model of cardiac lipotoxicity overexpressing ACSL1 (long-chain acyl-CoA s

149 inst the NAFLD-induced adverse effects, e.g. lipotoxicity, oxidative stress and endoplasmic reticulum

150 e have shown that palmitic acid (PA)-induced lipotoxicity (PA-LTx) in nerve growth factor-differentia

151 is study characterizes palmitic acid-induced lipotoxicity (PA-LTx) in Schwann cell cultures grown in

152 Lipotoxicity refers to the cytotoxic effects of excess f

153 in respiratory epithelial cells resulting in lipotoxicity-related lung inflammation and tissue remode

154 lecular mechanisms that underlie SFA-induced lipotoxicity remain unclear.

155 s from nonadipose tissues is known to induce lipotoxicity resulting in cellular dysfunction and death

156 flammation and reduced cardiac steatosis and lipotoxicity, resulting in normalization of heart failur

157 ocyte free fatty acid accumulation, however, lipotoxicity results.

158 t complications of human obesity may reflect lipotoxicity similar to that described in rodents.

159 an lead to further injury by contributing to lipotoxicity, sympathetic up-regulation, inflammation, o

160 at C youth are more susceptible to beta-cell lipotoxicity than AA youth, or alternatively, that AA yo

161 leptin resistance in the pathogenesis of the lipotoxicity that complicates obesity and results in the

162 This may cause a state of lipotoxicity that compromises left ventricular function

163 ll survival, their overaccumulation triggers lipotoxicity that leads to metabolic syndrome.

164 on (LMP) is an early event during PA-induced lipotoxicity that precedes MMP and apoptosis.

165 meliorates fatty acid oxidation avoiding the lipotoxicity that results from cell exposure to high fat

166 ing insulin sensitivity and preventing islet lipotoxicity, this activity of leptin may prevent adipog

167 ty acids serve a protective function against lipotoxicity though promotion of triglyceride accumulati

168 hepatocytes promotes lipid accumulation and lipotoxicity through lysosomal-mitochondrial permeabiliz

169 ubnetwork of beta cells that are targeted by lipotoxicity to suppress insulin secretion.

170 t beta-cells from glucose toxicity, and that lipotoxicity, to the extent it can be attributable to hy

171 buffer function of TAG accumulation against lipotoxicity under fatty acid overload.

172 eEF1A-1 involvement in lipotoxicity was confirmed in H9c2 cardiomyoblasts, in w

173 toleate induced an overt ER stress response, lipotoxicity was only observed in beta-cells exposed to

174 Ceramide, a mediator of lipotoxicity, was increased in PAH RVs versus controls.

175 To explore the mechanism of cellular lipotoxicity, we cultured Chinese hamster ovary cells in

176 date mechanisms of FA-induced cell death, or lipotoxicity, we generated Chinese hamster ovary (CHO) c

177 fed a high-fat diet, and in vitro models of lipotoxicity, we show that outer mitochondrial membrane

178 To elucidate molecular events critical for lipotoxicity, we used retroviral promoter trap mutagenes

179 Downregulation of SERCA2 and lipotoxicity were equivalent in Akita and Akita/ACE2KO h

180 ine whether the factors previously linked to lipotoxicity were uniquely increased by palmitate.

181 ance and metabolic complications of obesity (lipotoxicity), whereas comparable IMTG accumulation in e

182 xifies and stockpiles fatty acids to prevent lipotoxicity, whereas TAG hydrolysis (lipolysis) remobil

183 action results in unrestrained lipolysis and lipotoxicity, which are hallmarks of the metabolic syndr

184 Uncontrolled FA release from WAT promotes lipotoxicity, which is characterized by inflammation and

185 Lipotoxicity, which is triggered when cells are exposed

186 e ER is a key event for initiating beta-cell lipotoxicity, which leads to disruption of ER lipid raft

187 ose tissue, metabolic dysfunction, and liver lipotoxicity will result in improvements in the clinical

188 n, co-treatment of NGFDPC12 cells undergoing lipotoxicity with DHA significantly reduced LMP, suggest

189 implicated in insulin secretion thus linking lipotoxicity with early aspects of pancreatic beta-cell