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 ic flux and lysosome function contributed to lipotoxicity.

5 hat NHE1 functions as a metabolic sensor for lipotoxicity.

6 ikely by limiting macrophage survival during lipotoxicity.

7 turated fatty acid pools resulting in severe lipotoxicity.

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

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

10 nctional adaptations of clonal beta-cells to lipotoxicity.

11 oes not display features of acute myocardial lipotoxicity.

12 ts effect on obesity, insulin resistance and lipotoxicity.

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

14 sting that high FAO is distinct from cardiac lipotoxicity.

15 survival, yet their overaccumulation causes lipotoxicity.

16 long-chain fatty acids (VLCFAs) that mediate lipotoxicity.

17 ulated lipogenic program may protect against lipotoxicity.

18 t of pathological conditions associated with lipotoxicity.

19 logical basis for ectopic fat deposition and lipotoxicity.

20 ribute to organ failure, a phenomenon termed lipotoxicity.

21 nts and biomarkers in the setting of hepatic lipotoxicity.

22 may represent a protective mechanism against lipotoxicity.

23 of phosphatidylethanolamine as modifiers of lipotoxicity.

24 although they remain susceptible to hepatic lipotoxicity.

25 role of the lysosomal-mitochondrial axis on lipotoxicity.

26 acid oxidation, inflammation, and eventually lipotoxicity.

27 tes, and protected against palmitate-induced lipotoxicity.

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

29 e deposition, features suggestive of cardiac lipotoxicity.

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

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

32 usly been attributed to glucose toxicity and lipotoxicity.

33 evel hyperleptinemia protects the heart from lipotoxicity.

34 aired triglyceride synthesis, oleate induces lipotoxicity.

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

36 butes to dysfunctional lipid trafficking and lipotoxicity.

37 in nonadipocytes, thus protecting them from lipotoxicity.

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

39 nover while protecting against ER stress and lipotoxicity.

40 turation causing membrane rigidification and lipotoxicity.

41 accumulation in nonadipose tissues and cause lipotoxicity.

42 drogenase (Glud1) had no effect on palmitate lipotoxicity.

43 bition further promoted FFA accumulation and lipotoxicity.

44 ylglycerol (TAG) in lipid droplets (LDs) and lipotoxicity.

45 d to cellular metabolic dysfunction known as lipotoxicity.

46 d S-nitrosating agent (MitoSNO), alleviating lipotoxicity.

47 e investigate the role of IL11 in hepatocyte lipotoxicity.

48 RNA) screen identified >350 genes modulating lipotoxicity.

49 fatty acids (FFAs) are crucial in generating lipotoxicity.

50 , whereas MDA5 knockdown promotes hepatocyte lipotoxicity.

51 GI-58, to reduce free fatty acid release and lipotoxicity.

52 esis and lipid droplet formation to mitigate lipotoxicity.

53 rotecting against fatty acid-induced hepatic lipotoxicity.

54 al turnover and function in beta cells under lipotoxicity.

55 amoya vascular disease, protected cells from lipotoxicity.

56 , and the subsequent generation, from cardio-lipotoxicity.

57 creasing hepatic fat metabolism and reducing lipotoxicity.

58 lipid droplets protect sensory neurons from lipotoxicity.

59 es for treating metabolic diseases linked to lipotoxicity.

60 erase activity protected from all aspects of lipotoxicity.

61 orphology and sensitizes yeast to FA-induced lipotoxicity.

62 ROS production on the development of cardiac lipotoxicity.

63 gradation of membranous organelles, reducing lipotoxicity.

64 as obesity and cancer because of SFA-induced lipotoxicity.

65 :1, mol/mol) and does not induce significant lipotoxicity.

66 redict which patients with NAFL will develop lipotoxicity.

67 s an important mediator of glucotoxicity and lipotoxicity.

68 FL differ in their ability to defend against lipotoxicity.

69 ssociated with in vivo cardiac steatosis and lipotoxicity.

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

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

72 mice consuming a diet that promotes hepatic lipotoxicity.

73 herapeutic target for insulin resistance and lipotoxicity.

74 pendent manner and reduced palmitate-induced lipotoxicity.

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

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

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

78 leads to alterations in lipid metabolism and lipotoxicity, also contributing to the pro-inflammatory

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

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

81 Hepatocytes experience lipotoxicity and become senescent when Smoothened (Smo)

82 Adipocyte dysfunction contributes to lipotoxicity and cardiometabolic diseases.

83 PAK3 knockdown attenuated fatty acid-induced lipotoxicity and cell death in rat and human cardiomyocy

84 id droplets in regulating fatty acid flux in lipotoxicity and cell death.

85 Obesity-related renal lipotoxicity and chronic kidney disease (CKD) are preval

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

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

88 Lipotoxicity and ectopic fat deposition reduce insulin s

89 s, in promoting cell survival while limiting lipotoxicity and ferroptosis has been increasingly appre

90 Thus, the terms lipotoxicity and glucolipotoxicity should be used with g

91 druggable' target to reverse obesity-induced lipotoxicity and glucose intolerance.

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

93 In summary, empagliflozin reduces podocyte lipotoxicity and improves kidney function in experimenta

94 Hepatic lipotoxicity and inflammation are two key factors drivin

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

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

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

98 RING and RZ) implicated in Moyamoya disease, lipotoxicity and innate immunity(4).

99 hout an approved therapy, is associated with lipotoxicity and insulin resistance and is a major cause

100 evention of ectopic lipid deposition-induced lipotoxicity and insulin resistance.

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

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

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

104 However, the mechanisms underlying lipotoxicity and its influence on pathophysiology remain

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

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

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

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

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

110 ds of cells, and sequester lipids to prevent lipotoxicity and membrane damage.

111 n of fat excess-triggered defects, including lipotoxicity and metaflammation, but the causal mechanis

112 Inflammation, lipotoxicity and mitochondrial dysfunction have been imp

113 sed patients, lipid accumulation can promote lipotoxicity and mitochondrial dysfunction, thus trigger

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

115 e cardiometabolic disease (CMD) by promoting lipotoxicity and oxidative stress, yet their therapeutic

116 ith beta-cell function by reduction in gluco-lipotoxicity and possibly directly through PPAR-gamma ag

117 Conversely, AMPK activation mitigates lipotoxicity and renders GSCs resistant to the loss of D

118 ituents protection against oxidative stress, lipotoxicity and secretion of proinflammatory mediators

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

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

121 important metabolic pathway associated with lipotoxicity and the underlying inflammation, hepatocell

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

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

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

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

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

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

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

129 metabolism and mitochondrial bioenergetics, lipotoxicity, and altered signal transduction such as GR

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

131 SC activation is driven by metabolic stress, lipotoxicity, and chronic inflammation.

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

133 myopathy, with a special emphasis on cardiac lipotoxicity, and discuss the role of peroxisome prolife

134 The terms glucotoxicity, lipotoxicity, and glucolipotoxicity are used to describe

135 The terms glucotoxicity, lipotoxicity, and glucolipotoxicity have been widely use

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

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

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

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

140 balance, decreasing hepatic inflammation and lipotoxicity, and providing cardiovascular protection.

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

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

143 rculating glucose and fatty acid substrates, lipotoxicity, and tissue hypoxia.

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

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

146 While placental oxidative stress and lipotoxicity are hallmarks of placental dysfunction, the

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

148 Dyslipidemia and resulting lipotoxicity are pathologic signatures of metabolic synd

149 Defective autophagy and lipotoxicity are the hallmarks of nonalcoholic fatty liv

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

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

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

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

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

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

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

157 ORC1)-G9a-H3K9me2 axis in fatty acid-induced lipotoxicity blocks autophagy by repressing key autophag

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

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

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

161 s and ACSL1 knockdown in human cells prevent lipotoxicity by promoting increased levels of polyunsatu

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

163 urther show that the human ACSL1 potentiates lipotoxicity by the saturated fatty acid palmitate: sile

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

165 -6 PUFA represent a novel pathway of cardiac lipotoxicity caused by high n-6 PUFA diets.

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

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

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

169 ate, or dimethyl-alphaKG increased palmitate lipotoxicity compared with media that lacked these anapl

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

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

172 Intramyocardial lipotoxicity contributes to cardiac dysfunction.

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

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

175 mong previously unknown genetic modifiers of lipotoxicity, depletion of RNF213, a putative ubiquitin

176 activation of ATGL has beneficial effects on lipotoxicity-driven disorders including insulin resistan

177 etermine the pancreatic lipase(s) regulating lipotoxicity during AP.

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

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

180 epatitis (NASH), a disorder characterized by lipotoxicity, fibrosis, and progressive liver dysfunctio

181 Study of this process, known as lipotoxicity, has provided new insights into the regulat

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

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

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

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

186 etinal pigment epithelium (RPE) function and lipotoxicity in an S1P- and S1P receptor 3-dependent man

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

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

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

190 GLT2i affects energy metabolism and podocyte lipotoxicity in experimental Alport syndrome (AS).

191 nuated lipid accumulation, inflammation, and lipotoxicity in hepatocytes subjected to metabolic stres

192 vely profile the transcriptional response to lipotoxicity in hepatocytes, revealing new molecular ins

193 found to enhance lipid metabolism and reduce lipotoxicity in hFUSR521G mice and in cultured neurons a

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

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

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

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

198 Here, we induce ER stress and lipotoxicity in myotubes.

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

200 However, that lipotoxicity in nonadipose tissues of congenitally unlep

201 specific ceramide species promoting neuronal lipotoxicity in obesity have remained obscure.

202 Lipotoxicity in pancreatic beta-cells, arising from exce

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

204 r of stearoyl CoA desaturase (SCD), triggers lipotoxicity in patient-derived GBM stem-like cells (GSC

205 ivity of fatty acid synthase, which promotes lipotoxicity in photoreceptors.

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

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

208 ects of DIO were recapitulated by simulating lipotoxicity in skeletal muscle cells treated with satur

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

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

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

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

213 HAL-DBPs and HF also resulted in more severe lipotoxicity in these cells.

214 but not other lipid classes, are central to lipotoxicity in this model.

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

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

217 However, the molecular basis of lipotoxicity-induced NASH remains elusive.

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

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

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

221 Lipotoxicity is a presumed pathogenetic process whereby

222 Lipotoxicity is a recognized pathological trigger and ac

223 Hepatocyte lipotoxicity is characterized by aberrant mitochondrial

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

225 Lipotoxicity is emerging as a significant contributor to

226 Hepatocyte lipotoxicity is one of the main pathogenic factors of li

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

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

229 One hallmark of renal lipotoxicity is the ectopic accumulation of lipid drople

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

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

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

233 concentrations of free fatty acids leads to lipotoxicity (LT)-mediated suppression of glucose-stimul

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

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

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

237 protein abundance, and substantially reduced lipotoxicity-mediated oxidative and endoplasmic reticulu

238 pid homeostasis, while inhibition of cardiac lipotoxicity mitigates cardiac dysfunction.

239 Lipotoxicity occurred via the ferroptosis pathway.

240 f diabetic cardiomyopathy (DMCM) may involve lipotoxicity of cardiomyocytes in the context of hypergl

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

242 tDNA and lipid trafficking, the influence of lipotoxicity on mtDNA integrity, and how lipid metabolis

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

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

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

246 y acids in obese mice, which led to cellular lipotoxicity, oxidative stress, and mitochondrial dysfun

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

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

249 ed tubuloglomerular feedback, renal hypoxia, lipotoxicity, podocyte injury, inflammation, mitochondri

250 PTER transgenic expression mitigates cardiac lipotoxicity, preserves cardiac function and alleviates

251 These data suggest that hepatic fat (i.e., lipotoxicity) promotes HCC in this setting and may repre

252 Lipotoxicity refers to the cytotoxic effects of excess f

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

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

255 toxic to cells, although the basis for this lipotoxicity remains incompletely understood.

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

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

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

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

260 Moreover, in the context of lipotoxicity, some MAFK and TCF4 target genes were to th

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

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

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

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

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

266 stic insights into the ill-defined placental lipotoxicity that may inspire PLA2G6-targeted therapeuti

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

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

269 Ceramides contribute to the lipotoxicity that underlies diabetes, hepatic steatosis,

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

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

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

273 nding the metabolic mechanism of EPA-induced lipotoxicity to further enhance its anticancer effects.

274 letal muscle is a unifying mechanism linking lipotoxicity to metabolic disease.

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

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

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

278 erexpression aids LCFA oxidation and reduces lipotoxicity under pathological stress of transverse aor

279 By mitigating cardiac lipotoxicity, via redirected LCFA trafficking to ceramid

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

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

282 Lipotoxicity was recently reported in several forms of k

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

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

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

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

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

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

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

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

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

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

293 KO) cells manifest delayed FA processing and lipotoxicity, which can be rescued by SCD1 overexpressio

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

295 Lipotoxicity, which is triggered when cells are exposed

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

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

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

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

300 mportance of FFAs, an oversupply can trigger lipotoxicity with impaired membrane function, endoplasmi