ライフサイエンスコーパス: LDL cholesterol

1 ll as examples of trans-mediators (TAGAP for LDL cholesterol).

2 ds to a greater effect on HbA1c, weight, and LDL cholesterol.

3 No relationship was found with total or LDL cholesterol.

4 centrations without significantly increasing LDL cholesterol.

5 eptors on the cell surface and reduce plasma LDL cholesterol.

6 d to a 16-mg/dL (95% CI: 13, 20) increase in LDL cholesterol.

7 nmet medical need in the treatment of raised LDL cholesterol.

8 are linked to the abnormal levels of HDL and LDL cholesterol.

9 g plasma triacylglycerols, oxidized LDL, and LDL cholesterol.

10 ificantly according to the achieved level of LDL cholesterol.

11 able to achieve recommended target levels of LDL cholesterol.

12 ol also increases HDL cholesterol and lowers LDL cholesterol.

13 17-mmol/L (95% CI: 0.11-, 0.23-mmol/L) lower LDL cholesterol.

14 PUFAs, particularly in individuals with high LDL cholesterol.

15 ight, body mass index (BMI; in kg/m(2)), and LDL cholesterol.

16 trategy to help manage total cholesterol and LDL cholesterol.

17 or baseline factors associated with achieved LDL cholesterol.

18 erican diets decreases total cholesterol and LDL cholesterol.

19 L) receptors and increasing the clearance of LDL-cholesterol.

20 y severely elevated low density lipoprotein (LDL) cholesterol.

21 , reduces levels of low-density lipoprotein (LDL) cholesterol.

22 rogenic circulating low-density lipoprotein (LDL) cholesterol.

23 for the lowering of low-density lipoprotein (LDL) cholesterol.

24 d reduces levels of low-density lipoprotein (LDL) cholesterol.

25 SE, P < 0.0001 effect of HFCS-dose), fasting LDL cholesterol (0%: -1.0 +/- 3.1; 10%: 7.4 +/- 3.2; 17.

26 1.02-2.17), MI (OR 1.58, 95% CI 1.06-2.35), LDL-cholesterol (0.21 standard deviations, 95% CI 0.01-0

27 (TC; -0.25 +/- 0.05 mmol/L; P < 0.0001) and LDL cholesterol (-0.17 +/- 0.04 mmol/L; P < 0.0001) over

28 4 +/- 0.49 mmol/L, respectively (P = 0.024); LDL cholesterol: +0.36 +/- 0.50 compared with +0.04 +/-

29 triglycerides (reductions of 33.2 to 63.1%), LDL cholesterol (1.3 to 32.9%), very-low-density lipopro

30 Direct LDL-cholesterol (-1.00 mmol/L, 95% CI -1.38 to 0.61 vs 0

31 tio for each 10 mg per deciliter decrease in LDL cholesterol, 1.11 (95% CI, 1.04 to 1.19) for PCSK9 a

32 CI: 6.4, 15.9) and low-density lipoprotein (LDL) cholesterol (14 trials; net change: 6.7 mg/dL; 95%

33 apy for at least 6 months and dyslipidaemia (LDL cholesterol 3.4-5.7 mmol/L and triglycerides </=4.5

34 (2)): 28.5 +/- 4.0; low-density lipoprotein (LDL) cholesterol: 3.24 +/- 0.63 mmol/L].

35 g TC (-2.1% compared with 0.7%; P = 0.0004), LDL cholesterol (-4.1% compared with 0.9%; P < 0.0001) a

36 h 0.8% (95% CI: -1.5%, 4.5%), respectively], LDL cholesterol [-4.8% (95% CI: -12.6%, 3.1%) compared w

37 0.7% +/- 1.1%, respectively; P < 0.0001) and LDL cholesterol (6.9% +/- 1.8% compared with 2.2% +/- 1.

38 /=190 mg/dl, and adults 40-79 years old with LDL cholesterol=70-189 mg/dl and diabetes or a 10-year p

39 Both therapies are approved to lower LDL cholesterol, a causative agent for atherosclerotic c

40 Plant sterols (PSs) lower LDL cholesterol, an established risk factor for coronary

41 ensity lipoprotein (LDL) receptor, elevating LDL cholesterol and accelerating atherosclerotic heart d

42 itor anacetrapib exhibit a reduction in both LDL cholesterol and apolipoprotein B (ApoB) in response

43 tations in PCSK9 are associated with reduced LDL cholesterol and cardiovascular disease risk.

44 type 9 (PCSK9) inhibitor evolocumab reduced LDL cholesterol and cardiovascular events in the FOURIER

45 a mean 0.06 mmol/L (95% CI 0.05-0.07) lower LDL cholesterol and higher body weight (0.30 kg, 0.18-0.

46 as a monotonic relationship between achieved LDL cholesterol and major cardiovascular outcomes down t

47 of approximately 3 g KJM/d for reductions in LDL cholesterol and non-HDL cholesterol of 10% and 7%, r

48 oclonal antibodies have been shown to reduce LDL cholesterol and other lipids, but specific efficacy

49 y outcomes were the effects of evolocumab on LDL cholesterol and other lipids.

50 tion mutations in PCSK9 associated with high LDL cholesterol and premature cardiovascular disease hav

51 were available through day 210, and data on LDL cholesterol and proprotein convertase subtilisin-kex

52 caloric amount of carbohydrate-rich foods on LDL cholesterol and risk factors for the metabolic syndr

53 nt association was observed between achieved LDL cholesterol and safety outcomes, either for all seri

54 blood pressure, and weight, but to increase LDL cholesterol and the incidence of urogenital infectio

55 with reductions in both the concentration of LDL cholesterol and the risk of coronary heart disease,

56 LDL cholesterol and total cholesterol decreased signific

57 lesterol, and triacylglycerols, although for LDL cholesterol and triacylglycerols there was significa

58 anced the effect of free sugars on total and LDL cholesterol and triacylglycerols.

59 diabetes) and an unfavorable profile (higher LDL cholesterol and triglycerides).Choline and its metab

60 SK9), lowers plasma low-density lipoprotein (LDL) cholesterol and apolipoprotein B100 (apoB).

61 ctor profile [lower low-density lipoprotein (LDL) cholesterol and triglycerides] and lower odds of di

62 DLR) is a central determinant of circulating LDL-cholesterol and as such subject to tight regulation.

63 ent score and lower serum total cholesterol, LDL cholesterol, and albumin concentrations.

64 ated with FEV1, whereas serum triglycerides, LDL cholesterol, and apoB are associated with more sever

65 cohorts in association with serum total and LDL cholesterol, and AT lipidomics.

66 cholesterol, CELSR2, APOB and NCAN/MAU2 for LDL cholesterol, and GCKR, TRIB1, ZNF259/APOA5 and NCAN/

67 Plasma glucose, total cholesterol, LDL cholesterol, and insulin levels did not show any sig

68 re significant increases in HDL cholesterol, LDL cholesterol, and triacylglycerols, although for LDL

69 systolic blood pressure, total cholesterol, LDL cholesterol, and triglycerides but not with age, sex

70 n with non-HDL cholesterol, HDL cholesterol, LDL cholesterol, and triglycerides in up to 119,146 Icel

71 ve protein, hemoglobin A1c, HDL cholesterol, LDL cholesterol, and triglycerides, the LPIR score remai

72 -targeting drugs that can efficiently reduce LDL-cholesterol, and as tools to study the Cys-His-rich

73 positively associated with serum total- and LDL-cholesterol, and with AT-specific cholesterol metabo

74 Tree nut intake lowers total cholesterol, LDL cholesterol, ApoB, and triglycerides.

75 ndial concentrations of non-HDL cholesterol, LDL cholesterol, apolipoprotein B, apolipoprotein CIII,

76 triglycerides, and low-density lipoprotein (LDL) cholesterol, as well as reductions in liver triglyc

77 we found that TZD targets were enriched for LDL cholesterol associations, illustrating the utility o

78 ab significantly reduced ultracentrifugation LDL cholesterol at 12 weeks by 30.9% (95% CI -43.9% to -

79 Randomisation was stratified by LDL cholesterol at screening (<11 mmol/L or >/=11 mmol/L

80 dules led to a significant reduction in mean LDL cholesterol at week 12 (every-2-weeks dose: 59.2% re

81 ints were percentage change from baseline in LDL cholesterol at week 12 and at the mean of weeks 10 a

82 (P-interaction = 0.02), with the increase in LDL cholesterol being significantly greater with butter

83 For example, among participants with LDL cholesterol below 80 mg/dL, an interquartile range i

84 trend) once adjusted for age, sex, smoking, LDL-cholesterol, BMI, waist circumference, and HOMA-insu

85 The rs12916 SNP had similar effects on LDL cholesterol, bodyweight, and waist circumference.

86 iduals in randomised trials, statins lowered LDL cholesterol by 0.92 mmol/L (95% CI 0.18-1.67) at 1-y

87 For example, lowering LDL cholesterol by 2 mmol/L (77 mg/dL) with an effective

88 erapy alone, evolocumab reduced the level of LDL cholesterol by 61%, from a median of 120 mg per deci

89 ntiatherosclerotic effects through increased LDL cholesterol catabolism and LDL-derived cholesterol f

90 nts a potential strategy to increase hepatic LDL-cholesterol clearance.

91 plasma total cholesterol, triglycerides and LDL cholesterol comparable to oral ATV.

92 was well tolerated and significantly reduced LDL cholesterol compared with placebo.

93 yielded similar and rapid 60% reductions in LDL cholesterol compared with placebo.

94 iver-targeted IDOL-AAV-DJ/8 increased plasma LDL cholesterol compared with the control enhanced green

95 voice interactive system, and stratified by LDL cholesterol concentration at screening (higher or lo

96 therapy for at least 4 weeks, with a fasting LDL cholesterol concentration of 2.6 mmol/L or higher, w

97 iabetes evolocumab caused mean reductions in LDL cholesterol concentration that were 60% (95% CI 51-6

98 oking and alcohol use, waist:hip ratio, BMI, LDL cholesterol concentration, log-triglycerides, and HD

99 IER trial, the relationship between achieved LDL-cholesterol concentration at 4 weeks and subsequent

100 1 men and women (aged 21-73 y) with a median LDL-cholesterol concentration of 159 mg/dL (95% CI: 146,

101 e aorta by fluorodeoxyglucose (FDG)-PET, and LDL-cholesterol concentration of less than 3.37 mmol/L (

102 tatus, estimated glomerular filtration rate, LDL-cholesterol concentration, and use of lipid-lowering

103 uptake of LDL cholesterol, increased plasma LDL cholesterol concentrations, and premature cardiovasc

104 this decrease was not related to circulating LDL cholesterol concentrations, cholesterol synthesis ph

105 cumab, lower plasma low-density lipoprotein (LDL)-cholesterol concentrations.

106 the relationship between progressively lower LDL-cholesterol concentrations achieved at 4 weeks and c

107 LDL-cholesterol concentrations after the butter diet als

108 LDL-cholesterol concentrations after the cheese diet wer

109 gnificant monotonic relationship between low LDL-cholesterol concentrations and lower risk of the pri

110 as no difference in the change from baseline LDL-cholesterol concentrations between oral vitamin D3 a

111 t of vitamin D with UVB exposure would lower LDL-cholesterol concentrations compared with the effect

112 HDL cholesterol but differentially modifies LDL-cholesterol concentrations compared with the effects

113 The increase in LDL-cholesterol concentrations for DHA compared with EPA

114 ol and major cardiovascular outcomes down to LDL-cholesterol concentrations of less than 0.2 mmol/L.

115 ts extending to the bottom first percentile (LDL-cholesterol concentrations of less than 0.2 mmol/L;

116 2669 (10%) of 25 982 patients achieved LDL-cholesterol concentrations of less than 0.5 mmol/L,

117 ral vitamin D supplementation does not lower LDL-cholesterol concentrations or raise HDL-cholesterol

118 there were no safety concerns with very low LDL-cholesterol concentrations over a median of 2.2 year

119 The reduction in LDL-apoB and LDL-cholesterol concentrations was significantly greater

120 GTE significantly reduced circulating TC and LDL-cholesterol concentrations, especially in those with

121 se only among individuals with high baseline LDL-cholesterol concentrations.

122 KJM), a viscous soluble fiber, for improving LDL-cholesterol concentrations.

123 After 12 weeks, mean LDL cholesterol decreased from baseline by 20.6% (SD 24.

124 these observations suggest that, as well as LDL cholesterol, disordered metabolism of triglyceride-r

125 out one-quarter for each mmol/L reduction in LDL cholesterol during each year (after the first) that

126 ith the APOE4 allele associated with greater LDL-cholesterol elevation in response to saturated fatty

127 Secondary outcomes were HbA1c, LDL cholesterol, estimated glomerular filtration rate (e

128 associations of PCSK9 genetic variants with LDL cholesterol, fasting blood glucose, HbA1c, fasting i

129 s) significantly reduced levels of PCSK9 and LDL cholesterol for at least 6 months.

130 with significant increase in fasting plasma LDL cholesterol, free fatty acids, and total ketone bodi

131 was percentage change in ultracentrifugation LDL cholesterol from baseline at week 12 compared with p

132 point was percentage change in fasting serum LDL cholesterol from baseline to week 12 and the primary

133 ol (from 267 to 160, 157 and 184 mg/dL), and LDL cholesterol (from 193 mg/dL to 133, 115 and 124 mg/d

134 LDLR coding-sequence mutation and had plasma LDL cholesterol > 190 mg dl(-1).

135 clerotic cardiovascular disease, adults with LDL cholesterol>/=190 mg/dl, and adults 40-79 years old

136 In clinical trials, a small increase in LDL cholesterol has been reported with sodium-glucose co

137 in pharmacological interventions that reduce LDL cholesterol have been remarkable, coming more than a

138 not the HF-DASH diet, significantly reduced LDL cholesterol, HDL cholesterol, apolipoprotein A-I, in

139 -sensitivity check index, total cholesterol, LDL cholesterol, HDL cholesterol, or triglycerides (all

140 Among all subjects, TC, LDL cholesterol, HDL cholesterol, TC:HDL cholesterol, tr

141 cedure on the postintervention values of TC, LDL cholesterol, HDL cholesterol, TC:HDL cholesterol, tr

142 (BMI, systolic and diastolic blood pressure, LDL cholesterol, HDL cholesterol, total cholesterol, tri

143 risk factors [blood total cholesterol (TC), LDL cholesterol, HDL cholesterol, triglycerides, ratio o

144 Hg) and 0.1 mm Hg (-1.2, 1.5 mm Hg) for TC, LDL cholesterol, HDL cholesterol, triglycerides, TC:HDL

145 analysis of lipid traits (total cholesterol, LDL-cholesterol, HDL-cholesterol triglycerides) in up to

146 investigation to assess the causal roles of LDL-cholesterol, HDL-cholesterol, and triglycerides on A

147 total cholesterol, low-density lipoprotein (LDL) cholesterol, high-density lipoprotein (HDL) cholest

148 with at least 1 of low-density lipoprotein (LDL) cholesterol, high-density lipoprotein (HDL) cholest

149 [total cholesterol, low-density lipoprotein (LDL) cholesterol, high-density lipoprotein, and triglyce

150 cular disease, based on the concentration of LDL cholesterol in blood and individuals' responsiveness

151 TTR-ASO treatment decreased LDL cholesterol in high-fat diet-fed mice.

152 was associated with baseline serum total and LDL cholesterol in multivariable-adjusted models (beta:

153 In a post-hoc analysis, mean reductions in LDL cholesterol in patients on apheresis were significan

154 is an effective additional option to reduce LDL cholesterol in patients with homozygous familial hyp

155 CSK9 inhibition with evolocumab (AMG 145) on LDL cholesterol in patients with this disorder.

156 with the extent of reduction in circulating LDL cholesterol in response to PS consumption and could

157 he extent of reduction in circulating TC and LDL cholesterol in response to PS consumption.

158 NAs were able to reduce the triglyceride and LDL cholesterol in transgenic mice demonstrating pharmac

159 LDLR abundance and of circulating levels of LDL-cholesterol in humans.

160 rum lipids in adults with or at risk of high LDL cholesterol.In a randomized, crossover, isocaloric,

161 essure and elevated low-density lipoprotein (LDL) cholesterol increase the risk of cardiovascular dis

162 a is characterised by low cellular uptake of LDL cholesterol, increased plasma LDL cholesterol concen

163 LDL cholesterol is a well established risk factor for at

164 diet: -1.5 mmol/L (-2.1, -0.8 mmol/L)], and LDL cholesterol [LC diet: -0.1 mmol/L (-0.3, 0.1 mmol/L)

165 /m) revealed linear sensor characteristic to LDL cholesterol (LDL-C) from 4 to 400 mg/dL or 0.10-10.3

166 Alleles associated with lower levels of LDL cholesterol (LDL-C) have recently been associated wi

167 ronary heart disease (CHD), independently of LDL cholesterol (LDL-C) levels.

168 (LDLs) metabolism, and evolocumab can lower LDL cholesterol (LDL-C) to low levels.

169 between circulating HDL cholesterol (HDL-C), LDL cholesterol (LDL-C), and triglycerides and T2D and r

170 mutations that result in elevated levels of LDL cholesterol (LDL-C).

171 athway is essential for clearing circulating LDL cholesterol (LDL-C).

172 ndividuals with low low-density lipoprotein (LDL) cholesterol (LDL-C).

173 positive association between SFA intake and LDL cholesterol, LDL cholesterol was not associated with

174 goal of HbA1c less than 7.0% (53 mmol/mol), LDL cholesterol less than 2.59 mmol/L, and systolic bloo

175 84), and doses of 100 mg or more reduced the LDL cholesterol level (up to a least-squares mean reduct

176 ry end point was the change from baseline in LDL cholesterol level at 180 days.

177 the patients who received the regimen had an LDL cholesterol level below 50 mg per deciliter (1.3 mmo

178 The median time-weighted average LDL cholesterol level during the study was 53.7 mg per d

179 bococizumab had a reduction of 54.2% in the LDL cholesterol level from baseline, as compared with an

180 ontrast, p.R730W was associated with neither LDL cholesterol level nor altered in vitro activity.

181 trial (in which the patients had a baseline LDL cholesterol level of >/=100 mg per deciliter [2.6 mm

182 trial (in which the patients had a baseline LDL cholesterol level of >/=70 mg per deciliter [1.8 mmo

183 sive atorvastatin therapy and who had a mean LDL cholesterol level of 61 mg per deciliter (1.58 mmol

184 randomly assigned healthy volunteers with an LDL cholesterol level of at least 100 mg per deciliter i

185 mm(2)/mg/dL; P = .02); the association with LDL cholesterol level remained significant (P = .02) aft

186 The decrease in the LDL cholesterol level was 33.7 mg per deciliter (0.87 mm

187 , and pharmacodynamic measures (PCSK9 level, LDL cholesterol level, and exploratory lipid variables)

188 Conclusion LDL cholesterol level, systolic blood pressure, and diab

189 events and diabetes per unit decrease in the LDL cholesterol level.

190 g per deciliter (0.26 mmol per liter) in the LDL cholesterol level: odds ratio for cardiovascular eve

191 m(2); P = .03), and low-density lipoprotein (LDL) cholesterol level (beta = 0.04 mm(2)/mg/dL; P = .02

192 patients in the lowest quartile for baseline LDL cholesterol levels (median, 74 mg per deciliter [1.9

193 ed reduced blood pressure, triglyceride, and LDL cholesterol levels after the LFHCC n-3 diet and incr

194 ial, inclisiran was found to lower PCSK9 and LDL cholesterol levels among patients at high cardiovasc

195 analysis, there were no associations between LDL cholesterol levels and cognitive changes.

196 zetimibe resulted in incremental lowering of LDL cholesterol levels and improved cardiovascular outco

197 ansfer protein (CETP) by anacetrapib reduces LDL cholesterol levels and increases high-density lipopr

198 tandard therapy alone, significantly reduced LDL cholesterol levels and reduced the incidence of card

199 ease or familial hypercholesterolaemia whose LDL cholesterol levels are insufficiently controlled on

200 ere was wide variability in the reduction in LDL cholesterol levels at both 12 weeks and 52 weeks.

201 diovascular disease benefit from lowering of LDL cholesterol levels below current targets.

202 in the Netherlands and Denmark with fasting LDL cholesterol levels between 2.5 mmol/L and 4.5 mmol/L

203 n LDL cholesterol, while among subjects with LDL cholesterol levels close to 160 mg/dL, the same expo

204 rs or older and women 60 years or older with LDL cholesterol levels less than 130 mg/dL, high-sensiti

205 ed trials had a mean change from baseline in LDL cholesterol levels of -56.0% in the bococizumab grou

206 high risk for cardiovascular events who had LDL cholesterol levels of 70 mg per deciliter (1.8 mmol

207 h atherosclerotic cardiovascular disease and LDL cholesterol levels of 70 mg per deciliter (1.8 mmol

208 At day 240, PCSK9 and LDL cholesterol levels remained significantly lower than

209 We compared the effects of lower LDL cholesterol levels that were mediated by variants in

210 ab on a background of statin therapy lowered LDL cholesterol levels to a median of 30 mg per decilite

211 ay 180, the least-squares mean reductions in LDL cholesterol levels were 27.9 to 41.9% after a single

212 the SGLT2 inhibitor empagliflozin increases LDL cholesterol levels were investigated in hamsters wit

213 At week 12, LDL cholesterol levels were reduced by 27.4% in patients

214 LDL cholesterol levels were reduced by 68.2% in patients

215 e least-squares mean percentage reduction in LDL cholesterol levels with evolocumab, as compared with

216 d with coronary artery disease (CAD), plasma LDL cholesterol levels, and other energy metabolism phen

217 nal trials with different entry criteria for LDL cholesterol levels, we randomly assigned the 27,438

218 n had dose-dependent reductions in PCSK9 and LDL cholesterol levels.

219 at high cardiovascular risk who had elevated LDL cholesterol levels.

220 y serve as a potential strategy for lowering LDL cholesterol levels.

221 ic Commd1 knockout mice have elevated plasma LDL cholesterol levels.

222 , moderately increases ketone production and LDL cholesterol levels.

223 and significantly attenuated the lowering of LDL cholesterol levels.

224 aximum tolerated dose, significantly reduced LDL cholesterol levels.

225 magnitude and durability of the reduction in LDL cholesterol levels.

226 for cardiovascular disease who had elevated LDL cholesterol levels.

227 n regimen produced the greatest reduction in LDL cholesterol levels: 48% of the patients who received

228 tin therapy reduces low-density lipoprotein (LDL) cholesterol levels and the risk of cardiovascular e

229 (PCSK9) and lowers low-density lipoprotein (LDL) cholesterol levels by approximately 60%.

230 effect of lowering low-density lipoprotein (LDL) cholesterol levels by inhibiting PCSK9 on the risk

231 een shown to reduce low-density lipoprotein (LDL) cholesterol levels in patients who are receiving st

232 gnificantly reduced low-density lipoprotein (LDL) cholesterol levels in short-term studies.

233 l Trial by reducing low-density-lipoprotein (LDL) cholesterol levels more than statin therapy alone.

234 ained reductions in low-density lipoprotein (LDL) cholesterol levels over the course of 84 days in he

235 -based treatment of low-density lipoprotein (LDL) cholesterol levels.

236 esterol (LOC100996634 and COPB1) and one for LDL cholesterol (LINC00324/CTC1/PFAS).

237 dentify individuals who would derive maximum LDL cholesterol lowering with PS consumption.

238 tatin therapies for low-density lipoprotein (LDL)-cholesterol lowering in the management of atheroscl

239 r protective effects that are independent of LDL-cholesterol lowering called pleiotropic effects.

240 These data support further LDL-cholesterol lowering in patients with cardiovascular

241 abetes, to groups according to the number of LDL cholesterol-lowering alleles that they had inherited

242 Furthermore, AAT3 augments LDL cholesterol-lowering effects of ApoB-ASO.

243 We sought to investigate the associations of LDL cholesterol-lowering PCSK9 variants with type 2 diab

244 ial hypercholesterolaemia who were on stable LDL cholesterol-lowering therapy for at least 4 weeks; a

245 Within just a few years, four new LDL-cholesterol-lowering agents have received regulatory

246 than a decade after the approval of the last LDL-cholesterol-lowering drug, the cholesterol absorptio

247 behind the development of the newly approved LDL-cholesterol-lowering drugs and critically review the

248 s of antihyperglycaemic drugs and non-statin LDL-cholesterol-lowering drugs in patients with type 2 d

249 (LDLR-negative mutations), maximum untreated LDL-cholesterol (maxLDL), LDL-C, blood pressure, and cor

250 KJM significantly lowered LDL cholesterol (MD: -0.35 mmol/L; 95% CI: -0.46, -0.25

251 1025 (4%) patients did not have an LDL cholesterol measured at 4 weeks and 557 (2%) had alr

252 utter intake increased total cholesterol and LDL cholesterol more than did olive oil intake (P < 0.05

253 nalysis aimed to assess the effect of KJM on LDL cholesterol, non-HDL cholesterol, and apolipoprotein

254 f >/=3 wk that assessed the effect of KJM on LDL cholesterol, non-HDL cholesterol, or apolipoprotein

255 n changes from baseline in concentrations of LDL cholesterol, non-HDL cholesterol, total cholesterol,

256 (NSNPs = 73), HDL-cholesterol (NSNPs = 71), LDL-cholesterol (NSNPs = 57), triglycerides (NSNPs = 39)

257 weeks, with an additional mean reduction in LDL cholesterol of 8.3% (SD 13.0; mean absolute decrease

258 ults by the central laboratory not returning LDL cholesterol or any lipid results to the clinical sit

259 f regular-fat cheese for 12 wk did not alter LDL cholesterol or MetS risk factors differently than an

260 No causal effect of LDL-cholesterol or triglycerides was found.

261 ol/l increase), and low-density lipoprotein (LDL) cholesterol (OR, 0.83; 95% CI, 0.74-0.92, per mmol/

262 e same as those found against copper-induced LDL-cholesterol oxidation and supercoiled plasmid DNA st

263 led to a greater decrease in TC (P = 0.03), LDL cholesterol (P = 0.04), and HDL cholesterol (P = 0.0

264 cholesterol confers CAD risk beyond that of LDL cholesterol (P = 5.5 x 10(-8)), suggesting that targ

265 ificantly decreased triglycerides, total and LDL-cholesterol (p < 0.001).

266 droxyl and peroxyl radicals), copper-induced LDL-cholesterol peroxidation, as well as alpha-glucosida

267 lization, provide mechanisms for the greater LDL-cholesterol raising effect.

268 sorder characterised by substantially raised LDL cholesterol, reduced LDL receptor function, xanthoma

269 LDL cholesterol reduction was 31.1% with pitavastatin an

270 circulating lipid levels and statin-induced LDL cholesterol reduction.

271 correlates to some extent with the amount of LDL-cholesterol reduction.

272 otwithstanding the effectiveness of lowering LDL cholesterol, residual CVD risk remains in high-risk

273 The LDL-cholesterol response to treatment was significantly

274 vel non-coding rare variants associated with LDL cholesterol (rs17242388 in LDLR) and HDL cholesterol

275 09, and rs11206510) scaled to 1 mmol/L lower LDL cholesterol showed associations with increased fasti

276 After PS intervention, LDL cholesterol significantly decreased on average by 0.

277 w-density lipoprotein receptor [LDLR]), with LDL cholesterol statin response.

278 ascular events and the absolute reduction in LDL cholesterol that is achieved.

279 abetes, evolocumab caused mean reductions in LDL cholesterol that were 66% (62-70) versus placebo and

280 r the low levels of low-density lipoprotein (LDL) cholesterol that result from their use are associat

281 d TPCs include VEGF-induced neoangiogenesis, LDL-cholesterol trafficking and degradation, physical en

282 Total cholesterol (TC), LDL cholesterol, triacylglycerol, lipoprotein(a), and ap

283 rected QT interval, low density lipoprotein (LDL) cholesterol, triglyceride, and intercellular adhesi

284 d fasting glucose, hemoglobin A1C, total and LDL cholesterol, triglycerides, and coronary artery dise

285 (HDL) cholesterol, low-density lipoprotein (LDL) cholesterol, triglycerides, alanine transaminase (A

286 ghee increases the serum total cholesterol, LDL-cholesterols, triglycerides and decrease the serum g

287 Total, HDL, and LDL cholesterol; triglycerides; fasting glucose; AST; an

288 uction of 83.8% from baseline to day 84) and LDL cholesterol (up to a least-squares mean reduction of

289 ssociated with dyslipidemia: the increase in LDL cholesterol was 0.54 mmol/L (20.9 mg/dL) per allele

290 between nut intake and total cholesterol and LDL cholesterol was nonlinear (P-nonlinearity < 0.001 ea

291 tion between SFA intake and LDL cholesterol, LDL cholesterol was not associated with ASVD mortality i

292 LDL cholesterol was not significantly associated with ri

293 The primary outcome, LDL cholesterol, was not significantly different between

294 Overall, whole-grain intake lowered LDL cholesterol (weighted difference: -0.09 mmol/L; 95%

295 PCSK9 variants associated with lower LDL cholesterol were also associated with circulating hi

296 TATION: PCSK9 variants associated with lower LDL cholesterol were also associated with circulating hi

297 Reductions in the levels of PCSK9 and LDL cholesterol were maintained at day 180 for doses of

298 rs, LDLR mutation carriers had higher plasma LDL cholesterol, whereas APOA5 mutation carriers had hig

299 can increase plasma low density lipoprotein (LDL) cholesterol, which is a major risk factor for cardi

300 d with a 7-mg/dL (95% CI: 5, 10) increase in LDL cholesterol, while among subjects with LDL cholester