ライフサイエンスコーパス: SFA

1 SFA and MUFA models, developed using the first derivativ

2 SFA intake increases LDL cholesterol whereas PUFA intake

3 SFA were the main fatty acid group reduced (~80%), where

4 SFA-HFD impaired liver-to-feces RCT, increased hepatic i

5 SFAs from pastries and processed foods were associated w

6 y dietary restriction via splicing factor 1 (SFA-1; the C. elegans homologue of SF1, also known as br

7 Baseline (1993-1997) SFA intake was measured with a food-frequency questionna

8 y and/or Proximal Popliteal Artery [MDT-2113 SFA], NCT01947478; The IN.PACT SFA Clinical Study for th

9 a low-fat, high-carbohydrate diet (fat: 25%, SFAs: 5.8%).Serum HDL-cholesterol concentrations were si

10 A decrease in total saturated fatty acid (SFA) and monounsaturated fatty acid (MUFA) contents, and

11 reme quintiles, higher saturated fatty acid (SFA) and trans-fat intakes were associated with 81% (HR:

12 h the potential of its saturated fatty acid (SFA) content to raise low-density lipoprotein (LDL) chol

13 fatty acid (USFA) and saturated fatty acid (SFA) contents fluctuated under these treatments, the ole

14 Saturated fatty acid (SFA) high-fat diets (HFDs) enhance interleukin (IL)-1bet

15 fatty acid (PUFA), and saturated fatty acid (SFA) in the breast adipose tissue.

16 endothelial cells with saturated fatty acid (SFA) increased the accumulation of lipid droplets and im

17 he association between saturated fatty acid (SFA) intake and ischemic heart disease (IHD) risk is deb

18 The reduction of saturated fatty acid (SFA) intake has been the basis of long-standing dietary

19 ation to limit dietary saturated fatty acid (SFA) intake has persisted despite mounting evidence to t

20 volve reducing dietary saturated fatty acid (SFA) intake to </=10% of total energy (%TE).

21 d fatty acid (PUFA) to saturated fatty acid (SFA) ratio were higher and C18:2n-6 and monounsaturated

22 amplified response to saturated fatty acid (SFA) reduction, and increased cardiovascular disease.

23 palmitate, a prevalent saturated fatty acid (SFA), could drive solid-like domain separation from the

24 atty acids, especially saturated fatty acid (SFA), on cardiovascular disease (CVD).

25 gh fat diet (HFD) and saturated fatty acids (SFA) modulate fundamental circadian properties of periph

26 Overall, saturated fatty acids (SFA) were predominant, accounting for 71 to 80% of fatty

27 posing macrophages to saturated fatty acids (SFA), and endoplasmic reticulum (ER) stress responses es

28 the concentrations of saturated fatty acids (SFA), mono-unsaturated fatty acids (MUFA), gamma-oryzano

29 oped and proposed for Saturated Fatty Acids (SFA), Monounsatured Fatty Acids (MUFA), Polyunsatured Fa

30 toleate (16:1n7) from saturated fatty acids (SFA), stearate (18:0) and palmitate (16:0), respectively

31 vation in response to saturated fatty acids (SFA).

32 Saturated fatty acids (SFAs) (the "bad" fat), especially palmitate (PA), in the

33 een intake of dietary saturated fatty acids (SFAs) and cardiovascular disease risk.We compared the im

34 asis via synthesis of saturated fatty acids (SFAs) and monounsaturated fatty acids (MUFAs).

35 Circulating saturated fatty acids (SFAs) are integrated biomarkers of diet and metabolism t

36 utrients and specific saturated fatty acids (SFAs) in food.

37 than 55% of the total saturated fatty acids (SFAs) in salty snacks.

38 ration of excess saturated free fatty acids (SFAs) into membrane phospholipids within the ER promotes

39 Saturated fatty acids (SFAs) of different chain lengths have unique metabolic a

40 The effects of saturated fatty acids (SFAs) on cardiovascular disease (CVD) risk are modulated

41 s of reducing dietary saturated fatty acids (SFAs) on insulin resistance (IR) and other metabolic ris

42 iets that are high in saturated fatty acids (SFAs) or polyunsaturated fatty acids (PUFAs) have differ

43 levels of circulating saturated fatty acids (SFAs) that associate with the progression of neuropathy.

44 aturase that converts saturated fatty acids (SFAs) to unsaturated fatty acids (UFAs), at low temperat

45 Replacing dietary saturated fatty acids (SFAs) with polyunsaturated fatty acids (PUFA) reduces th

46 Replacement of saturated fatty acids (SFAs) with unsaturated fatty acids (UFAs), especially po

47 that NoDGAT2A prefers saturated fatty acids (SFAs), NoDGAT2D prefers monounsaturated fatty acids (MUF

48 % kcal) diets rich in saturated fatty acids (SFAs), omega-6 or omega-3 polyunsaturated FAs (PUFAs).

49 grams per day), total saturated fatty acids (SFAs), percentage of energy from SFAs, and total trans f

50 ary fibres, red meat, saturated fatty acids (SFAs), sodium, sugar-sweetened beverages (SSBs), and add

51 ich in saturated fat [saturated fatty acids (SFAs)] and can increase plasma low density lipoprotein (

52 e a reduction in spike-frequency adaptation (SFA) and a shift in the phase response curve (PRC).

53 mopexin) and depleted of paraoxonase-1 after SFA-HFD in comparison with MUFA-HFD.

54 c-derived inflammatory proteins on HDL after SFA-HFD in comparison with MUFA-HFD, which reflected dif

55 R binding affinity of postprandial TRL after SFA, and lower LDL binding and hepatocyte internalizatio

56 Although SFAs increase low-density lipoprotein (LDL) cholesterol,

57 nsaturated sphingomyelins (even if having an SFA base) were not associated with risk of diabetes.

58 hed with oil-based margarine ( n = 42) or an SFA diet enriched with butter (n = 41) for 6 wk.

59 Using stationary fluctuation analysis (SFA), we demonstrate that single-channel conductance of

60 0.38 +/- 0.06 vs 0.46 +/- 0.10; P < .05) and SFA was higher (0.31 +/- 0.07 vs 0.19 +/- 0.11; P < .05)

61 to its highest concentration (30-55 DAF) and SFA and PUFA reached their lowest.

62 test meals rich in SFA, unsaturated fat and SFA with fish oil.

63 NFalpha and IL-6 are key signals in HFD- and SFA-induced proinflammatory responses that ultimately le

64 1beta secretion from lipopolysaccharide- and SFA-primed cells in an AMPK-dependent manner.

65 be improved by replacing atherogenic TFA and SFA with beneficial ones, in order to avoid adverse effe

66 ecylic and margaric acid, myristic acid, and SFAs from dairy sources.

67 intakes of total SFAs, individual SFAs, and SFAs from different food sources.

68 to many exotic phenomena, such as anomalous SFA-mediated quantum oscillations, chiral magnetic effec

69 s conducted with a surface forces apparatus (SFA) allow adhesive failure to be distinguished from coh

70 d a combination of surface forces apparatus (SFA) measurements and replica-exchange molecular dynamic

71 combined with a buccal single flap approach (SFA) in the regenerative treatment of intraosseous defec

72 ect cohort accessed by Single Flap Approach (SFA).

73 Surface Fermi arcs (SFAs), the unique open Fermi-surfaces (FSs) discovered r

74 ry, unprocessed meat, and dark chocolate are SFA-rich foods with a complex matrix that are not associ

75 the Treatment of Superficial Femoral Artery [SFA] and Proximal Popliteal Artery [PPA] [INPACT SFA II]

76 c Lesions in the Superficial Femoral Artery [SFA] and/or Proximal Popliteal Artery [PPA]) that enroll

77 Baseline SFA intake was associated with baseline serum total and

78 gy intake) at 3 months adjusted for baseline SFA and GP practice using intention-to-treat analysis.

79 re was a strong positive association between SFA intake and LDL cholesterol, LDL cholesterol was not

80 conflicting evidence in the relation between SFA consumption and risk of atherosclerotic vascular dis

81 e effects of isocaloric replacements between SFA, MUFA, PUFA, and carbohydrate, adjusted for protein,

82 Direct comparisons between SFAs varying in chain length, specifically palmitic acid

83 intraosseous defects accessed with a buccal SFA and treated with different modalities were selected

84 duction, adjunctive use of a CTG to a buccal SFA in the regenerative treatment of periodontal intraos

85 an intraosseous defect treated with a buccal SFA with (SFA+CTG group; n = 15) or without (SFA group;

86 After buccal SFA, greater post-surgery increase in bREC must be expec

87 th buccal bone dehiscence accessed by buccal SFA may support the stability of the gingival profile.

88 domain containing (ADIPOQ)] were changed by SFA overfeeding.

89 modulation of peripheral circadian clocks by SFA-induced inflammatory signaling.

90 hypoxia-potentiated inflammation induced by SFA palmitate, we found that the AMP-mimetic AMPK activa

91 n; 0.2, 0.8) whether replacing carbohydrate, SFA, or even MUFA.

92 In comparison to carbohydrate, SFA, or MUFA, most consistent favourable effects were se

93 ls of pentadecylic acid (C15:0, an odd-chain SFA) and palmitoleic acid were inversely correlated with

94 lating concentrations of the very-long-chain SFAs (VLSFAs) arachidic acid (20:0), behenic acid (22:0)

95 Very-long-chain SFAs (VLSFAs) have recently gained considerable attentio

96 ated with diabetes; however, very-long-chain SFAs (VLSFAs), with 20 or more carbons, differ from palm

97 vestigated associations of major circulating SFAs [palmitic acid (16:0) and stearic acid (18:0)] and

98 Fatty acid composition (SFA:MUFA:PUFA) (1:1.5:2) of rice bran oil+palm oil (80:2

99 k, consumption of a high-fat diet containing SFA-reduced, MUFA-enriched dairy products for 12 wk show

100 In contrast, SFAs from either cheese or butter have no significant ef

101 current dietary recommendations to decrease SFA and replace it with unsaturated fat should continue

102 monounsaturated fatty acid (MUFA)-rich diet (SFAs: 5.8%, MUFAs: 19.6%); a polyunsaturated fatty acid

103 polyunsaturated fatty acid (PUFA)-rich diet (SFAs: 5.8%, PUFAs: 11.5%); and a low-fat, high-carbohydr

104 6 single nucleotide polymorphism and dietary SFA:carbohydrate ratio intake for the homeostasis model

105 The impact of dietary SFA consumption and insulin resistance on HDL efflux fun

106 nt is a potential strategy to reduce dietary SFA intake for cardiovascular disease (CVD) prevention i

107 redictive of reduced CVD risk, 3) do dietary SFAs affect factors other than LDL cholesterol that may

108 ccenic acid (18:1n-7)] and estimated dietary SFAs and MUFAs.

109 fatty acid biomarkers and estimated dietary SFAs or MUFAs were not significantly associated with inc

110 The effects of dietary SFAs on insulin sensitivity, inflammation, vascular func

111 4 major questions: 1) does reducing dietary SFAs lower the incidence of CVD, 2) is the LDL-cholester

112 ting a target for maximally reducing dietary SFAs?

113 gated the substitution of 9.5-9.6%TE dietary SFAs with either monounsaturated fatty acids (MUFAs) or

114 Substitution of 9.5-9.6%TE dietary SFAs with either MUFAs or n-6 PUFAs did not significantl

115 The proposition that dietary SFAs should be restricted to the maximal extent possible

116 We sought to investigate whether dietary SFAs were associated with IHD risk and whether associati

117 rger differences in SFA intake and different SFA food sources.

118 need to distinguish the effects of different SFAs and to explore determinants of circulating VLSFAs.

119 on, the existence of SFAs is robust and each SFA remains tied to a pair of Weyl points of opposite ch

120 electrochemical surface forces apparatus (EC-SFA) on confined metallic surfaces, we observe in situ n

121 large proportion of the population exceeding SFA recommendations.

122 .We studied the effects of 7 wk of excessive SFA (n = 17) or PUFA (n = 14) intake (+750 kcal/d) on th

123 systems, but FR milk had less saturated FA (SFA) and/or palmitic acid, and/or greater alpha-linoleni

124 We show that following saturated FA (SFA) treatment, the ER integrity of SNX14 (KO) cells is

125 Saturated FA (SFA) were present with 22.76-51.17%.

126 Another longevity promoting splicing factor, SFA-1, similarly exerts an immuno-suppressive effect, wo

127 Guidelines recommend reducing saturated fat (SFA) intake to decrease cardiovascular disease (CVD) ris

128 We aimed to assess how saturated fat (SFA), monounsaturated fat (MUFA), polyunsaturated fat (P

129 ic diets (%TE target compositions, total fat:SFA:MUFA:n-6 PUFA) that were rich in SFAs (36:17:11:4, n

130 ed Fluorescence Surface Forces Apparatus (FL-SFA), migration of liquid-disordered clusters and deplet

131 Importantly, the FL-SFA can unambiguously correlate interaction forces and i

132 id (HRSD: 0.91: 95% CI: 0.83, 0.99), and for SFAs from dairy sources, including butter (HRSD: 0.94; 9

133 nsumed an average of 12-18% of calories from SFA.

134 metformin protects vascular endothelium from SFA-induced ectopic lipid accumulation and pro-inflammat

135 rsely, in a regression study, switching from SFA- to MUFA-HFD failed to reverse insulin resistance bu

136 The additional 2% of energy from SFAs in the cheese diet was replaced by n-6 PUFAs in the

137 atty acids (SFAs), percentage of energy from SFAs, and total trans fatty acids with serum PLFAs in bo

138 /100g DM), whereas the Mon-thong variety had SFA>MUFA>PUFA (5.1, 4.0, 1.1g/100g DM, respectively).

139 High SFA intake was associated with the risk of ASVD mortalit

140 so observed with insulin resistance and high SFA consumption in humans.

141 between two and 21 DAF characterized by high SFA and PUFA, which decreased 21 DAF.

142 l 3 dietary protein assignments (61 for high SFA; 52 for low SFA).

143 In humans, high-SFA consumers, but not high-MUFA consumers, displayed re

144 In this Dutch population, higher SFA intake was not associated with higher IHD risks.

145 ant reduction in CVD risk can be achieved if SFAs are replaced by unsaturated fats, especially polyun

146 as the between-group difference in change in SFA intake (% total energy intake) at 3 months adjusted

147 There were small decreases in SFA intake at 3 months: control = -0.1% (95% CI -1.8 to

148 ed in populations with larger differences in SFA intake and different SFA food sources.

149 wed differences of ~9 energy percent (E%) in SFA and ~4 E% in PUFA between the SFA and PUFA groups.

150 E4-), both groups had a greater reduction in SFA (percentage of total energy) intake than at level 0

151 N was associated with a smaller reduction in SFA intake than in nongene-based PN (level 2) for E4- pa

152 s powered to detect an absolute reduction in SFA of 3% (SD3).

153 e of this current recreates the reduction in SFA the shift from a type 2 to a type 1 PRC observed in

154 e in primary care to encourage reductions in SFA intake and to provide personalized advice to encoura

155 There was no evidence of large reductions in SFA, but we are unable to exclude more modest benefits.

156 sting and 4-6 h following test meals rich in SFA, unsaturated fat and SFA with fish oil.

157 herapy and trans fat or limited variation in SFA and PUFA intake may explain our findings.

158 separated by 4-wk washouts: 2 diets rich in SFAs (12.4-12.6% of calories) from either cheese or butt

159 tal fat:SFA:MUFA:n-6 PUFA) that were rich in SFAs (36:17:11:4, n = 65), MUFAs (36:9:19:4, n = 64), or

160 ice Mus musculus fed a high-fat diet rich in SFAs developed robust peripheral neuropathy.

161 the association between 12-month change in %SFA and blood lipids in 208 HLC participants with comple

162 The association between increase in %SFA and decrease in triglycerides was no longer signific

163 s who had the highest 12-month increases in %SFA.

164 There were similar trends in %SFA based on supermarket purchases: control = -0.5% (95%

165 Secondary outcomes included %SFA in purchases, LDL cholesterol, and feasibility outco

166 fferences in health impacts among individual SFA-containing foods.

167 e, including the heterogeneity of individual SFAs, the likelihood of clinically meaningful interindiv

168 for higher intakes of total SFAs, individual SFAs, and SFAs from different food sources.

169 indicates that saturated fatty acid-induced (SFA-induced) lipotoxicity contributes to the pathogenesi

170 Proximal Popliteal Arterial Disease [INPACT SFA I], NCT01175850; IN.PACT Admiral Drug-Coated Balloon

171 and Proximal Popliteal Artery [PPA] [INPACT SFA II], NCT01566461; MDT-2113 Drug-Eluting Balloon vs.

172 age of dietary saturated fatty acid intake (%SFA) and changes in low-density lipoproteins, high-densi

173 increase in response to extra energy intake.SFA overfeeding and PUFA overfeeding induce distinct epi

174 st a guideline focused primarily on limiting SFA intake, including the heterogeneity of individual SF

175 ype may be more likely to benefit from a low SFA:carbohydrate ratio intake to improve insulin resista

176 ed 4 milk fatty acid patterns: "MUFA and low SFA," "high n-6 PUFA," "high n-3 PUFA," and "high medium

177 ein assignments (61 for high SFA; 52 for low SFA).

178 ssigned to 1 of 2 parallel arms (high or low SFA) and within each, allocated to red meat, white meat,

179 nt of protein source, high compared with low SFA increased LDL cholesterol (P = 0.0003), apoB (P = 0.

180 concomitant intake of high compared with low SFAs.

181 0% CLA), combining to produce milk 16% lower SFA and higher in MUFA (43%), PUFA (55%) and CLA (59%).

182 /- 0.06 vs 0.27 +/- 0.05; P < .01) and lower SFA (0.19 +/- 0.11 vs 0.30 +/- 0.12; P < .05) than preme

183 grocery purchases and suggestions for lower SFA swaps.

184 is the LDL-cholesterol reduction with lower SFA intake predictive of reduced CVD risk, 3) do dietary

185 ucagon, or GIP related to protein type or MC-SFA content.

186 n and medium-chain saturated fatty acids (MC-SFAs) improved postprandial lipid metabolism in humans w

187 as 1,2-distearoyl-PA (18:0/18:0-PA) mediate SFA-induced lipotoxicity and vascular calcification.

188 We investigated the association of SFA intake with serum lipid profiles and ASVD mortality

189 risks such as obesity and cancer because of SFA-induced lipotoxicity.

190 white meat than with nonmeat, independent of SFA content (P < 0.0001 for all, except apoB: red meat c

191 We also demonstrate that overexpression of SFA-1 is sufficient to extend lifespan.

192 The highest quartile of SFA intake (>31.28 g/d) had an ~16% cumulative mortality

193 We hypothesized that the replacement of SFA for monounsaturated fatty acid (MUFA) in HFDs would

194 Balloon vs Standard PTA for the Treatment of SFA and Proximal Popliteal Arterial Disease [INPACT SFA

195 red the impact of consuming equal amounts of SFAs from cheese and butter on cardiometabolic risk fact

196 ical results demonstrate a latent benefit of SFAs, and it remains elusive whether a certain low level

197 t is believed to derive from the capacity of SFAs to raise LDL cholesterol, and the evidence that LDL

198 the shape, size and even the connections of SFAs in a model TWS, NbAs, and observe their evolution t

199 of our study suggest that the consumption of SFAs from cheese and butter has similar effects on HDL c

200 is study examines the differential effect of SFAs and MUFAs on the development of neuropathy and the

201 of energy of total UFAs, 13.0% of energy of SFAs, and <1% of energy of TFAs.

202 dramatic surface evolution, the existence of SFAs is robust and each SFA remains tied to a pair of We

203 The results indicate a high daily intake of SFAs and trans fatty acids, which may have an unfavourab

204 though it is possible that dietary intake of SFAs has a causal role in CVD, the evidence to support t

205 etary recommendations to decrease intakes of SFAs and, more recently, to replace SFAs with unsaturate

206 macronutrient, 2) the carbon chain length of SFAs, and 3) the SFA food source.

207 mains elusive whether a certain low level of SFAs is physiologically essential for maintaining cell m

208 uration were created, in which proportion of SFAs, MUFAs, and PUFAs in TAG varied by 1.3-, 3.7-, and

209 In continuous analyses, replacement of SFAs plus TFAs with total UFAs, PUFAs, or cis MUFAs (per

210 In contrast, replacement of SFAs with carbohydrates, particularly sugar, has been as

211 The replacement of SFAs with MUFAs and PUFAs or of trans fat with MUFAs was

212 Replacement of SFAs with polyunsaturated fatty acids has been associate

213 logic research has shown that replacement of SFAs with unsaturated fat, but not refined carbohydrate

214 Isocaloric replacements of SFAs with MUFAs and PUFAs or trans fat with MUFAs were a

215 s with cheese and meat as primary sources of SFAs cause higher HDL cholesterol and apo A-I and, there

216 the effects of cheese and meat as sources of SFAs or isocaloric replacement with carbohydrates on blo

217 to a health effect from the substitution of SFAs in the HMUFA and LFHCC n-3 diets.

218 secondary outcome measures, substitution of SFAs with MUFAs attenuated the increase in night systoli

219 iable Cox regression for the substitution of SFAs with other macronutrients and for higher intakes of

220 ease (CVD) and IHD mortality when the sum of SFAs and trans fatty acids (TFAs) was theoretically repl

221 An increase of %SFA, without significant changes in absolute saturated f

222 we tested the effects of the intervention on SFA intake and low-density lipoprotein (LDL) cholesterol

223 mined in C57BL/6j mice following 24 weeks on SFA- or MUFA-enriched high-fat diets (HFDs) or low-fat d

224 ery [MDT-2113 SFA], NCT01947478; The IN.PACT SFA Clinical Study for the Treatment of Atherosclerotic

225 Methods and Results IN.PACT SFA is a prospective, multicenter, randomized single-bli

226 Unique identifier: NCT01175850 (IN.PACT SFA phase I) and NCT01566461 (IN.PACT SFA phase II).

227 N.PACT SFA phase I) and NCT01566461 (IN.PACT SFA phase II).

228 Conclusions The IN.PACT SFA randomized trial demonstrates that the IN.PACT Admir

229 The IN.PACT SFA Trial is a prospective, multicenter, single-blinded,

230 Preconception SFA concentration was associated with higher methylation

231 eral circadian clocks by the proinflammatory SFA, palmitate.

232 negatively correlated with C20:5n-3 and PUFA/SFA ratio, but differences in sensory attributes (tender

233 o was found in all studied species, and PUFA/SFA ratios ranged between 0.94 and 1.72, which is desira

234 The lipid indices (PUFA/SFA ratio, atherogenic and thrombogenic indices) for bot

235 (20:5n-3+22:6n-3+22:5n-3) and omega-6 PUFAs, SFAs, MUFAs, and trans FAs were 4.7 +/- 1.2, 38.0 +/- 2.

236 around one-third of the maximum recommended SFA intake.

237 these data support dietary advice to reduce SFA intake.

238 c health guidelines should advocate reducing SFA consumption as much as possible to reduce the risk o

239 geted to APOE was more effective in reducing SFA intake than standard dietary advice, there was no di

240 dies found no beneficial effects of reducing SFA intake on cardiovascular disease (CVD) and total mor

241 takes of SFAs and, more recently, to replace SFAs with unsaturated fat, including PUFAs and MUFAs.

242 ietary macronutrient isocalorically replaces SFA, the greatest LDL-cholesterol-lowering effect is see

243 Replacing SFA with PUFA significantly lowered glucose, HbA1c, C-pe

244 Replacing SFAs with MUFAs or n-6 PUFAs did not affect the percenta

245 eral blood mononuclear cells after replacing SFAs with PUFAs.

246 mount of dietary fat and recommend replacing SFAs with unsaturated fats, especially polyunsaturated f

247 blind, randomized controlled trial replacing SFAs with PUFAs in healthy subjects with moderate hyperc

248 lower risks of CVD mortality when replacing SFAs plus TFAs with total UFAs [HR in quintile 5 compare

249 specific inhibition of SCD and the resulting SFA accumulation plays a causative role in the pathogene

250 script abundance ratio that underlie a rigid SFA:MUFA:PUFA hierarchy in triacylglycerol (TAG).

251 turated (MUFA) (6.1-7.8g/100g DM)>saturated (SFA) (4.2-5.7g/100g DM)>polyunsaturated fatty acid (PUFA

252 category, while the proportion of saturated (SFA) and polyunsaturated (PUFA) fatty acids had increase

253 tigated if dietary replacement of saturated (SFA) for monounsaturated (MUFA) fatty acids modulates RC

254 Substituting SFAs with animal protein, cis monounsaturated fatty acid

255 r pharmacological AMPK activation suppresses SFA-induced inflammation in a human system is unclear.

256 : 19%TE SFA; 11%TE MUFA) and modified (16%TE SFA; 14%TE MUFA) diet].

257 TE) from fat: control (dietary target: 19%TE SFA; 11%TE MUFA) and modified (16%TE SFA; 14%TE MUFA) di

258 for cardiometabolic and general health than SFA intake alone.

259 We show that SFA-1 is specifically required for lifespan extension by

260 This study also suggests that SFA palmitic acid may play an important role in MetS-ass

261 ntrolled clinical studies demonstrating that SFAs increase LDL cholesterol, a major causal factor in

262 There is growing evidence that SFAs in the context of dairy foods, particularly ferment

263 the carbon chain length of SFAs, and 3) the SFA food source.

264 In addition, the SFA diet significantly altered the expression of 28 tran

265 rons treated with mixtures of oleate and the SFA palmitate.

266 nt (E%) in SFA and ~4 E% in PUFA between the SFA and PUFA groups.

267 Furthermore, both the SFA and PUFA diets increased the mean degree of DNA meth

268 ereas treatment with metformin decreased the SFA-induced leukocyte adhesion.

269 tely reversed by switching the mice from the SFA-rich high-fat diet to a MUFA-rich high-fat diet; ner

270 3% (95% CI: -0.7%, 11.2%), P = 0.206, in the SFA group, and -10.4% (95% CI: -15.2%, -5.7%) compared w

271 .0% (95% CI: -1.7%, 7.7%), P = 0.140, in the SFA group, and -8.9% (95% CI: -12.6%, -5.2%) compared wi

272 dback comprised a personalized report on the SFA content of grocery purchases and suggestions for low

273 rial and a bioactive agent in adjunct to the SFA may limit the postoperative increase in iREC.

274 population, the PUFA diet compared with the SFA diet lowered LDL cholesterol (-0.31 mmol/L; 95% CI:

275 The phase transition teleports the SFAs between different parts of the surface Brillouin zo

276 HCP to motivate participants to reduce their SFA intake.

277 patient-derived cells are hypersensitive to SFA-mediated lipotoxic cell death.

278 ful interindividual variation in response to SFA reduction, the potential for unintended health conse

279 Total SFA intake was associated with a lower IHD risk (HR per

280 Individual and total SFAs, MUFAs, and n-3 and n-6 PUFAs were analyzed using S

281 5 common groups of fatty acids [i.e., total SFAs, total MUFAs, total omega-3 (n-3) PUFAs, total mari

282 s independently associated with higher total SFAs, the "high medium-chain fatty acid" pattern, and lo

283 cronutrients and for higher intakes of total SFAs, individual SFAs, and SFAs from different food sour

284 and PC-TP play critical roles in trafficking SFAs into the glycerolipid biosynthetic pathway to form

285 then demonstrate that maintaining a high UFA/SFA ratio is essential for proteostasis at low temperatu

286 ever, the molecular mechanisms that underlie SFA-induced lipotoxicity remain unclear.

287 her unsaturated/saturated fatty acids (unSFA/SFA) ratio.

288 When SFA is present (decreasing ACh), traveling waves of acti

289 N, and P = 0.046 for the BPRHS) but not when SFA:carbohydrate ratio intake was low.

290 had a significantly higher HOMA-IR only when SFA:carbohydrate intake was high (P = 0.045 for the CORD

291 lcarnitine, and kynurenine were reduced when SFAs were replaced with PUFAs.

292 with a lower risk of CVD and death, whereas SFA and trans-fat intakes were associated with a higher

293 y that the overall dietary patterns in which SFAs are consumed are of greater significance for cardio

294 ergy profiles that quantitatively agree with SFA measurements and are used to extract the adhesive pr

295 Replacing 5% energy from carbohydrate with SFA had no significant effect on fasting glucose (+0.02

296 tained adipose AMPK activation compared with SFA-HFD-fed mice.

297 Furthermore, treatment with SFA or inhibition of autophagy increased leukocyte adhes

298 I modifies the effect of PUFAs compared with SFAs, with smaller improvements in atherogenic lipid con

299 seous defect treated with a buccal SFA with (SFA+CTG group; n = 15) or without (SFA group; n = 15) pl

300 SFA with (SFA+CTG group; n = 15) or without (SFA group; n = 15) placement of a CTG and regenerative t