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 impairment of insulin-responsive Akt phosphorylation

3 SFA intake was negatively associated with both forms of

4 SFA participants faced similar problems, but to a lesser

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

6 SFAs accounted for 46% of total plasma phospholipid fatt

7 SFAs decreased wakefulness and increased non-rapid eye m

8 SFAs from pastries and processed foods were associated w

9 SFAs, however, markedly increased liver fat compared wit

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

11 to the HS diet or diets that contained <10% SFAs and were high in either MUFAs or carbohydrates.

12 each of the 4 diets (HAD: 33% total fat, 12% SFA, 17% protein, and 20 g beef/d), DASH (27% total fat,

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

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

15 n, and 20 g beef/d), DASH (27% total fat, 6% SFA, 18% protein, and 28 g beef/d), BOLD (28% total fat,

16 n, and 28 g beef/d), BOLD (28% total fat, 6% SFA, 19% protein, and 113 g beef/d), and BOLD+ (28% tota

17 113 g beef/d), and BOLD+ (28% total fat, 6% SFA, 27% protein, and 153 g beef/d) for 5 wk.

18 s have evaluated a low-saturated fatty acid (SFA) (<7% calories) diet that contains lean beef.

19 acid-the most abundant saturated fatty acid (SFA) and the major SFA in the HFD used in our animal stu

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

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

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

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

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

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

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

27 n shown to depend upon saturated fatty acid (SFA) oversupply and de novo sphingolipid synthesis.

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

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

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

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

32 Fatty acid (SFA, MUFA, PUFA and n6/n3 and h/H ratios) and amino acid

33 contained lower total saturated fatty acid (SFA; 67 vs 72 g/100g fatty acids) and higher cis-monouns

34 Brain capillaries from S-folinic acid (SFA; 40 mg/kg)-treated PCFT-nullizygous mice exhibited i

35 fatty acids and lower saturated fatty acids (SFA) than those from pigs raised in the Intensive system

36 ng enzymes converting saturated fatty acids (SFA) to monounsaturated fatty acids (MUFA) in HCC and th

37 he highest amounts of saturated fatty acids (SFA) were found in low-fat yogurts, of monounsaturated f

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

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

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

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

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

43 od levels of specific saturated fatty acids (SFAs) and monounsaturated fatty acids (MUFAs) could refl

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

45 atty acids (MUFAs) or saturated fatty acids (SFAs) and their impact on glucose homeostasis, locomotio

46 e association between saturated fatty acids (SFAs) and type 2 diabetes.

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

48 is uncertain whether saturated fatty acids (SFAs) impair endothelial function and contribute to arte

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

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

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

52 for the conversion of saturated fatty acids (SFAs) into MUFAs.

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

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

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

56 on during overfeeding saturated fatty acids (SFAs) or polyunsaturated fatty acids (PUFAs).

57 placement options for saturated fatty acids (SFAs) to optimize cardiovascular disease (CVD) risk redu

58 educing the intake of saturated fatty acids (SFAs) to reduce coronary artery disease (CAD).

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

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

61 stern diet, including saturated fatty acids (SFAs), omega-3 (n-3) fatty acids, and refined sugar, wit

62 % kcal) diets rich in saturated fatty acids (SFAs), omega-6 or omega-3 polyunsaturated FAs (PUFAs).

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

64 tty acids (MUFAs) and saturated fatty acids (SFAs).

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

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

67 I), firing rate, spike frequency adaptation (SFA) and the steady-state gain of firing.

68 otable degree of spike frequency adaptation (SFA).

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

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

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

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

73 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)

74 otal fat area], VFA [visceral fat area], and SFA [subcutaneous fat area], respectively).

75 en products had much higher fat contents and SFA than had whole meat.

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

77 1beta secretion from lipopolysaccharide- and SFA-primed cells in an AMPK-dependent manner.

78 ssociated with lower milk fat percentage and SFA concentrations but higher monounsaturated FA and pol

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

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

81 MUFAs and SFAs led to a significant increase in fat mass but only

82 reciprocal increases in plasma cis-MUFAs and SFAs.

83 ongitudinal trends for PUFAs, cis-MUFAs, and SFAs were weak and not significant.

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

85 rgy from foods, higher energy from total and SFAs, and lower probability of adherence to prudent and

86 y data taken with a surface force apparatus (SFA).

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

88 , assessed using a Surface Forces Apparatus (SFA), between two mica surfaces fully covered by the pol

89 The single-flap approach (SFA) consists of the elevation of a limited mucoperioste

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

91 seous defects with the single flap approach (SFA).

92 the treatment of superficial femoral artery (SFA) in-stent restenosis (ISR).

93 Parasite striated fiber assemblins (SFA) polymerize into a dynamic fiber that emerges from t

94 Baseline SFA intake was associated with baseline serum total and

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

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

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

98 We used gas chromatography to measure blood SFA and MUFA levels in prediagnostic samples from 476 in

99 949488, and rs8066956) were related to blood SFA and MUFA levels.

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

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

102 l is to assess the effectiveness of a buccal SFA used for the surgical debridement of deep intraosseo

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

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

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

106 n whether these effects are mediated by bulk SFAs and sphingolipids or by individual lipid species.

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

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

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

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

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

112 Even-chain SFAs that were measured (14:0 [myristic acid], 16:0 [pal

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

114 ecanoic acid), as were measured longer-chain SFAs (20:0 [arachidic acid], 22:0 [behenic acid], 23:0 [

115 By contrast, measured odd-chain SFAs (15:0 [pentadecanoic acid] and 17:0 [heptadecanoic

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

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

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

119 with the thickness measured by conventional SFA methods.

120 All patients underwent conventional SFA PTA and final post-dilation with paclitaxel-eluting

121 Dietary recommendations advise decreasing SFAs.

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

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

124 6 single nucleotide polymorphism and dietary SFA:carbohydrate ratio intake for the homeostasis model

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

126 fic sphingolipid metabolic route and dietary SFAs in the molecular pathogenesis of lipotoxic cardiomy

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

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

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

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

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

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

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

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

135 ratios (HRs) for associations per SD of each SFA with incident type 2 diabetes using Prentice-weighte

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

137 Serum cholesterol ester SFA and PUFA associations were supported by dietary inta

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

139 through selection can decrease saturated FA (SFA) consumption, improve human health and provide a mea

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

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

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

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

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

145 eaker [for SBP: B = 0.36, P = 0.638 (NS) for SFA; B = 0.44, P = 0.019 for MUFA; B = 1.18, P = 0.376 (

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

147 ned significant, whereas the association for SFAs was no longer significant.

148 Monounsaturated fatty acid substitution for SFAs also decreases CVD risk.

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

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

151 /100g DM), whereas the Mon-thong variety had SFA>MUFA>PUFA (5.1, 4.0, 1.1g/100g DM, respectively).

152 fat (HF(MUFA)), or a high-saturated fat (HF(SFA)) diet for 16 weeks.

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

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

155 Thus, despite the high SFA content, additive supplementation of M. oleifera lea

156 function after 1 mo of consumption of a high-SFA (HS) diet and after 24 wk after random assignment to

157 assigned to a low-fat diet, a high-fat high-SFA (HSF) diet, and the HSF diet with 3.45 g DHA/d (HSF-

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

159 Higher SFA intake was associated with worse global cognitive (p

160 INTERPRETATION: Higher SFA intake was associated with worse global cognitive an

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

162 In humans, SFA-enriched diet led to a decrease in hippocampal and c

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

164 significant decrease in cortical activity in SFA-mice whereas MUFAs even improved activity.

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

166 he effects of random and systematic error in SFA data analysis and modeling via simulations of interf

167 s report, we demonstrate that a diet high in SFA induced cardiac hypertrophy, left ventricular systol

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

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

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

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

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

173 ght individuals were overfed muffins high in SFAs (palm oil) or n-6 PUFAs (sunflower oil) for 7 weeks

174 fat mixed meals (2.6 MJ), which were high in SFAs, MUFAs, or PUFAs.

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

176 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

177 In adjusted analyses, different individual SFAs were associated with incident type 2 diabetes in op

178 ding of differences in sources of individual SFAs from dietary intake versus endogenous metabolism is

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

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

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

182 , self-reported food-allergic or intolerant (SFA) and nonfood-allergic (NFA) consumers, and explored

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

184 Low-SFA, heart-healthy dietary patterns that contain lean be

185 /- 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

186 tive change, comparing highest versus lowest SFA quintiles; the multivariate-adjusted odds ratio (OR)

187 ant saturated fatty acid (SFA) and the major SFA in the HFD used in our animal study-potently enhance

188 sein) and 63 g milk fat (with high or low MC-SFA content) daily.

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

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

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

192 cross-sectional analysis of TFAs, cis-MUFAs, SFAs, and PUFAs measured in plasma before intervention (

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

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

195 10, 39 consecutive patients underwent PTA of SFA-ISR in our institution.

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

197 highest compared with the lowest quintile of SFA intake had an RR of SCD of 1.44 (95% CI: 1.04, 1.98)

198 tinol stent has improved the patency rate of SFA after percutaneous transluminal angioplasty (PTA).

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

200 t adjunctive use of DEB for the treatment of SFA-ISR represents a potentially safe and effective ther

201 ated FAs, and the subsequent accumulation of SFAs in vascular smooth muscle cells (VSMCs), are charac

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

203 which regulate the intracellular balance of SFAs and unsaturated FAs, and the subsequent accumulatio

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

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

206 ant increase in fat mass but only feeding of SFAs was accompanied by glucose intolerance in mice.

207 n, and sleep, whereas a comparable intake of SFAs acted as a negative modulator of brain activity in

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

209 e dietary fat quality by replacing intake of SFAs with n-6 and n-3 PUFAs.

210 onal and item memory accuracy with intake of SFAs.

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

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

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

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

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

216 The replacement of SFAs with MUFAs or carbohydrates in healthy subjects doe

217 Replacement of SFAs with polyunsaturated fatty acids has been associate

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

219 Recent studies question the role of SFAs in cardiovascular disease (CVD) and have found that

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

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

222 se (CVD) and have found that substitution of SFAs in the diet with omega-6 (n-6) polyunsaturated fatt

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

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

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

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

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

228 In conclusion, overeating SFAs promotes hepatic and visceral fat storage, whereas

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

230 vely measured individual plasma phospholipid SFAs and incident type 2 diabetes in EPIC-InterAct parti

231 Different individual plasma phospholipid SFAs were associated with incident type 2 diabetes in op

232 t directly correlated with changes in plasma SFAs and inversely with PUFAs.

233 PUFA/SFA (0.61 at t=0) and omega-6/omega-3 (14.05 at t=0) wer

234 yunsaturated and saturated fatty acids (PUFA/SFA), and polyunsaturated and monounsaturated fatty acid

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

236 It also gave better PUFA/SFA and n-6/n-3 ratios.

237 these data support dietary advice to reduce SFA intake.

238 ling to SK channels accounts for the reduced SFA of Ca(v)1.3(-/-) MCCs.

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

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

241 Replacing SFAs with carbohydrates with a high glycemic index is al

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

243 Replacing SFAs with refined carbohydrate does little to alter CVD

244 Replacing SFAs with vegetable PUFAs has cardiometabolic benefits,

245 utrient composition of the diet by replacing SFAs with unsaturated fatty acids, as well as lean prote

246 We tested the effects of replacing SFAs with monounsaturated fatty acids (MUFAs) or carbohy

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

248 There is convincing evidence that replacing SFAs with unsaturated fat, both omega-6 and omega-3 poly

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

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

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

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

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

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

255 ated intake of major fatty acids (saturated [SFA], monounsaturated [MUFA], total polyunsaturated [PUF

256 Substituting SFAs with animal protein, cis monounsaturated fatty acid

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

258 hreefold larger increase in lean tissue than SFAs.

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 This suggests that SFA supplementation restored the normal BBB function.

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

263 in opposite directions, which suggests that SFAs are not homogeneous in their effects.

264 The SFA fiber provides a robust spatial and temporal organiz

265 e results of the study indicate that: 1) the SFA and DFA resulted in significant CAL gains and PD red

266 uctions at 6 months post-surgery; and 2) the SFA was similarly effective compared to the DFA in terms

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

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

269 nsulin and glucose responses (AUC) after the SFA meal were significantly higher than those after the

270 as higher after the MUFA meal than after the SFA meal.

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

272 e lower during the PUFA diet than during the SFA diet (P < 0.05).

273 s lower during the PUFA diet than during the SFA diet [between-group difference in relative change fr

274 in (P = 0.06) tended to be higher during the SFA diet.

275 Few significant differences in the SFA, MUFA and PUFA composition of breast and leg meat po

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

277 Furthermore, treatment with the SFA myristate, but not palmitate, induced hypertrophy an

278 ncreases when defects were accessed with the SFA or DFA.

279 Fourteen patients were treated according to SFA principles and 14 patients received the DFA.

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

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

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

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

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

285 When SFA is minimal (in waking or REM sleep state, high ACh)

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

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

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

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

290 ith the percentage of abdominal fat, whereas SFA (b = 0.27; P = 0.04) and PUFA (b = -0.48; P = 0.03)

291 locomotor activity in MUFA-fed mice, whereas SFA-mice were resistant.

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

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

294 Compared with SFA intake, n-6 PUFAs reduce liver fat and modestly impr

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

296 As the population with SFA stenting continues to increase, occurrence of ISR ha

297 EC increase compared to defects treated with SFA alone.

298 reatment modality, with defects treated with SFA in combination with a graft material and a bioactive

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