ライフサイエンスコーパス: postprandial

1 , there was no difference between fasting or postprandial abdominal and femoral ATBF.

2 ype 7), urgency, nocturnal diarrhea, FI, and postprandial abdominal discomfort before administration

3 to a single high-fat meal did not change the postprandial accumulation of fat in the liver (P = 0.93)

4 Postprandial accumulation of gastric secretions in the p

5 Lipasin-deficient mice exhibited elevated postprandial activity of LPL in the heart and skeletal m

6 amycin complex 1 (mTORC1) regulates numerous postprandial adaptations, we investigated the potential

7 e protein digestion and absorption kinetics, postprandial amino acid availability, anabolic signaling

8 Both a postprandial and supraphysiological insulin clamp signif

9 We found that the postprandial apoB-48 response decreased significantly af

10 The postprandial appetite response was determined for 180 mi

11 [1.7-7.5], p=0.465), and increased abdominal postprandial ATBF (3.5 [1.9-4.2] to 4.7 [2.1-9.0], p=0.2

12 GH PRO (1.5 g . kg(-1) . d(-1)) augments the postprandial availability of dietary protein-derived ami

13 d with HIGH PRO (1.5 g . d(-1)) augments the postprandial availability of dietary protein-derived ami

14 use of sodium caseinate or chitosan, on the postprandial bioavailability of interesterified-lipids i

15 or sucrose in food or beverages lowers peak postprandial blood glucose and insulin concentrations.

16 Fasting and postprandial blood glucose and plasma total GLP-1 as wel

17 omegranate (supplement) on the bread-derived postprandial blood glucose concentration in 2 randomized

18 se uptake into fat and muscle cells to lower postprandial blood glucose, an enforced change in cellul

19 The main outcomes analyzed were peak postprandial blood glucose, insulin, and triglyceride co

20 ctose resulted in significantly lowered peak postprandial blood glucose, particularly in people with

21 s 1 and 28 of each intervention, fasting and postprandial blood samples were collected before and aft

22 Peak postprandial blood triglyceride concentrations did not s

23 eeding (400%), while clamping PFH glucose at postprandial brain levels blunted the Epi response to hy

24 seline, a greater C-peptide index and 90-min postprandial C-peptide level were predictive of lower Hb

25 hylomicron-TG level but that increase in 6-h postprandial cardiac DFA partitioning nevertheless occur

26 ody or with lipasin deficiency had increased postprandial cardiac LPL activity and lower TAG levels o

27 mooth (<0.2-mm particles) wheat porridge, on postprandial changes in blood glucose, insulin, C-peptid

28 clude accelerated gastric emptying, enhanced postprandial cholecystokinin and glucagon-like peptide 1

29 west ghrelin concentrations and higher early postprandial cholecystokinin and glucagon-like peptide 1

30 LCn3s reduced postprandial chylomicron cholesterol and VLDL apolipopro

31 Postprandial chylomicron lutein responses measured after

32 that a whey protein supplement decreased the postprandial chylomicron response compared with casein i

33 uptake is higher in men driven by change in postprandial chylomicron-TG level but that increase in 6

34 ing compared with that of jejunal feeding on postprandial circulating plasma glucose and amino acid c

35 f plasma TGs in mice fed a high-fat diet, in postprandial clearance studies, and when ApoC-III-rich o

36 VLDL particle size (P = 0.04), and a reduced postprandial concentration of medium-sized VLDL particle

37 During ER, postprandial concentrations of acylated ghrelin were low

38 the 2 higher doses increased fasting and/or postprandial concentrations of non-HDL cholesterol, LDL

39 ere rectally administered during fasting and postprandial conditions (oral glucose load).

40 nents, including lipids, under nutrient-rich postprandial conditions.

41 The regulatory mechanisms underlying the postprandial control of VLDL-TAG secretion remain unclea

42 (Ptime x age = 0.008), and the shape of the postprandial curves was different between young and old

43 Despite the postprandial decrease in FFA-driven esterification and o

44 Anxiety was associated with postprandial distress syndrome at baseline (OR, 4.83; 99

45 Postprandial distress syndrome was associated with pain

46 Metabolic alterations relevant to postprandial dyslipidemia were previously identified in

47 Postprandial dysmetabolism-an exaggerated spike in trigl

48 her the addition of protein can modulate the postprandial ectopic lipid storage.

49 group, hesperidin protected individuals from postprandial ED (P = 0.050) and significantly downregula

50 At rest, postprandial EE and CHOx, as well as adipose tissue perf

51 During exercise, postprandial EE was lower after EGCG than after placebo,

52 In conclusion, exenatide augmented postprandial EF in subjects with diabetes and prevented

53 ed the effect of GLP-1R agonist exenatide on postprandial EF in type 2 diabetes and the mechanisms un

54 Subcutaneous exenatide increased postprandial EF independent of reductions in plasma gluc

55 enols, but there is little research on their postprandial effects.

56 ting in faster and higher but more transient postprandial elevation of plasma amino acids.

57 effect of high potassium and high sodium on postprandial endothelial function as assessed by using f

58 ssium and reduced sodium intakes can improve postprandial endothelial function.

59 After each intervention, fasting and postprandial energy expenditure (EE), as well as fat oxi

60 ast growth factor 19 (FGF19) is an important postprandial enterokine which regulates liver metabolism

61 hat Small Heterodimer Partner (SHP) mediates postprandial epigenetic repression of hepatic autophagy

62 tolerance in muscle and the liver, excessive postprandial excursion of plasma glucose and insulin, an

63 Fasting and postprandial fat oxidation was not significantly affecte

64 Wilcoxon signed rank test p=0.08), increased postprandial femoral ATBF (2.4 [1.6-4.0] to 6.9 [3.4-8.7

65 Baseline FMD was reduced in IR, and postprandial FMD attenuation occurred after each meal, p

66 on of hesperidin 2S did not improve basal or postprandial FMD in our total study population.

67 No significant change in fasting or postprandial FMD was observed after 6 wk of hesperidin i

68 l suppresses feelings of hunger and augments postprandial fullness sensations more so than an otherwi

69 given gastric content volume, self-reported postprandial fullness was greater in AN than in HC or OB

70 n AN tended to become shorter (p = 0.09) and postprandial fullness was less marked (p < 0.01).

71 and symptom scores (nausea, abdominal pain, postprandial fullness, and bloating) on a 0-10 scale.

72 abdominal symptoms, including discomfort or postprandial fullness.

73 with solid fat (LE3), different dynamics of postprandial gallbladder volume were induced (P </= 0.00

74 emptying of solids and liquids, fasting and postprandial gastric volume, satiation by nutrient drink

75 tolerated volume), satiety, and fasting and postprandial gastric volumes at 16 weeks.

76 volume to fullness, satiety, or fasting and postprandial gastric volumes at week 16.

77 This work assessed postprandial gastrointestinal function and concurrent se

78 were similar (P = 0.58) for both groups, but postprandial GLP-1 and PYY responses were significantly

79 in resulted in a significant increase in the postprandial GLP-1 response compared with whey (P = 0.00

80 Postprandial glucagon-like peptide 17-36 (P = 0.784) and

81 ; DBs: -0.057 +/- 0.042, P < 0.001), and 2-h postprandial glucose (mean +/- SD: water: -1.02 +/- 0.25

82 - 0.32, LF = -0.42 +/- 0.20; P = 0.002), 2-h postprandial glucose (PY = -0.61 +/- 0.24 mmol/L, LF = -

83 glucose, fructose ingestion results in lower postprandial glucose and higher lactate and triglyceride

84 erated GLP-1 response after RYGB, changes in postprandial glucose and insulin responses did not signi

85 I meal produced an approximately 60% greater postprandial glucose area under the curve (AUC) than did

86 igher fiber intake was associated with lower postprandial glucose at breakfast, and the intake of sol

87 lasma glucose at week 2 and week 28, and 2 h postprandial glucose at week 28; the proportion of patie

88 (12-h behavioral cycle inversion) increased postprandial glucose by 6%.

89 We showed that 1) both interventions reduce postprandial glucose concentration, 2) acute interruptio

90 Co-cultures maintained postprandial glucose concentrations in the circulation w

91 ts in a substantial reduction of fasting and postprandial glucose concentrations.

92 y by decreased insulin sensitivity (elevated postprandial glucose despite 14% higher late-phase insul

93 Genetic activation of this pathway improved postprandial glucose disposal in mice, whereas its muscl

94 Skeletal muscle is a major site of postprandial glucose disposal.

95 Finally, combination treatment blunted postprandial glucose excursions and improved HbA1c level

96 ced serum cholesterol and the attenuation of postprandial glucose excursions.

97 ith restored preprandial lipid oxidation and postprandial glucose flux in ZDF rats.

98 The only difference between meals was higher postprandial glucose following sunflower oil compared wi

99 tance and could be an important regulator of postprandial glucose homeostasis and 2) the insulin-dese

100 anner, leading to improvement of fasting and postprandial glucose homeostasis.

101 ablation impaired insulin action and led to postprandial glucose intolerance.

102 sts are empirically evaluated against actual postprandial glucose measurements captured by individual

103 ute to a mechanistic explanation of improved postprandial glucose metabolism with regular interruptio

104 ssion is associated with full restoration of postprandial glucose profile and/or the potentially nonr

105 e observed in blood pressure, heart rate, or postprandial glucose response.

106 First, postprandial glucose was 17% higher (i.e., lower glucose

107 Postprandial glucose, insulin, and inflammatory response

108 se replacement of glucose or sucrose on peak postprandial glucose, insulin, and triglyceride concentr

109 ith greater reductions in fasting plasma and postprandial glucose, more patients with an HbA1c less t

110 has an equally beneficial effect on lowering postprandial glucose.The aim of our study was to compare

111 randomized controlled trials measuring peak postprandial glycemia after isoenergetic replacement of

112 Postprandial glycemia and insulinemia were measured in c

113 t acute activation of intestinal ECS reduced postprandial glycemia independently on intestinal glucos

114 ely by the carbohydrate content, even though postprandial glycemia is vastly influenced by glycemic i

115 peptide 1 receptor agonist exenatide reduces postprandial glycemia, partly by slowing gastric emptyin

116 l mechanism by which exenatide can attenuate postprandial glycemia.

117 accessibility of starch has implications for postprandial glycemia.

118 of this study was to review the evidence for postprandial glycemic and insulinemic responses after is

119 ight-loss-independent therapeutic effects on postprandial glycemic control.

120 tial impact of prior meal composition on the postprandial glycemic response and glycemic index (GI) a

121 rage but not in a supplement, can reduce the postprandial glycemic response of bread, whereas microbi

122 cterize changes in body weight, satiety, and postprandial gut hormone profiles following esophagectom

123 of the gastrointestinal lining, increases in postprandial gut hormone secretions, glycemic control, p

124 lactate concentrations were monitored over 7 postprandial h.

125 obese, nondiabetic humans exhibit augmented postprandial hepatic energy metabolism, whereas elderly

126 important for minute-to-minute regulation of postprandial hepatic glucose production, although condit

127 roach might bring new opportunities to study postprandial hepatic lipid dynamics.

128 Fasting and postprandial (HFMM) lipid metabolism was assessed by usi

129 The postprandial homeostasis model assessment index (+54%) a

130 ere below basal concentrations in the fourth postprandial hour.

131 termined under basal conditions and during 4 postprandial hours by intravenous infusions of [3,3,3-(2

132 Fasting and postprandial hunger, satiation, hormone concentrations,

133 or retinopathy, or prevalent fasting versus postprandial hyperglycaemia, could also be considered in

134 phasic analogues can target both fasting and postprandial hyperglycaemia, with the added advantage of

135 liberation from starches and alleviation of postprandial hyperglycaemia.

136 Diet-induced postprandial hyperglycemia and fasting hyperinsulinemia

137 ses likely leads to the early development of postprandial hyperglycemia in CF.

138 patic gluconeogenesis, promoting fasting and postprandial hyperglycemia through increased fatty acid

139 ly permits a transient and optimal degree of postprandial hyperglycemia to efficiently enhance insuli

140 emia and glycemia after correcting excessive postprandial hyperglycemia using treatment with a sodium

141 s functional food ingredients for regulating postprandial hyperglycemia.

142 pring normalizes body temperature and causes postprandial hyperglycemia.

143 ts on glucose absorption, in order to manage postprandial hyperglycemia.

144 During a postprandial hyperglycemic-hyperinsulinemic clamp after

145 algorithm may be a useful tool for reducing postprandial hyperinsulinemia in T2DM, thereby potential

146 Postprandial hyperinsulinemic hypoglycemia (PHH) is ofte

147 ptive (hypoinsulinemic-euglycemic clamp) and postprandial (hyperinsulinemic hyperaminoacidemic-euglyc

148 However, the postprandial hyperleucinemia was transient, and concentr

149 s, accumulation of remnant lipoproteins, and postprandial hyperlipidemia.

150 Group A (four patients with fasting and/or postprandial hypoglycemic episodes) showed qualitatively

151 pain (P = .054), reflecting a steeper early postprandial increase in symptoms among subjects with hi

152 hepatic gammaATP concentrations, the maximum postprandial increase of gammaATP was 6-fold higher in O

153 l phenolics improved vascular function, with postprandial increases in FMD from baseline of 1.4% at 2

154 ic beta cells secrete insulin in response to postprandial increases in glucose levels to prevent hype

155 n amplitude of glycemic excursion (MAGE) and postprandial incremental area under the curve (AUCpp).

156 ith higher peak concentrations and a greater postprandial incremental AUC for GLP-1 and cholecystokin

157 n of energy balance, glucose metabolism, and postprandial inflammatory responses.In a randomized cont

158 te after feeding, which effectively sustains postprandial inhibition of autophagy.

159 LOWCAL diet led to reductions in weight and postprandial insulin area under the curve.

160 Postprandial insulin clamps increased ISF and plasma Abe

161 In contrast, higher postprandial insulin concentrations and increased fat ox

162 However, the first postprandial insulin peak (after breakfast) and the iAUC

163 rom the saline condition in both groups, but postprandial insulin release was markedly attenuated aft

164 effect, accounts for as much as half of the postprandial insulin response and is exploited therapeut

165 Compared with the high-FII diet, mean postprandial insulin response over 8 h was 53% lower wit

166 The reduction in postprandial insulin secretion by Ex-9 was greater in th

167 d in ZDF rats during fasting and near-normal postprandial insulinemia and glycemia after correcting e

168 Postprandial levels of BCAAs and methionine were signifi

169 ide tyrosine tyrosine (P = .003), and higher postprandial levels of glucagon-like peptide 1 (P < .001

170 for solids and P = .011 for liquids), lower postprandial levels of peptide tyrosine tyrosine (P = .0

171 Lower postprandial LGD in obese subjects and blunting of MPS r

172 Abdominal obesity and exaggerated postprandial lipemia are independent risk factors for ca

173 matrix modulates the impact of dairy fat on postprandial lipemia in healthy subjects.

174 nowledge, the impact of the cheese matrix on postprandial lipemia in humans has not yet been evaluate

175 upport a role of TM6SF2 in the regulation of postprandial lipemia, potentially through a similar func

176 g that these agents also improve fasting and postprandial lipemia, the latter more significantly than

177 raction between milk protein and milk fat on postprandial lipemia.

178 e energy content and an attenuated impact on postprandial lipemia.

179 FXR also regulates postprandial lipid and glucose metabolism.

180 ain saturated fatty acids (MC-SFAs) improved postprandial lipid metabolism in humans with abdominal o

181 he bioavailability of plasma carotenoids and postprandial lipid response.

182 ietary protein source determines fasting and postprandial lipids in healthy individuals in a manner t

183 afood and nonseafood to modulate fasting and postprandial lipids in healthy subjects.

184 he meat protein absorption rate and estimate postprandial meat protein utilization in elderly subject

185 did not alter vascular function or attenuate postprandial metabolic derangements in triglycerides, gl

186 GF19) is an intestinal hormone that mediates postprandial metabolic responses in the liver.

187 ferent degrees of starch bioaccessibility on postprandial metabolism (e.g., glycemia) and to gain ins

188 Postprandial metabolism was assessed over 6 h, and glyco

189 rate of starch amylolysis and, consequently, postprandial metabolism.

190 e novel insights regarding the regulation of postprandial metabolism.

191 l muscle protein synthesis rates or increase postprandial muscle protein synthesis rates after ingest

192 l muscle protein synthesis rates or increase postprandial muscle protein synthesis rates after ingest

193 LOW PRO compared with HIGH PRO on basal and postprandial muscle protein synthesis rates after the in

194 LOW PRO compared with HIGH PRO on basal and postprandial muscle protein synthesis rates after the in

195 RO) or high protein intake (HIGH PRO) on the postprandial muscle protein synthetic response.

196 These data indicate that impaired postprandial myofibrillar protein synthetic response may

197 Fructose consumption in FRU increased postprandial net carbohydrate oxidation and decreased ne

198 ding or insulin-stimulated conditions (lower postprandial or clamp RQ).

199 idised lipids in a single meal may influence postprandial oxidative stress and inflammation.

200 ies) could be largely restricted to fighting postprandial oxidative stress in the gastric compartment

201 in docosahexaenoic acid (DHA-OR) on lipidic postprandial oxidative stress in Wistar rats.

202 Postprandial oxidised-LDL concentrations decreased with

203 scuits, it is highly bioavailable and lowers postprandial oxidised-LDL levels.

204 hildren with both preprandial (P = .039) and postprandial (P = .008) status than those in adults.

205 ference by diets: 0.31 mmol/L; P = 0.03) and postprandial (P = 0.01) serum triacylglycerol concentrat

206 oxytyrosol sulphate, a metabolite of OOPC 2h postprandial (P=0.05).

207 ation of symptoms including epigastric pain, postprandial pain, nausea, vomiting, and weight loss.

208 L concentrations were not altered during the postprandial period (P = 0.74).

209 d SNAT2 protein content increased during the postprandial period in all groups (time effect, P < 0.05

210 Blood samples were collected during the 12-h postprandial period to assess the rise in plasma glucose

211 nous phenylalanine availability over the 5-h postprandial period was greater after LOW PRO than after

212 sma availability of leucine over the 300-min postprandial period was similar (P= 0.75) between the in

213 l chymes were kinetically collected over the postprandial period.

214 modulate sugar metabolism much later in the postprandial period.

215 er, clamp conditions do not adequately mimic postprandial physiological responses.

216 g of how these systems collectively regulate postprandial physiology will further facilitate the deve

217 ding in healthy young men results in similar postprandial plasma amino acid and glucose concentration

218 ns; many of these functions are sensitive to postprandial plasma and intracellular amino acid concent

219 Fasting and postprandial plasma glucagon-like peptide 1 (GLP-1), pep

220 It decreased fasting and postprandial plasma glucose (-5%, P < 0.01, and -8%, P <

221 Primary outcomes were postprandial plasma glucose and insulin (0-180 min).

222 foods or supplements after a common meal on postprandial plasma glucose and plasma insulin in patien

223 ht loss caused a similar decrease in the 6-h postprandial plasma glucose area under the curve in both

224 nt interruptions to prolonged sitting reduce postprandial plasma glucose.

225 Postprandial plasma inflammatory markers tended to remai

226 and on other disease risk markers, including postprandial plasma insulin, glucose, and oxidative stre

227 ood (13)C glucose, VLDL-(13)C palmitate, and postprandial plasma lactate concentrations was not signi

228 ll three SCFA mixtures increased fasting and postprandial plasma peptide YY (PYY) concentrations, and

229 entrations were similar to those observed on postprandial plasma triglyceride concentrations.

230 low-density lipoproteins triglycerides or on postprandial plasma triglycerides or apoB48 concentratio

231 ing fatty acids (FA) during fasting supports postprandial (PP) insulin secretion that is critical for

232 protein digestion, which is known to affect postprandial protein metabolism in the elderly.The prese

233 tein within its natural whole-food matrix on postprandial protein metabolism remains understudied in

234 eat cooking conditions have little effect on postprandial protein utilization in young adults, the pr

235 OOPC=961 mg/kg) or VOO (OOPC=289 mg/kg) in a postprandial randomised, double blind, crossover trial.

236 uced fasting (P-time x treatment = 0.03) and postprandial respiratory quotient (P-time x treatment =

237 cheese, soft cream cheese, and butter on the postprandial response at 4 h and on the incremental area

238 il supplemented with DHA inhibited vitamin D postprandial response in rats (-25%, p<0.05).

239 rt rate variability (HRV)) on hunger and the postprandial response to GL.

240 nondiabetic and T2DM subjects, mimicking the postprandial response.

241 conducted to determine any contributions to postprandial responses caused by acidic beverages.As pri

242 other polyphenol-rich interventions improve postprandial responses, and future studies should take i

243 No differences were observed in the postprandial rise in circulating plasma amino acid and g

244 The postprandial rise in plasma cholecystokinin, peptide YY

245 thesize and secrete insulin in proportion to postprandial rises in blood glucose.

246 A fasting first-void urine sample and postprandial samples (2, 4, 6 h) were collected after SS

247 kfast (0 h) and at 24, 48, and 72 h and from postprandial samples collected at 4, 5, 6, 7, 9, 12, and

248 ES demonstrated an exaggerated postprandial satiety gut hormone response that was atten

249 gectomy, patients demonstrate an exaggerated postprandial satiety gut hormone response, which may med

250 aintenance of feeding from pellet-to-pellet; postprandial satiety was unaffected.

251 Postprandial secretion volume (SV), formation of a secre

252 Moreover, studies relating continuous postprandial sensations of satiation to measurable patho

253 olesterol in the fasted serum (P = 0.03) and postprandial serum (P = 0.01) that was observed after th

254 e-bread challenge attenuated the rise in the postprandial serum glucose response (P < 0.0001) and res

255 Program cohort exhibited significantly lower postprandial serum triglycerides, suggestive of a role f

256 However, little is known about how postprandial sleep is regulated.

257 Postprandial sleep was positively correlated with ingest

258 l to Lkr neurons that rhythmically increased postprandial sleep when silenced, suggesting that these

259 whereas Lk downregulation by RNAi increased postprandial sleep, suggestive of an inhibitory connecti

260 these findings reveal the dynamic nature of postprandial sleep.

261 ancreatic beta cells and is required for the postprandial spike in insulin secretion.

262 fibrillar protein synthesis during the early postprandial stage after milk ingestion.

263 41 probes were observed to be altered in the postprandial state (5% FDR).

264 05% compared with 0.057% +/- 0.005%/h in the postprandial state after LOW PRO compared with HIGH PRO,

265 05% compared with 0.057% +/- 0.005%/h in the postprandial state after LOW PRO compared with HIGH PRO,

266 assium in the presence of high sodium in the postprandial state is not known.

267 ction in key gluconeogenic substrates in the postprandial state may contribute to increased susceptib

268 scription factor activated by insulin in the postprandial state.

269 al depot, an effect further augmented in the postprandial state.

270 rculating hormones secreted in the basal and postprandial state.

271 ion (HGP) and allowing the transition to the postprandial state.

272 Delta)(hep) mice relative to controls in the postprandial state.

273 ositional difference between preprandial and postprandial states, demonstrating the utility of such a

274 and net liver fat content in the fasted and postprandial states, we used stable-isotope tracer metho

275 acerbating the hyperlipidemia of fasting and postprandial states.

276 in children and young adults in fasting and postprandial states.

277 biscuits (C-B), and the effects on oxidative postprandial status.

278 lial cells (EC) from large vessels process a postprandial surge of FA.

279 rritable bowel syndrome (IBS) have increased postprandial symptom responses and more psychosocial mor

280 relationship between psychosocial status and postprandial symptom responses in patients with IBS is u

281 s are associated specifically with increased postprandial symptoms.

282 ent VLDL-TAG secretion, leading to increased postprandial TAG secretion.

283 h the use of (15)N enrichment of amino acids.Postprandial time course observations showed a lower con

284 easured changes from baseline in fasting and postprandial triacylglycerol, apolipoprotein B-48 (apoB-

285 We found no difference in postprandial triacylglycerol, FFA, insulin, glucose, glu

286 oprotein risk factors for CVD and uric acid: postprandial triglyceride (0%: 0 +/- 4; 10%: 22 +/- 8; 1

287 ow glycemic index, has been shown to elevate postprandial triglyceride compared with glucose.

288 aining beverages increased concentrations of postprandial triglyceride, and the 2 higher doses increa

289 Mechanisms of postprandial triglyceridemia and SR-B1 regulation were s

290 Reducing postprandial triglyceridemia may be a promising strategy

291 In 10 participants, postprandial triglycerides and apoB48 levels were measur

292 e small intestine, both 1 and 9 can suppress postprandial triglycerides during acute oral lipid chall

293 al investigation and successfully suppressed postprandial triglycerides during an acute meal challeng

294 In APOE4s a greater LDLR binding affinity of postprandial TRL after SFA, and lower LDL binding and he

295 tide 1 (GLP-1) reduces hyperglucagonemia and postprandial TRL, the latter in part through a decreased

296 Fasting and postprandial urine samples were analyzed using (1)H nucl

297 ries) to a high-fat (50 g total fat) meal on postprandial vascular function, as well as triglyceride,

298 ne cleavage and its relative contribution to postprandial vitamin A in humans after consumption of ra

299 ribution of newly absorbed alpha-carotene to postprandial vitamin A should not be estimated but shoul

300 This was associated with decreased postprandial whole-body protein synthesis with RM than w