ライフサイエンスコーパス: postprandial

1 ies was used to determine postabsorptive and postprandial (20 g milk protein) MyoPS and MitoPS, fiber

2 Postprandial activation of leukocyte-endothelium interac

3 ory effects of the parasympathetic branch in postprandial adaptation.

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

5 ity-risk A-allele (AAs) would exhibit higher postprandial AG and energy intake than individuals homoz

6 Furthermore, higher fasting and postprandial amino acid removal were observed after habi

7 nterestingly, cholestyramine feeding reduced postprandial Areg up-regulation in both tissues.

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

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

10 Crohn's disease (CD) patients suffer postprandial aversive symptoms, which can lead to anorex

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

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

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

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

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

16 Peak postprandial blood triglyceride concentrations did not s

17 ributions of endogenous GIP and GLP-1 to the postprandial changes in glucose and glucoregulatory horm

18 Postprandial changes in hepatic lipids were measured [De

19 Black women had smaller postprandial changes in large (P=0.005) and medium TRLPs

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

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

22 During ER, postprandial concentrations of acylated ghrelin were low

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

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

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

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

27 hanges in serum and urine metabolomes during postprandial dairy product tests through the association

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

29 ugs affecting gastric accommodation to treat postprandial distress and nausea.

30 Postprandial distress syndrome was associated with pain

31 between lactase persistence genotype and the postprandial dynamics of lactose-derived metabolites.

32 Postprandial dysmetabolism-an exaggerated spike in trigl

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

34 Randomized controlled trials comparing acute postprandial effects on PPG and/or PPI after exposure to

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

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

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

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

39 recapitulated in vivo under hypoglycemic and postprandial (fed) conditions.

40 Postprandial FGF19 and SHP inhibit SREBF2, which leads t

41 Postprandial fibroblast growth factor 19 (human FGF19, m

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

43 Postprandial FSRs trended to be greater in MYCO compared

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

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

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

47 act and includes epigastric pain or burning, postprandial fullness, or early satiety.

48 Postprandial galactitol and galactonate after lactose ov

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

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

51 This work assessed postprandial gastrointestinal function and concurrent se

52 Basal and postprandial GLP-1 and postprandial PYY (all P < 0.05) w

53 Fasting ghrelin levels decreased, whereas postprandial GLP-1 and PYY increased after sleeve gastre

54 decreased only in males (P < 0.001), whereas postprandial GLP-1 was increased only in females (P < 0.

55 and post-procedure hormones fasting ghrelin, postprandial GLP-1, postprandial PYY, and fasting GIP le

56 ics of the dual-hormone therapy and enhances postprandial glucagon suppression in diabetic pigs.

57 a weight loss of 14.6% +/- 2.6% and elevated postprandial glucagon-like peptide 1 compared with contr

58 551) influence the effect of caffeine on the postprandial glucose (GLU) response to a carbohydrate me

59 examining the acute effect of LES intake on postprandial glucose (PPG) and postprandial insulin (PPI

60 - 0.32, LF = -0.42 +/- 0.20; P = 0.002), 2-h postprandial glucose (PY = -0.61 +/- 0.24 mmol/L, LF = -

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

62 Postprandial glucose and insulin responses as well as gl

63 Postprandial glucose and protein absorption and gastro-e

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

65 nclusion, CHADN has the potential to enhance postprandial glucose clearance in states of diet-induced

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

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

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

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

70 High postprandial glucose excursions may increase risk for di

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

72 -phase insulin secretion is a determinant of postprandial glucose homeostasis.

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

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

75 al role of immune cells in the regulation of postprandial glucose metabolism has not been fully eluci

76 a neutral effect on metabolic flexibility or postprandial glucose metabolism in middle-aged overweigh

77 as a class of lipid messengers that improve postprandial glucose regulation and may have potential a

78 1, but the hormones contribute additively to postprandial glucose regulation in healthy individuals.

79 inuous glucose monitoring was used to assess postprandial glucose responses over 24 h, and visual ana

80 postprandially and contribute importantly to postprandial glucose tolerance.

81 that OBG viscosity determines its effect on postprandial glucose, insulin, and gastric emptying.

82 Postprandial glucose, insulin, and inflammatory response

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

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

85 suggest that caffeine-induced impairments in postprandial glycaemia are related to 1976T > C and -163

86 eful dietary supplements capable of blunting postprandial glycaemia in humans, including those with o

87 (3.6%) for postprandial lipemia, but not for postprandial glycemia (6.0% and 15.4%, respectively); ge

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

89 that polyphenol-rich purple potatoes lowered postprandial glycemia and insulinemia compared to yellow

90 These results indicate that PPE alleviates postprandial glycemia and insulinemia, and affects postp

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

92 l mechanism by which exenatide can attenuate postprandial glycemia.

93 environment to feeding is a key regulator of postprandial glycemia.

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

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

96 explored whether meal rankings according to postprandial glycemic excursions differ between 2 simult

97 ult in concordant meal rankings according to postprandial glycemic excursions.

98 , has no acute effects on the mean change in postprandial glycemic or insulinemic responses compared

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

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

101 ficacy of a predictive model of personalized postprandial glycemic response to foods that was develop

102 often seek to personalize diets to minimize postprandial glycemic responses as measured by continuou

103 Ectopic lipid deposition and postprandial glycogen storage in the liver and skeletal

104 emodeling of oscillatory gene expression and postprandial GR binding results from a concomitant incre

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

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

107 lactate concentrations were monitored over 7 postprandial h.

108 ose metabolism was evaluated, by determining postprandial hepatic and intra-myocellular lipid and gly

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

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

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

112 nally, we argue that glucagon is a bona fide postprandial hormone that evolved to concurrently and sy

113 mportance of the autonomic nervous system in postprandial human metabolism.

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

115 liberation from starches and alleviation of postprandial hyperglycaemia.

116 As such, overall postprandial hyperglycemia (24-h incremental area under

117 The LCBF significantly reduced postprandial hyperglycemia after breakfast (P < 0.01) an

118 Diet-induced postprandial hyperglycemia and fasting hyperinsulinemia

119 o be sufficient to lower overall exposure to postprandial hyperglycemia and improve glycemic variabil

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

121 tivity can offer facile routes to ameliorate postprandial hyperglycemia in diabetes via control of st

122 hyperglycemic activity against sugar-induced postprandial hyperglycemia in rats plausibly due to the

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

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

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

126 easible strategy to reduce daily exposure to postprandial hyperglycemia.

127 s functional food ingredients for regulating postprandial hyperglycemia.

128 pring normalizes body temperature and causes postprandial hyperglycemia.

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

130 rus-mediated expression of IL-10 ameliorates postprandial hyperglycemia.

131 breakfast meal often results in the largest postprandial hyperglycemic excursion in people with type

132 During a postprandial hyperglycemic-hyperinsulinemic clamp after

133 l-selective D2R knockout mice exhibit marked postprandial hyperinsulinemia in vivo.

134 Postprandial hyperinsulinemic hypoglycemia (PHH) is ofte

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

136 nistic role in order to decrease the risk of postprandial hypoglycaemia in this specific cohort.

137 bypass (RYGB) operation with a high risk of postprandial hypoglycaemia.

138 history of RYGB operation and a high risk of postprandial hypoglycaemic events have lower levels of b

139 nant women with RYGB and exaggerated risk of postprandial hypoglycaemic events, basal and dynamic bet

140 6 kg/m2; 6 +/- 3 y post-RYGB) with recurrent postprandial hypoglycemia documented by plasma glucose (

141 Postprandial hypoglycemia is a risk after Roux-en-Y gast

142 reased glucose variability and lower risk of postprandial hypoglycemia.

143 ethod, which allows continuous collection of postprandial ileal digesta.

144 The postprandial increase following the ingestion of 6 g BCA

145 The meal challenge induced a significant postprandial increase in aversive symptom scores (fullne

146 Recent studies have suggested that postprandial increases in insulin directly contribute to

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

148 andial glycemia and insulinemia, and affects postprandial inflammation.

149 emonstrate that inhibition of this transient postprandial inflammatory response fails to correct meta

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

151 on can stimulate glucose Rd and EGP, 2) that postprandial inhibition of adipose lipolysis does not su

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

153 LES intake on postprandial glucose (PPG) and postprandial insulin (PPI) responses, in order to compre

154 Postprandial insulin clamps increased ISF and plasma Abe

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

156 e traffic to the cell surface in response to postprandial insulin for blood glucose clearance.

157 rt-term dietary reduction of BCAAs decreases postprandial insulin secretion and improves white adipos

158 Basal and postprandial insulin secretion rates were >50% greater i

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

160 -step hyperinsulinemic euglycemic clamp, and postprandial interorgan crosstalk of lipid and glucose m

161 Fasting and postprandial large, medium, and small TRLPs, but not ver

162 Failure to stimulate postprandial LCN2 in individuals with obesity may contri

163 Postprandial LCN2 serum levels correlate inversely with

164 Postprandial levels of BCAAs and methionine were signifi

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

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

167 nce) than did meal macronutrients (3.6%) for postprandial lipemia, but not for postprandial glycemia

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

169 FXR also regulates postprandial lipid and glucose metabolism.

170 adipocytes and was associated with increased postprandial lipoprotein lipase activity in adipose tiss

171 n D1 gene ablation caused markedly increased postprandial liver glycogen levels (in a HNF4alpha-depen

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

173 Postprandial mesenteric vascular dysfunction is associat

174 Thereby, we could compare fasted and postprandial metabolic consequences of RYGB and VLCD in

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

176 Kingdom to the PREDICT 1 study and assessed postprandial metabolic responses in a clinical setting a

177 Postprandial metabolism was assessed over 6 h, and glyco

178 IMB than in CTL (-14% +/- 5%; P < 0.01) and postprandial MitoPS rates significantly declined in resp

179 They underwent baseline and postprandial MRI scans, symptom questionnaires, and bloo

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

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

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

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

184 branched-chain ketoacid (BCKA) ingestion on postprandial muscle protein synthesis rates.

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

186 Basal and postprandial myofibrillar protein synthesis rates were a

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

188 In response to 20 g milk protein, postprandial MyoPS rates were significantly lower in IMB

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

190 receptors previously found to play roles in postprandial nutrient detection.

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

192 Postprandial oxidised-LDL concentrations decreased with

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

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

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

196 CR induces pronounced postprandial peaks in hepatic adropin expression.

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

198 e and protein ingestion, and following a 4-h postprandial period to assess mixed muscle fractional pr

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

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

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

202 Sampling throughout a 6 h postprandial period, and at different locations in the s

203 and plasma samples were collected over a 9-h postprandial period.

204 modulate sugar metabolism much later in the postprandial period.

205 l chymes were kinetically collected over the postprandial period.

206 y but gave rise to a paradoxical increase in postprandial PG excursion, which was annulled by empagli

207 Empagliflozin reduced postprandial PG through increased urinary glucose excret

208 lar protein synthesis rates during the early postprandial phase (0-2 h) in vivo in healthy older male

209 llar protein synthesis rates during the late postprandial phase (2-5 h) remained elevated in the MILK

210 tract and may explain, at least partly, the postprandial physiological effects of the breads identif

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

212 Fasting and postprandial plasma concentrations of glucose and insuli

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

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

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

216 In conclusion, endogenous GIP affects postprandial plasma glucose excursions and insulin secre

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

218 stion by pigs resulted in a concentration of postprandial plasma leucine between 2 h and 5 h30 twice

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

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

221 SAT microcirculations respond differently to postprandial processing of dietary fat.

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

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

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

225 Basal and postprandial GLP-1 and postprandial PYY (all P < 0.05) were significantly diffe

226 No significant changes in postprandial PYY were observed over time for either sex.

227 ormones fasting ghrelin, postprandial GLP-1, postprandial PYY, and fasting GIP levels were included.

228 otal expression of NCC, NKCC2, or NKA in the postprandial rats.

229 Postprandial repression of Cyp7a1 was impaired in Areg(-

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

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

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

233 regression analyses on the residuals of the postprandial response of 149 nuclear magnetic resonance-

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

235 In vivo, the vitamin K postprandial response was higher in male Abcb1(-/-) mice

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

237 coefficient of variation (s.d./mean, %)) in postprandial responses of blood triglyceride (103%), glu

238 Postprandial responses to ad libitum meals were highly v

239 lso tested whether inhibition of endothelial postprandial responses to high-fat meals (HFMs) preserve

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

241 There were 2 distinct postprandial responses, classified as high and low metab

242 g BCKA, and 30 g milk protein (MILK) on the postprandial rise in circulating amino acid concentratio

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

244 0.004%.h-1, respectively; P = 0.093) and the postprandial rise in FSRs was greater in MYCO compared w

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

246 Attenuation of the exaggerated postprandial satiety gut hormone response is associated

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

248 and this cohort demonstrates an exaggerated postprandial satiety gut hormone response.

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

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

251 We characterized the 6-h postprandial serum kinetics and urinary excretion of lac

252 GWAS of fasting TG and postprandial serum TG at 150 minutes resulted in complet

253 GWAS of fasting and postprandial serum TG at 150 minutes were performed.

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

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

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

257 these findings reveal the dynamic nature of postprandial sleep.

258 Postprandial small-bowel water content showed a signific

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

260 To test this, we used fasted or 4 hour postprandial Sprague Dawley rats to analyze ENaC express

261 henotype is defined by hyperglycaemia in the postprandial state (impaired glucose tolerance) and/or f

262 05% compared with 0.057% +/- 0.005%/h in the postprandial state after LOW PRO compared with HIGH PRO,

263 05% compared with 0.057% +/- 0.005%/h in the postprandial state after LOW PRO compared with HIGH PRO,

264 Interventions were performed in the postprandial state and included: (i) prolonged uninterru

265 hm-transformed insulin concentrations of the postprandial state at 30 min after a meal challenge and

266 ical activity when fed ad libitum and in the postprandial state but not during the unfed period.

267 nditions (e.g., uncontrolled diabetes or the postprandial state), the in situ-generated insulin analo

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

269 scription factor activated by insulin in the postprandial state.

270 ose and decreased with fasting, RYGB, and in postprandial states following VSG.

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

272 te cohorts were studied in the fasted or 1-h postprandial states.

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

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

275 We hypothesized that blunted postprandial superior mesenteric blood flow responses wo

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

277 Blunted postprandial sympathetic regulation of gut blood flow ha

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

279 ch reconstruction on perioperative outcomes, postprandial symptoms, nutritional and anthropometric pa

280 s are associated specifically with increased postprandial symptoms.

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

282 To identify genetic variation of postprandial TG independent of fasting TG, we calculated

283 a variant near LIPC as a main contributor to postprandial TG metabolism independent of fasting TG con

284 We aimed to elucidate the genetics of the postprandial TG response through genome-wide association

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

286 from subjects' plasma at fasting and 3.5 hrs postprandial to a test meal high in saturated fat.

287 ross-sectional study, to compare fasting and postprandial triglyceride-rich lipoprotein particle (TRL

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

289 Reducing postprandial triglyceridemia may be a promising strategy

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

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

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

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

294 paradoxical association of lower fasting and postprandial TRLP subfractions despite insulin resistanc

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

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

297 of the vascular endothelium that instigates postprandial VAT inflammation.

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