ライフサイエンスコーパス: IUGR

1 IUGR affects most organ systems by either interrupting d

2 IUGR altered the developmental pattern of H3K4me3 and K9

3 IUGR cases included 23 foetuses with clinical severity s

4 IUGR changes cytosine methylation at approximately 1,400

5 IUGR establishes risk for developing diabetes.

6 IUGR FcCM had a reduced ability to stimulate endothelial

7 IUGR FcCM was found to have reduced levels of the pro-an

8 IUGR infants were more likely to be older at worst stage

9 IUGR infants were more likely to have a worse stage of R

10 IUGR is a common complication of human pregnancy that li

11 IUGR is a strong predictor of reduced short-term neonata

12 IUGR is accompanied by changes in the quantity and activ

13 IUGR is associated with vascular remodeling of the stem

14 IUGR livers, however, had increased basal FOXO1 phosphor

15 IUGR myoblasts also replicated less (P < 0.05) than cont

16 IUGR programming in baboons produces myocardial remodell

17 IUGR semitendinosus muscles had similar percentages of p

18 IUGR was induced through a well-characterized model of b

19 healthy term infants, their mothers, and 10 IUGR infants and their mothers.

20 llous cytotrophoblasts from control (n = 3), IUGR (n = 3), PE (n = 3), PE/IUGR (n = 3) and HELLP/IUGR

21 Among 7 IUGR cases, we identified 2 primary and 3 recurrent HCMV

22 in 0 of 6 sham-chow, 5 of 8 sham-HF, 4 of 8 IUGR-chow, and 8 of 9 IUGR-HF rats (chi-square, P = 0.00

23 5 of 8 sham-HF, 4 of 8 IUGR-chow, and 8 of 9 IUGR-HF rats (chi-square, P = 0.007).

24 nutrient supplementation (ENS) may abrogate IUGR-conferred multigenerational MetS.

25 ility, and blood flow pattern in young adult IUGR baboons, which may contribute to cardiac stress.

26 he suspicion of pulmonary hypertension after IUGR.

27 rated two-phased perinatal programming after IUGR.

28 le there was no significant difference among IUGR groups.

29 he IGF-1 P2 transcriptional start site among IUGR lineage F2 offspring was reversed in ENS (P < 0.04)

30 ly life functional decline with ageing in an IUGR non-human primate model.

31 dlimb muscle of control (CON, n = 11-12) and IUGR (n = 12) late gestation fetal sheep.

32 le, late gestation control (CON) (n = 8) and IUGR (n = 13) fetal sheep were catheterized with aortic

33 and forkhead box class O (FOXO)1 in CON and IUGR fetal livers.

34 ipheral glucose utilization rates in CON and IUGR fetuses.

35 isolated pancreatic islets from control and IUGR (induced by bilateral uterine artery ligation at da

36 colemmal membranes isolated from control and IUGR hindlimb skeletal muscle.

37 ceptor was not different between control and IUGR islets, but VEGFA was lower and the high-affinity V

38 gnalling activity was similar in control and IUGR muscle.

39 ystem L activity were similar in control and IUGR sarcolemma, although ex vivo Na(+) K(+) -ATPase act

40 apamycin pathway were similar in control and IUGR skeletal muscle homogenate.

41 Developmental and IUGR-induced DNA methylation occurred in a GHRE-, CpG si

42 Weanlings grouped distinctly for ENS and IUGR by partial least-squares discriminate analysis (PLS

43 etween non-Hispanic Black race/ethnicity and IUGR, 12% of the association in Hispanic women, and 10%

44 This suggests that both HF and IUGR can induce islet injury via converging pathways.

45 In conclusion, HF and IUGR independently contribute to islet injury characteri

46 pathogenesis of placental insufficiency and IUGR are largely unknown.

47 a sheep model of placental insufficiency and IUGR, we have previously demonstrated lower net total up

48 l sheep model of placental insufficiency and IUGR.

49 In IUGR and IUGR-AR lambs heart rates were greater, which was indepe

50 In IUGR and IUGR-AR lambs, hindlimb GURs were greater but fractional

51 transporter 4 (GLUT4) was lower in IUGR and IUGR-AR skeletal muscle than in controls but GLUT1 was g

52 re measured in control lambs, IUGR lambs and IUGR lambs treated with adrenergic receptor modifiers: c

53 In studies of PTB, LBW, and IUGR that used a categorical depression measure, pooled

54 However, normal and IUGR FcCM produced in chronic hypoxia did not alter endo

55 ould decrease the ability of both normal and IUGR fibrocyte-like cells to stimulate angiogenesis.

56 te the response to oxygenation in normal and IUGR FPUs.

57 n control but strongly correlated in OLD and IUGR baboons.

58 pathway protects against hypoxia-associated IUGR, we used an experimental murine model to determine

59 Hypoxia resulted in asymmetric IUGR, placental insufficiency, and reduced placental PPA

60 No difference was seen between IUGR infants and controls in total serum or skin caroten

61 Change in T2* differed significantly between IUGR cases and controls for placenta (5.25 msec vs 11.25

62 ignificant differences in ADC values between IUGR subtypes.

63 beta-Cell mass was not altered by IUGR.

64 however, this was not aggravated further by IUGR.

65 Hierarchical clustering revealed grouping by IUGR lineage and supplementation at d21 and d160.

66 nt bilateral uterine artery ligation causing IUGR in F1.

67 or NR (50%) lactating mothers generated CON, IUGR, PNGR and IPGR male (M) and female (F) offspring th

68 Conversely, IUGR lineage ENS-fed rats did not manifest MetS, with si

69 At 134 days, IUGR fetuses weighed 67% less (P < 0.05) than controls a

70 Experimental IUGR identifies an intrauterine phase with inhibition of

71 In differentiation-promoting media (2% FBS), IUGR and control myoblasts had similar percentages of my

72 We developed a baboon model for IUGR studies using a moderate 30% global calorie restric

73 he identification of pregnancies at risk for IUGR and the generation of clinical interventional strat

74 n into PPARgamma as a therapeutic target for IUGR in pregnancies complicated by hypoxia.

75 mentally programmed MetS, adult F2, formerly IUGR rats, were obese (621 vs. 461 g; P < 0.0001), dysli

76 Perirenal adipose tissue was collected from IUGR and control fetuses at 133 days of gestational age

77 er in islet EC-conditioned media (ECCM) from IUGR, and islets incubated with control islet ECCM respo

78 Thus, we hypothesized that FcCM from IUGR cells would have a reduced ability to stimulate ang

79 20% fetal bovine serum, FBS), myoblasts from IUGR fetuses had 34% fewer (P < 0.05) myoD-positive cell

80 f TP (TPbeta) is increased in placentae from IUGR pregnancies, compared to healthy pregnancies.

81 Among the F2 generation, IUGR lineage rats were underweight at birth (6.7 vs. 8.0

82 We also found that the LG-H IUGR offspring exhibit increased risk for CVD at 4 month

83 = 3), PE (n = 3), PE/IUGR (n = 3) and HELLP/IUGR (n = 2) placentae were used to determine the mean m

84 , 53% in PE, 47% in PE/IUGR and 64% in HELLP/IUGR indicating an epigenetic down-regulation of Syncyti

85 ations in the metabolome accompany heritable IUGR, precede adult-onset MetS, and are partially amenab

86 Stem villus arteries in human IUGR placentas displaying absent or reversed end-diastol

87 fficiency are consistent with cases of human IUGR.

88 (miRNAs) significantly higher in term human IUGR vs. normal placentas.

89 rlying HCMV infection in cases of idiopathic IUGR, we studied maternal and cord sera and placentas fr

90 In IUGR and IUGR-AR lambs heart rates were greater, which w

91 In IUGR and IUGR-AR lambs, hindlimb GURs were greater but f

92 In IUGR baboons there was increased carotid arterial blood

93 In IUGR lambs ADRbeta2 activation increased whole-body gluc

94 In IUGR lambs we identified disparities in key aspects of g

95 In IUGR lambs, islet insulin content and GSIS were less tha

96 ATP content was lower by 25% (P = 0.007) in IUGR muscle.

97 ase activity was lower by 64% (P = 0.019) in IUGR sarcolemma.

98 rations were 59% and 74% lower (P < 0.05) in IUGR fetuses and lambs compared to controls, respectivel

99 mRNA concentrations were lower (P < 0.05) in IUGR fetuses but not in lambs.

100 nificantly from 29% in control CTs to 49% in IUGR, 53% in PE, 47% in PE/IUGR and 64% in HELLP/IUGR in

101 regulating processes known to be abnormal in IUGR islets, such as vascularization, beta-cell prolifer

102 ears) revealed long-term LV abnormalities in IUGR offspring.

103 r (RV) filling and ejection abnormalities in IUGR young adult baboons using cardiac magnetic resonanc

104 ely correlated to mTOR signaling activity in IUGR.

105 m ECs increase islet insulin content, and in IUGR ECs, secretion of HGF was diminished.

106 c elevation in circulating catecholamines in IUGR fetuses persistently inhibits insulin concentration

107 luate the prognostic value of ADC changes in IUGR foetuses.

108 d circumference (HC) < 5% was more common in IUGR group A compared to IUGR group B (56.5% vs. 13.3%,

109 lopment, and this regulation is decreased in IUGR fetuses, resulting in lower pancreatic islet insuli

110 lude that intrinsic cellular deficiencies in IUGR myoblasts and factors in IUGR serum diminish myobla

111 w, blood vessel sizes, and distensibility in IUGR baboons (8 males, 8 females, 8.8 years, similar to

112 eficiencies in IUGR myoblasts and factors in IUGR serum diminish myoblast proliferation and myofibre

113 le than in controls but GLUT1 was greater in IUGR-AR.

114 independent of postnatal catch-up growth in IUGR lambs as early as 1 month of age and are inherent t

115 iciencies that explain poor muscle growth in IUGR newborn offspring.

116 he high-affinity VEGF receptor was higher in IUGR islets and ECs, respectively.

117 erum factors reduces myofibre hypertrophy in IUGR fetal sheep.

118 -1 (ET-1) production, has been implicated in IUGR.

119 cyte nuclear factor-4alpha were increased in IUGR livers during basal and insulin periods.

120 and contribute to placental insufficiency in IUGR pregnancies.

121 Vessel density was less in IUGR pancreata than in controls.

122 oups, whereas amino acid uptake was lower in IUGR (IUGR: 1.3 +/- 0.5 mumol min(-1) 100 g(-1) ; CON: 2

123 Glucose transporter 4 (GLUT4) was lower in IUGR and IUGR-AR skeletal muscle than in controls but GL

124 and fractional synthetic rate were lower in IUGR compared to CON (P < 0.05).

125 amino acid uptake was significantly lower in IUGR fetal sheep.

126 ATP content was lower in IUGR skeletal muscle.

127 lami, CN, and CH were significantly lower in IUGR than control foetuses, while there was no significa

128 the development of vascular malformation in IUGR, but in vitro these changes cannot be attributed to

129 ght partially explain early onset obesity in IUGR offspring.

130 of the placental vasculature is observed in IUGR and may be due to the development of the placenta i

131 nd systolic cardiac function was observed in IUGR offspring with differences between male and female

132 hough their transport across the placenta in IUGR pregnancies is poorly understood.

133 b blood flow and oxygen consumption rates in IUGR fetal sheep.

134 ons resulted in hindlimb blood flow rates in IUGR that were similar to control fetuses on a weight-sp

135 Absolute hindlimb blood flow was reduced in IUGR (IUGR: 32.9 +/- 5.6 ml min(-1) ; CON: 60.9 +/- 6.5

136 orter function, was significantly reduced in IUGR skeletal muscle sarcolemma compared to control.

137 Furthermore, the persistent reduction in IUGR myoblast replication shows adaptive deficiencies th

138 nutrients and oxygen to the fetus result in IUGR.

139 ational hypoxia (LG-H) exposure resulting in IUGR would result in (1) placental transcriptome changes

140 ired glucose-stimulated insulin secretion in IUGR lambs is due to lower intra-islet insulin availabil

141 or cessation of catecholamine signalling in IUGR fetuses.

142 myoblast proliferation and myofibre size in IUGR fetuses, but intrinsic myoblast deficiencies do not

143 Our left ventricular (LV) CMRI studies in IUGR baboons (8 M, 8 F, 5.7 years - human equivalent app

144 d amino acid uptake and protein synthesis in IUGR fetal skeletal muscle.

145 about placental fatty acid (FA) transport in IUGR.

146 ed, but wall thickness remained unchanged in IUGR placentas.

147 tivity and whole-body glucose utilization in IUGR lambs.

148 rison to the normal group, the ADC values in IUGR foetuses were significantly lower in cerebellar hem

149 lize NEFA was 55 +/- 15% lower (P < 0.05) in IUGRs than controls.

150 factor in pregnancy complications, including IUGR; however, the role of TP isoforms during pregnancy

151 itazone (PIO) for preventing hypoxia-induced IUGR.

152 estriction with ad libitum postnatal intake (IUGR), pre- and postnatal nutrient restriction (IPGR), o

153 al motion may provide valuable insights into IUGR cardiovascular physiology.

154 Isolated IUGR hepatocytes maintained increased glucose production

155 whereas amino acid uptake was lower in IUGR (IUGR: 1.3 +/- 0.5 mumol min(-1) 100 g(-1) ; CON: 2.9 +/-

156 ute hindlimb blood flow was reduced in IUGR (IUGR: 32.9 +/- 5.6 ml min(-1) ; CON: 60.9 +/- 6.5 ml min

157 < 0.01), whereas paternal and maternal IUGR (IUGR(pat)/IUGR(mat), respectively) control-fed rats, des

158 rates (GURs) were measured in control lambs, IUGR lambs and IUGR lambs treated with adrenergic recept

159 Based on evidence in humans linking IUGR to adult CVD, we hypothesized that in murine pregna

160 The 10-month-old male IUGR group had a 1.5- to 2.0-fold increase in subcutaneo

161 DA; P < 0.01), whereas paternal and maternal IUGR (IUGR(pat)/IUGR(mat), respectively) control-fed rat

162 postnatal growth failure (p = 0.01) than non-IUGR infants.

163 uiring ROP (both p < 0.0001) compared to non-IUGR infants.

164 ng ROP treatment (p < 0.001) compared to non-IUGR infants.

165 Thus, alterations in the ability of IUGR fibrocyte-like cells to stimulate angiogenesis may

166 Understanding early cardiac biomarkers of IUGR using non-invasive imaging in this susceptible popu

167 thelium indicated transmission in 2 cases of IUGR with primary infection and 3 asymptomatic recurrent

168 n developed nations the most common cause of IUGR is impaired placentation resulting from poor tropho

169 ould be considered as an underlying cause of IUGR, regardless of virus transmission to the fetus.

170 y the changes that occur as a consequence of IUGR.

171 lacentation, and promotes the development of IUGR, and represents an underappreciated pathogenic fact

172 ipogenic programming; however, the effect of IUGR on white adipose tissue (WAT) progenitors is unknow

173 A surgical model of IUGR (bilateral uterine artery ligation) in Sprague-Dawl

174 The present study used a baboon model of IUGR (maternal nutrient restriction, MNR) to investigate

175 In summary, this animal model of IUGR links the placental transcriptional response to the

176 iogenesis in a low protein diet rat model of IUGR.

177 s are decreased at term in a baboon model of IUGR.

178 Mothers of IUGR infants had lower total serum carotenoids (P = 0.01

179 d has been implicated in the pathogenesis of IUGR and preeclampsia.

180 n of placental development and the rescue of IUGR by tetraploid embryo complementation did not restor

181 56 singleton live births, the excess risk of IUGR among Black women, Hispanic women, and women of oth

182 ensitized in the perirenal adipose tissue of IUGR fetuses and lambs by measuring adrenergic receptor

183 The birth weight of IUGR pups was 13% lower than that of sham pups.

184 Data on IUGR and SGA status, worst stage of and need for treatme

185 Here, we assessed the impact of malaria on IUGR, using data from a longitudinal, ultrasonography-ba

186 e that therapeutically superimposing PNGR on IUGR (IPGR) should be carefully weighed in light of unin

187 th growth restriction (PNGR) superimposed on IUGR (IPGR) protects young and aging adults from this ph

188 stnatal nutrient restriction superimposed on IUGR was protective, restoring metabolic normalcy to a l

189 tatin after the onset of preeclampsia and/or IUGR compared with women in the control group.

190 gnant women with APS who developed PE and/or IUGR during treatment with LDA+LMWH.

191 dition to LDA+LMWH at the onset of PE and/or IUGR.

192 er 3 days in media containing 10% control or IUGR fetal sheep serum (FSS).

193 TB (<37 weeks' gestation), LBW (<2500 g), or IUGR (<10th percentile for gestational age).

194 stetric APS when taken at the onset of PE or IUGR until the end of pregnancy.

195 hereas paternal and maternal IUGR (IUGR(pat)/IUGR(mat), respectively) control-fed rats, destined for

196 ontrol (n = 3), IUGR (n = 3), PE (n = 3), PE/IUGR (n = 3) and HELLP/IUGR (n = 2) placentae were used

197 rol CTs to 49% in IUGR, 53% in PE, 47% in PE/IUGR and 64% in HELLP/IUGR indicating an epigenetic down

198 ities in pathophysiology among preeclampsia, IUGR, and atherosclerotic cardiovascular disease, statin

199 ation is a potential strategy for preventing IUGR in pregnancies complicated by hypoxia, although fur

200 d restriction (MFR) during pregnancy-related IUGR rat model, bone marrow stem cells showed enhanced a

201 knowledge, this is the first study reporting IUGR-induced programmed adult RV dysfunction in an exper

202 , and RPS6 phosphorylation, without rescuing IUGR.

203 wo groups of intrauterine growth restricted (IUGR) foetuses and control cases.

204 Intrauterine growth restriction (IUGR) affects up to 10% of pregnancies in Western societ

205 ency causes intrauterine growth restriction (IUGR) and disturbances in glucose homeostasis with assoc

206 ors such as intrauterine growth restriction (IUGR) and high-fat (HF) diet contribute to type 2 diabet

207 ion induces intrauterine growth restriction (IUGR) and leads to heightened cardiovascular risks later

208 Intrauterine growth restriction (IUGR) and low birth weigth (LBW) are risk factors for ne

209 the risk of intrauterine growth restriction (IUGR) and preeclampsia 3-fold, augmenting perinatal morb

210 ciated with intrauterine growth restriction (IUGR) and small-for-gestational age (SGA) birth.

211 ncidence of intrauterine growth restriction (IUGR) approximately threefold.

212 cy loss and intrauterine growth restriction (IUGR) are serious pregnancy complications, and the trigg

213 (SGA) from intrauterine growth restriction (IUGR) as independent predictors of ROP, we performed a r

214 Intrauterine growth restriction (IUGR) confers heritable alterations in DNA methylation,

215 Intrauterine growth restriction (IUGR) decreases serum IGF-1 levels.

216 Intrauterine growth restriction (IUGR) enhances risk for adult onset cardiovascular disea

217 ncy-induced intrauterine growth restriction (IUGR) fetuses have chronic hypoxaemia and elevated plasm

218 etuses with intrauterine growth restriction (IUGR) have lower muscle mass that persists postnatally.

219 etuses with intrauterine growth restriction (IUGR) have reduced muscle mass that persists postnatally

220 etuses with intrauterine growth restriction (IUGR) have shown that adrenergic dysregulation was assoc

221 ia (PE) and intrauterine growth restriction (IUGR) in 20% of patients.

222 KEY POINTS: Intrauterine growth restriction (IUGR) increases offspring risk of chronic diseases later

223 Intrauterine growth restriction (IUGR) increases susceptibility to age-related diseases,

224 Intrauterine growth restriction (IUGR) increases the risk for metabolic disease and diabe

225 Intrauterine growth restriction (IUGR) is a common complication of pregnancy whereby the

226 Intrauterine growth restriction (IUGR) is a failure to achieve the growth potential of a

227 Intrauterine growth restriction (IUGR) is a pathology of pregnancy that results in failur

228 rimposed on intrauterine growth restriction (IUGR) is associated with adult-onset obesity, insulin re

229 Intrauterine growth restriction (IUGR) is associated with an increased propensity to deve

230 Intrauterine growth restriction (IUGR) is associated with perinatal morbidity and increas

231 Intrauterine growth restriction (IUGR) is associated with specific changes in placental t

232 Intrauterine fetal growth restriction (IUGR) is often associated with compromised umbilical art

233 Intrauterine growth restriction (IUGR) leads to development of type 2 diabetes (T2D) in a

234 Intrauterine growth restriction (IUGR) leads to offspring obesity.

235 iciency and intrauterine growth restriction (IUGR) of the fetus affects approximately 8% of all pregn

236 esized that intrauterine growth restriction (IUGR) offspring hearts would show impaired function and

237 effects of intrauterine growth restriction (IUGR) on carotenoid status in term newborn infants.

238 e impact of intrauterine growth restriction (IUGR) on pancreatic vascularity and paracrine signaling

239 fetus with intrauterine growth restriction (IUGR) persists into adulthood and may contribute to incr

240 Intrauterine growth restriction (IUGR) reduces skeletal muscle mass in fetuses and offspr

241 t models of intrauterine growth restriction (IUGR) successfully identify mechanisms that can lead to

242 t models of intrauterine growth restriction (IUGR) successfully identify mechanisms that can lead to

243 affected by intrauterine growth restriction (IUGR) suffer from reductions in muscle mass, which may c

244 cterized by intrauterine growth restriction (IUGR) with gonadal, adrenal, and bone marrow failure, pr

245 inating in intra-uterine growth restriction (IUGR) with postnatal catch up growth leads to diabesity.

246 ell growth, intrauterine growth restriction (IUGR), and impaired placental development.

247 ion induces intrauterine growth restriction (IUGR), increasing later life chronic disease including c

248 ion induces intrauterine growth restriction (IUGR), increasing risks of chronic diseases later in lif

249 , following intrauterine growth restriction (IUGR), is epigenetically heritable.

250 ciated with Intrauterine Growth Restriction (IUGR), Preeclampsia (PE) and High Elevated Liver and Low

251 clampsia or intrauterine growth restriction (IUGR).

252 thality and intrauterine growth restriction (IUGR).

253 ciated with intrauterine growth restriction (IUGR).

254 (LBW), and intrauterine growth restriction (IUGR).

255 nfants with intrauterine growth restriction (IUGR).

256 factors for intrauterine growth restriction (IUGR).

257 Smaller IUGR normalized blood vessel sizes were observed in the

258 nt hyperinsulinism and hypoglycaemia in some IUGR infants.

259 odifiers: clenbuterol atenolol and SR59230A (IUGR-AR).

260 ependent of postnatal growth failure status, IUGR infants had a 4-5 x increased risk of needing ROP t

261 We studied IUGR baboons (8 male, 8 female, 5.7 years), control offs

262 Our findings suggest IUGR-induced pulmonary hypertension should be further in

263 In summary, IUGR programs WAT preadipocytes to greater adipogenic po

264 rinsic beta cell S6K1 signaling, rather than IUGR, during fetal development may underlie reduced beta

265 We conclude that IUGR disrupts developmental epigenetics around distal GH

266 We conclude that IUGR resulted in obesity without insulin resistance and

267 This study establishes that IUGR also leads to impairment of the right ventricle in

268 We hypothesized that IUGR disrupts the normal developmental maturation of hep

269 We hypothesized that IUGR in the rat would affect hepatic IGF-1 expression an

270 The IUGR model based on the ligation of the left uterine vas

271 (RV) function is dependent on LV health, the IUGR right ventricle remains poorly studied.

272 catecholamine concentrations observed in the IUGR fetus produce developmental adaptations in pancreat

273 ood flow and oxygen consumption rates in the IUGR fetus.

274 s a significant fetal weight decrease in the IUGR FPUs (-21.9%; P < .001).

275 Mild decrease in distensibility in the IUGR group was seen in the iliac but not the carotid art

276 Aspects of cardiac impairment found in the IUGR offspring were similar to those found in normal con

277 g sex-specific adipogenic programming in the IUGR offspring.

278 e sex-specific adipogenic programming in the IUGR offspring.

279 r CVD, and 2) adult phenotypes of CVD in the IUGR offspring.

280 are lower in hindlimb skeletal muscle of the IUGR fetus.

281 was more common in IUGR group A compared to IUGR group B (56.5% vs. 13.3%, p < 0.0001).

282 stance arteries in stem villi contributes to IUGR by compromising umbilical blood flow via oxidative

283 The mechanisms underlying IUGR are poorly understood, though inadequate blood flow

284 PUs in the left and right uterine horns were IUGR cases and controls, respectively.

285 and vascular impairment in baboons who were IUGR at birth because of moderate maternal nutrient redu

286 Our aim was to determine whether IUGR and HF diets interact in type 2 diabetes pathogenes

287 Here we show that the mechanism by which IUGR leads to the development of T2D in adulthood is via

288 oblast types replicated less (P < 0.05) with IUGR FSS-supplemented media compared to control FSS-supp

289 asing insulin content, which was absent with IUGR ECCM.

290 ental insufficiency is often associated with IUGR; however, the molecular mechanisms involved in the

291 ng triglycerides and very-LDLs compared with IUGR control-fed F2 offspring (P < 0.01).

292 er that seems to be unique in the fetus with IUGR.

293 red with control fetuses (CON), fetuses with IUGR had increased basal glucose production rates and he

294 A total of 38 foetuses with IUGR and 18 normal control foetuses with similar gestati

295 ve glucose metabolism in neonatal lambs with IUGR and to determine whether daily treatment with ADRbe

296 clearance is normal, 1-month-old lambs with IUGR at birth have higher rates of hindlimb glucose upta

297 vascular and haemodynamic changes occur with IUGR, which may contribute to the occurrence of later li

298 gests that vascular redistribution seen with IUGR in fetal life may continue into adulthood.

299 In summary, fetal sheep with IUGR have increased hepatic glucose production, which is

300 suboptimal placental performance that yields IUGR.