ライフサイエンスコーパス: IUGR

1 IUGR affected hepatic DUSP5 mRNA levels and exon 2 DNA m

2 IUGR affects most organ systems by either interrupting d

3 IUGR altered the developmental pattern of H3K4me3 and K9

4 IUGR changes cytosine methylation at approximately 1,400

5 IUGR decreased hepatic and serum IGF-1.

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 fetuses are both hypoxic and hypoglycaemic, and hav

9 IUGR is a common complication of human pregnancy that li

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

11 IUGR is accompanied by changes in the quantity and activ

12 IUGR is associated with vascular remodeling of the stem

13 IUGR livers, however, had increased basal FOXO1 phosphor

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

15 IUGR programming in baboons produces myocardial remodell

16 IUGR rat liver is characterized by persistent changes in

17 IUGR semitendinosus muscles had similar percentages of p

18 IUGR was induced through a bilateral uterine artery liga

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

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

21 m term placentas of 12 normal, 12 PE, and 12 IUGR pregnancies.

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

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

24 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

25 5 of 8 sham-HF, 4 of 8 IUGR-chow, and 8 of 9 IUGR-HF rats (chi-square, P = 0.007).

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

27 ch partially inactivates postnatal and adult IUGR glut4 gene transcription.

28 Further increased interactions in the adult IUGR between DNMT3a/DNMT3b and HDAC1 and MEF2D and HDAC1

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

30 he suspicion of pulmonary hypertension after IUGR.

31 However, between 7 and 10 weeks of age, IUGR rats developed mild fasting hyperglycemia and hyper

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

33 We developed an IUGR model in rats whereby at age 3-6 months the animals

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

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

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

37 ipheral glucose utilization rates in CON and IUGR fetuses.

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

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

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

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

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

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

44 pathogenesis of placental insufficiency and IUGR are largely unknown.

45 l sheep model of placental insufficiency and IUGR.

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

47 t mouse model of spontaneous miscarriage and IUGR, and that complement activation causes dysregulatio

48 nt for women with recurrent miscarriages and IUGR.

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

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

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

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

53 g of CTs were significantly raised in PE and IUGR as compared with normal pregnancy.

54 s in isolated villous trophoblasts in PE and IUGR.

55 of villous trophoblasts from normal, PE, and IUGR pregnancies.

56 Prematurity and IUGR may have different etiologies and consequences.

57 causative factor of preeclampsia-associated IUGR and offer two possible underlying mechanisms: a dir

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

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

60 beta-Cell mass was not altered by IUGR.

61 however, this was not aggravated further by IUGR.

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

63 nt bilateral uterine artery ligation causing IUGR in F1.

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

65 Concurrently, IUGR modified epigenetic characteristics, particularly t

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

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

68 s confirmed in Akt1 null mice, which display IUGR.

69 e sheep to reduce IGF bioavailability during IUGR and increase IGF bioavailability during prepubertal

70 cental circulation at risk of pre-eclampsia, IUGR, or both have raised concentrations of ADMA, which

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

72 natal period and persist in the adult female IUGR offspring.

73 The fetal IUGR state was characterized by loss of USF-1 binding at

74 ntrauterine growth restriction of the fetus (IUGR) results from impaired placental development, frequ

75 ntrauterine growth restriction of the fetus (IUGR), and pre-eclampsia arose in ten (23%).

76 the development of type 2 diabetes following IUGR and we believe they are the first to describe the o

77 the development of adult diabetes following IUGR, we used a rodent model of IUGR that expresses lowe

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

79 cid levels in dams from two mouse models for IUGR: 1) feeding C57BL/6J dams a protein-restricted diet

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

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

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

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

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

85 20% fetal bovine serum, FBS), myoblasts from IUGR fetuses had 34% fewer (P < 0.05) myoD-positive cell

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

87 ion and was significantly raised in STs from IUGR pregnancies after stimulation with both agonists.

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

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

90 , 53% in PE, 47% in PE/IUGR and 64% in HELLP/IUGR indicating an epigenetic down-regulation of Syncyti

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

92 and molecular evidence of ER stress in human IUGR and PE+IUGR placentas, providing a potential mechan

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

94 fficiency are consistent with cases of human IUGR.

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

96 In IUGR baboons there was increased carotid arterial blood

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

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

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

100 However, the exact role of AT(1)-AAs in IUGR and the underlying mechanisms have not been identif

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

105 hosphorylation were significantly blunted in IUGR rats.

106 Insulin suppression of HGP was blunted in IUGR versus control rats (10.4 +/- 0.6 vs. 6.5 +/- 1.0 m

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

108 on transport chain progressively declined in IUGR islets.

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 er understanding of placental dysfunction in IUGR will lead to targeted therapeutic options for this

113 n CTs and STs were significantly elevated in IUGR.

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

115 al pregnancy which is exacerbated further in IUGR, diabetic and pre-eclamptic pregnancies and may als

116 expression of mitochondria-encoded genes in IUGR islets.

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

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

119 production (HGP) was significantly higher in IUGR than in control rats (14.6 +/- 0.4 vs. 12.3 +/- 0.3

120 erum factors reduces myofibre hypertrophy in IUGR fetal sheep.

121 and oxidative stress gradually increased in IUGR islets.

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

123 sts suppression of translation initiation in IUGR placentas, with a further increase in PE+IUGR cases

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

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

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

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

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 producing beta-cell mass that is observed in IUGR rats over time.

133 Histopathological studies of the placenta in IUGR indicate that abnormalities of the maternal spiral

134 needed to ensure developmental plasticity in IUGR are provided by epigenetic modulation of critical g

135 -activator) binding to the glut4 promoter in IUGR versus control was observed.

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

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

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

139 xpression of Pdx1 was permanently reduced in IUGR beta cells and underwent epigenetic modifications t

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

141 nutrients and oxygen to the fetus result in IUGR.

142 smic reticulum (ER) stress play key roles in IUGR pathophysiology.

143 or cessation of catecholamine signalling in IUGR fetuses.

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

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

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

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

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

149 Finally, autoantibody-induced IUGR and placental apoptosis are diminished by either lo

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

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

152 Isolated IUGR hepatocytes maintained increased glucose production

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

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

155 < 0.01), whereas paternal and maternal IUGR (IUGR(pat)/IUGR(mat), respectively) control-fed rats, des

156 In adult rat liver, IUGR increased Erk1/Erk2 phosphorylation and p612 IRS-1

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

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

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

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

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

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

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

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

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

166 t model in which to study the development of IUGR.

167 ted postnatally, and the postnatal effect of IUGR on the histone code was gender-specific.

168 The likelihood of IUGR increased 21% for every one standard deviation chan

169 ere increased at least threefold in liver of IUGR compared with control rats.

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

171 es following IUGR, we used a rodent model of IUGR that expresses lower levels of Pdx1, a pancreatic a

172 pregnant rat, a well-characterized model of IUGR.

173 In two mouse models of IUGR, we found reduced concentrations of essential amino

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

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

176 rtile were associated with increased risk of IUGR (adjusted odds ratio=3.29, 95% confidence interval:

177 artiles were associated with reduced risk of IUGR.

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

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

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

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

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

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

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

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

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

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

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

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

190 Two natural models of ovine IUGR are those of hyperthermic exposure during pregnancy

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

192 PE+IUGR placentas showed elevated ER stress with the additi

193 r evidence of ER stress in human IUGR and PE+IUGR placentas, providing a potential mechanism for euka

194 UGR placentas, with a further increase in PE+IUGR cases.

195 are complicated further by preeclampsia (PE+IUGR).

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 or binding protein (IGFBP) system to promote IUGR and subsequent postnatal catch-up growth in female

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

201 , and RPS6 phosphorylation, without rescuing IUGR.

202 LUT4 mRNA in intrauterine growth-restricted (IUGR) female rat offspring.

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

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

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

206 onment, but intrauterine growth restriction (IUGR) and pre-eclampsia are associated with a greater de

207 maturity or intrauterine growth restriction (IUGR) and result in small-for-gestational-age (SGA) infa

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

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

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

211 Intrauterine growth restriction (IUGR) decreases serum insulin growth factor-1 (IGF-1) le

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

230 Intrauterine growth restriction (IUGR) still accounts for a large incidence of infant mor

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

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

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

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

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

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

237 rriages and intrauterine growth restriction (IUGR), but the mediators are undefined.

238 In cases of intrauterine growth restriction (IUGR), fetal weight-specific tissue glucose uptake rates

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

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

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

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

243 thality and intrauterine growth restriction (IUGR).

244 ciated with intrauterine growth restriction (IUGR).

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

246 suffer from intrauterine growth restriction (IUGR).

247 blood with intrauterine growth restriction (IUGR).

248 ia (PE) and intrauterine growth restriction (IUGR).

249 clampsia or intrauterine growth restriction (IUGR).

250 models for intrauterine growth restriction (IUGR): maternal protein restriction and hypercholesterol

251 cy leads to intrauterine growth retardation (IUGR) and adult onset insulin resistance in both humans

252 on leads to intrauterine growth retardation (IUGR) and increased prepubertal growth rate in female la

253 Intrauterine growth retardation (IUGR) has been linked to the development of type 2 diabe

254 Intrauterine growth retardation (IUGR) has been linked to the onset of diseases in adulth

255 a model of intrauterine growth retardation (IUGR) in the rat that leads to diabetes in adulthood.

256 rth weights of intrauterine growth-retarded (IUGR) animals were significantly lower than those of con

257 was developed; intrauterine growth-retarded (IUGR) rats develop diabetes with a phenotype similar to

258 stern diet also had litters with significant IUGR.

259 nt dams resulted in litters with significant IUGR.

260 Smaller IUGR normalized blood vessel sizes were observed in the

261 nt hyperinsulinism and hypoglycaemia in some IUGR infants.

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

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

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 modifies epigenetic characteristics of the rat hepa

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

268 These results demonstrate that IUGR induces mitochondrial dysfunction in the fetal beta

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

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

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

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

273 -binding protein) concentrations to bind the IUGR glut4 gene.

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

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

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

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

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

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

280 so that gluconeogenesis is augmented in the IUGR rat.

281 tions demonstrate the mixed phenotype of the IUGR fetus that includes enhanced glucose utilization ca

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

283 teristics and mRNA levels are altered due to IUGR using chromatin immunoprecipitation (ChIP) coupled

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 ols until approximately 7 weeks of age, when IUGR rats caught up to controls.

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

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

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

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

291 e clear that the morbidities associated with IUGR are complex and result from disruptions to multiple

292 2) metabolic activity may be associated with IUGR, so the ratio of paraxanthine to caffeine was then

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

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

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

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

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.