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1 rategy to prevent fetal overgrowth caused by maternal obesity.
2 rweight, and 1.26 (95% CI, 1.05 to 1.52) for maternal obesity.
3 es in a model of high fat diet (HFD)-induced maternal obesity.
4 ogated with diet reversal despite persistent maternal obesity.
5 hat are associated with high birthweight and maternal obesity.
6 as in preeclampsia, placental infection, or maternal obesity.
7 D, allergy, or autism spectrum disorder; and maternal obesity.
8 f lipolytic genes in mouse hearts exposed to maternal obesity.
9 D development in the offspring programmed by maternal obesity.
10 e phenotype observed in offspring exposed to maternal obesity.
11 silience to emotional dysfunction induced by maternal obesity.
12 oncentrations in pregnancy may be altered by maternal obesity.
13 was no difference in insulin action based on maternal obesity.
14 in the developing embryo brain cortex due to maternal obesity.
15 environment of pregnancies with and without maternal obesity.
16 overweight (OR 1.80, 95% CI 1.25, 2.59) with maternal obesity.
17 Ts) isolated from pregnancies complicated by maternal obesity.
18 n kinase, which was inhibited as a result of maternal obesity.
19 tabolic dysfunction linked to programming by maternal obesity.
20 Human milk composition is altered by maternal obesity.
21 o decrease the health burden associated with maternal obesity.
22 e was seen in DNV count per patient based on maternal obesity (72.0 versus 72.2 for maternal body mas
25 and function can be modified as a result of maternal obesity affecting materno-fetal fatty acids (FA
26 results support our hypothesis and show that maternal obesity affects offspring cardiac metabolism in
30 dies of both rodents and non-human primates, maternal obesity also predicts a preference for palatabl
33 consistent regarding the association between maternal obesity and Apgar score or cord pH in humans.
35 on, and other factors that often covary with maternal obesity and breast-feeding did not change these
39 r studies have reported associations between maternal obesity and childhood wheeze, asthma as well as
40 prolactin and prolactin receptor mutations, maternal obesity and diabetes mellitus, interventions du
42 is study aimed to elucidate the influence of maternal obesity and early life exposure to high-fat die
46 Evidence points to prenatal exposures to maternal obesity and gestational diabetes mellitus (GDM)
51 We aimed to analyze relationships between maternal obesity and human milk metabolites, infant body
54 ng evidence of a causal relationship between maternal obesity and impaired fetal and infant survival,
58 nt mechanisms explain why the combination of maternal obesity and offspring obesity leads to the most
62 ive of this study was to evaluate effects of maternal obesity and over-nutrition on signalling of the
63 is no difference in the association between maternal obesity and periodontitis between females with
65 ectin is a critical mechanistic link between maternal obesity and the development of metabolic diseas
66 men, there is a negative association between maternal obesity and the initiation as well as the conti
69 l to understand the developmental effects of maternal obesity and/or type 2 diabetes mellitus and fur
71 valence attributable to maternal overweight, maternal obesity, and excessive gestational weight gain
72 s among prenatal maternal cortisol profiles, maternal obesity, and repeated wheeze up to age 2 years
73 a significant role of early-life exposure to maternal obesity- and fetal growth-related factors in ch
74 3.27], and OR 4.47 [95% CI: 3.99, 5.23] for maternal obesity; and OR 1.39 [95% CI: 1.30, 1.49], OR 1
75 ed fertility, and pregnancies complicated by maternal obesity are associated with adverse outcomes, i
77 logical changes of pregnancy associated with maternal obesity are present from early pregnancy onward
78 omplications, increasing evidence implicates maternal obesity as a major determinant of offspring hea
80 structure and efficiency are not affected by maternal obesity at E13.5, suggesting that the reduction
81 resent from early pregnancy onward, reducing maternal obesity before conception is probably the best
84 llustrating that high fat diet (HFD)-induced maternal obesity can regulate fetal bone development.
87 propose that low circulating adiponectin in maternal obesity causes fetal overgrowth and programs th
88 apanese macaque model to investigate whether maternal obesity combined with a Western-style diet (WSD
89 es include a role for in utero influences of maternal obesity compounded by the availability of energ
90 nor sleeping energy expenditure at 3 mo nor maternal obesity contributed to measures of body size at
103 This research highlights that exposure to maternal obesity during lactation alone can programme ad
106 is to investigate the programming effects of maternal obesity during preconception and the preconcept
114 utilized integrative multi-omics to examine maternal obesity effects on offspring neurodevelopment i
115 ate immune system in liver injury induced by maternal obesity followed by a postnatal obesogenic diet
116 However, little is known about the effect of maternal obesity, GDM and their interaction, on placenta
117 nal age, maternal hypertension of pregnancy, maternal obesity, gestational diabetes and pregnancy at
121 nt and nonhuman primate models investigating maternal obesity have highlighted the importance of the
127 nant maternal HF feeding resembles pregravid maternal obesity in mice, which reduces fetal and neonat
136 ed obese mouse models, our study showed that maternal obesity increased fetal fat tissue mass, with a
138 ition hypothesis, intrauterine influences of maternal obesity increased lifelong obesity risk in the
140 this study were to test the hypothesis that maternal obesity increases oxidative stress during fetal
147 ss the relative contributions of exposure to maternal obesity, induced by a highly varied cafeteria d
149 ectin gene knockout (Adipoq(-/-)) attenuated maternal obesity-induced high fetal fat tissue mass.
152 othesis that neonatal hyperleptinemia due to maternal obesity induces persistent changes in the centr
153 ampal co-methylation network correlated with maternal obesity, infant behavior, infant hippocampal li
171 exposure to in-utero inflammation induced by maternal obesity is proposed as an underlying mechanism
172 intervention studies have been done in which maternal obesity is reversed and the consequences for of
174 and fetal development, and we now know that maternal obesity leads to increased inflammation, oxidat
175 odel, which posits that prenatal exposure to maternal obesity leads to neurobehavioral flexibility de
181 assessed whether peripheral inflammation in maternal obesity may be transferred to the offspring bra
182 enin signaling in MSCs of infants exposed to maternal obesity may have important consequences for MSC
186 e region overlapping mir-663 correlated with maternal obesity, metabolic and immune markers, and infa
188 d of pregnant women in the USA are obese and maternal obesity (MO) negatively affects fetal developme
193 ACT: Human epidemiological studies show that maternal obesity (MO) shortens offspring life and health
194 to rise worldwide and parallels the rise in maternal obesity (MO) that predisposes offspring to card
195 , the authors examined the association among maternal obesity, obesity subtypes, and spontaneous and
196 icantly increased odds of child obesity with maternal obesity (odds ratio [OR] 3.64, 95% CI 2.68-4.95
197 g for obesity in adolescent females included maternal obesity (odds ratio [OR], 3.46; 95% confidence
198 2.2; 95% confidence interval, 1.09-4.09) and maternal obesity (odds ratio, 3.43; 95% confidence inter
199 hich was exacerbated by previous exposure to maternal obesity (OffOb-OD), as demonstrated by raised a
201 ummarize recent research on the influence of maternal obesity on breastmilk composition and discuss t
203 the cellular and molecular repercussions of maternal obesity on embryonic cortical neurogenesis.
204 onal studies provide evidence for effects of maternal obesity on her offspring's risks of obesity, co
205 egies for preventing the negative effects of maternal obesity on offspring development and adult heal
206 t can mitigate the adverse health effects of maternal obesity on offspring development and disease ri
209 perimental studies support causal effects of maternal obesity on offspring outcomes, which are mediat
210 this study was to investigate the effect of maternal obesity on offspring's glucose metabolism durin
211 plementation reversed the adverse effects of maternal obesity on placental function and fetal growth.
212 f research investigating the consequences of maternal obesity on pregnancy and offspring health.
213 This study sought to examine the effect of maternal obesity on pregnancy complications in women wit
214 miologic evidence regarding the influence of maternal obesity on the risk of oral clefts is inconsist
218 in childhood but it remains unclear whether maternal obesity or underweight associate with adult off
222 ow that in utero exposure to a MHFD, but not maternal obesity per se, increases fetal H3K14ac with co
223 lycemia or dyslipidemia, particularly due to maternal obesity, poses a threat to the optimal developm
230 study identifies a novel mechanism by which maternal obesity programs obesity in offspring via incre
231 tment for lean body mass, sex, birth weight, maternal obesity, race, and other sociodemographic varia
241 CI, 1.35-6.42) and more than quadrupled with maternal obesity status (BMI >/=30.0 kg/m(2); AOR, 4.34;
242 fetal heart lipidomes are more sensitive to maternal obesity than males; (3) changes in lipid supply
244 model of diet-induced (high sugar/high fat) maternal obesity to explore the impact of metformin on m
246 skeletal development and mechanisms linking maternal obesity to osteoblast differentiation in offspr
259 his association was stronger with increasing maternal obesity, was modified by gestational weight gai
263 reduced H3K27me3 at genes upregulated due to maternal obesity, which could have resulted from reduced