Foetal growth of kidneys, liver and spleen in intrauterine growth restriction: “programming” causing “metabolic syndrome” in adult age

2007 ◽  
Vol 93 (12) ◽  
pp. 1635-1639 ◽  
Author(s):  
G Latini ◽  
B Mitri ◽  
A Vecchio ◽  
G Chitano ◽  
C Felice ◽  
...  
2004 ◽  
Vol 93 (12) ◽  
pp. 1635-1639 ◽  
Author(s):  
Latini G ◽  
B De Mitri ◽  
A Del Vecchio ◽  
Chitano G ◽  
C De Felice ◽  
...  

2001 ◽  
Vol 21 (1) ◽  
pp. 95-112 ◽  
Author(s):  
Peter M. Hooper ◽  
Damon C. Mayes ◽  
Nestor N. Demianczuk

2021 ◽  
Vol 89 (1) ◽  
pp. 27-36
Author(s):  
Iván Acevedo Monterrosa ◽  
Damián A. Soria ◽  
Analía Tomat ◽  
Rosana Elesgaray ◽  
Cristina Arranz ◽  
...  

Background: Intrauterine growth restriction is an abnormal fetal development characterized by a fetal growth rate lower than the potential genetic growth for the gestational age. This condition represents a major burden for public health systems, as it increases short and long-term morbidity and mortality in the offspring, particularly because of its association with the development of cardiovascular and metabolic disease in adult life. Objectives: The aim of the present study was to identify possible cardinal genes involved in intrauterine growth restriction associated with the development of obesity, hypertension and metabolic syndrome using bioinformatics tools. Methods: A total of 343 genes involved in the phenotypes of interest were obtained and 20 genes were identified as significantly relevant in the interaction network analysis. Specifically, four of these identified genes encode for growth factors or their receptors, VEGFA, PDGFRB, IGF1R and EGFR. We also identified genes related to insulin and cardiovascular homeostasis as CTNNB1, APP, MYC and MDMD2. Cluster analysis provided the most significant gene ontology terms, including those related to the biological processes of proliferation and programmed cell death, intercellular communication, protein metabolism and development of the cardiovascular system. Conclusions: The genes found in this study could be useful as putative biomarkers for the presence of cardiovascular and metabolic disorders associated with intrauterine growth restriction, or as potential therapeutic targets for treatment strategies directed to the patient's genotype.


2009 ◽  
Vol 297 (3) ◽  
pp. R813-R824 ◽  
Author(s):  
Bérengère Coupé ◽  
Isabelle Grit ◽  
Dominique Darmaun ◽  
Patricia Parnet

Epidemiological studies demonstrated a relationship between low birth weight mainly caused by intrauterine growth restriction (IUGR) and adult metabolic disorders. The concept of metabolic programming centers on the idea that nutritional and hormonal status during the key period of development determines the long-term control of energy balance by programming future feeding behavior and energy expenditure. The present study examined the consequence of early or late “catch-up growth” after IUGR on feeding behavior and metabolic cues of male offspring of rat dams exposed to protein restriction during gestation and/or lactation. Our results suggest that early catch-up growth may be favorable for fasting metabolic parameters at weaning, as no differences were observed on plasma leptin, triglyceride, glucose, and insulin levels compared with controls. In contrast, if pups remained malnourished until weaning, low insulin concentration was detected and was accompanied by hyperphagia associated with a large increase in hypothalamic NPY and AgRP mRNA expression. At adult age, on a regular chow diet, only the meal structure was modified by fetal programming. The two IUGR groups demonstrated a reduced meal duration that enhanced the speed of food ingestion and consequently increased the rest period associated to the satiety state without changes in the hypothalamic expression of appetite neuropeptides. Our findings demonstrate that in IUGR, regardless of postnatal growth magnitude, metabolic programming occurred in utero and was responsible for both feeding behavior alteration and postprandial higher insulin level in adults. Additionally, catch-up growth immediately after early malnutrition could be a key point for the programming of postprandial hyperleptinemia.


2018 ◽  
Vol 50 (5) ◽  
pp. 1764-1778 ◽  
Author(s):  
Linyuan Shen ◽  
Shunhua Zhang ◽  
Qiang Li ◽  
Yuhua Fu ◽  
Guoqing Tang ◽  
...  

Background/Aims: Intrauterine growth restriction (IUGR) is a risk factor for adult metabolic syndrome, but how this disease is regulated by lncRNAs and circRNAs remains elusive. Methods: Here, we employed adult IUGR and normal pigs as models to evaluate the expression of various global lncRNAs and circRNAs in pig livers using RNA-seq. Results: In total, we obtained 1,162 million raw reads of approximately 104.54 Gb high quality data. After a strict five-step filtering process, 3,368 lncRNAs were identified, including 300 differentially expressed lncRNAs (p < 0.05) in the IUGR group relative to the control group. The cis-regulatory analysis identified target genes that were enriched in specific GO terms and pathways (p < 0.05), including amino acid metabolism, oxidoreductase activity, PPAR signaling pathway, and insulin signaling pathway. These are closely related to the observed phenotypes of increased gluconeogenesis and impaired mitochondrial oxidative phosphorylation in adulthood of the IUGR group. Additionally, we also identified 403 circRNAs, of which 44 were differentially expressed (p < 0.05). Interestingly, our results identified ATF4-miR214-circRNA7964 and TCF7-miR22-3p-circRNA16347 as two competing endogenous networks, which were closely associated with the observed increase in hepatic gluconeogenesis in the IUGR group. Conclusion: Together, this study reveals a multitude of candidate lncRNAs and circRNAs involved in the development of IUGR pigs, which could facilitate further researches on the molecular mechanisms of metabolic syndrome.


Diabetes ◽  
2011 ◽  
Vol 60 (2) ◽  
pp. 507-516 ◽  
Author(s):  
C. F. Rueda-Clausen ◽  
V. W. Dolinsky ◽  
J. S. Morton ◽  
S. D. Proctor ◽  
J. R. B. Dyck ◽  
...  

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