Maternal metabolic syndrome, induced by increased fructose consumption, is associated with subfertility and impaired fetal growth in mice

2014 ◽  
Author(s):  
Jessica L Saben ◽  
Laura T Lawrence ◽  
Julie Rhee ◽  
Zeenat Asghar ◽  
Joan K Riley ◽  
...  
Diabetologia ◽  
2005 ◽  
Vol 48 (5) ◽  
pp. 849-855 ◽  
Author(s):  
D. Jaquet ◽  
S. Deghmoun ◽  
D. Chevenne ◽  
D. Collin ◽  
P. Czernichow ◽  
...  

2017 ◽  
Vol 102 (5) ◽  
pp. 1606-1613 ◽  
Author(s):  
Kyoung Eun Joung ◽  
Sule Umit Cataltepe ◽  
Zoe Michael ◽  
Helen Christou ◽  
Christos S. Mantzoros

AbstractContext:Infants born small for gestational age (SGA) have increased risk for obesity and metabolic syndrome, but the underlying mechanisms are not fully elucidated. Adipocyte fatty acid–binding protein (AFABP) is an adipokine that has been implicated in modulation of insulin sensitivity and lipid metabolism. Higher plasma AFABP levels are associated with increased risk of metabolic syndrome and cardiovascular morbidity in adults. Alterations in AFABP levels during fetal growth have not been characterized.Objective:To examine AFABP levels in neonatal cord blood in relation to gestational age and birth weight.Design:A cross-sectional study of 361 neonates born at a tertiary academic center.Outcome Measures:Plasma AFABP levels were measured by enzyme-linked immunosorbent assay. For comparison, venous samples from 26 adults were analyzed.Results:AFABP levels were higher in neonates compared with adults (P < 0.01). Preterm infants had higher AFABP levels [48.2 (31.2 to 73.3) ng/mL] compared with full-term infants [35.8 (25.1 to 51.5)] ng/mL, P < 0.01). There was a negative correlation between AFABP and gestational age (r = 0.28, P = 0.02). Among full-term infants, AFABP levels in SGA infants were lower [28.6 (24.2 to 37.3) ng/mL], compared with appropriate for gestational age [36.1 (25.5 to 50.4) ng/mL] and large for gestational age infants [45.0 (24.6 to 62.4) ng/mL, P < 0.05].Conclusions:These associations may reflect the higher metabolic activity during fetal development. AFABP may also be involved in fetal growth and the association between SGA status and obesity and metabolic syndrome in later life.


2021 ◽  
Vol 12 ◽  
Author(s):  
Satoru Ikenoue ◽  
Yoshifumi Kasuga ◽  
Toyohide Endo ◽  
Mamoru Tanaka ◽  
Daigo Ochiai

Based on epidemiological and experimental evidence, the origins of childhood obesity and early onset metabolic syndrome can be extended back to developmental processes during intrauterine life. It is necessary to actively investigate antecedent conditions that affect fetal growth by developing reliable measures to identify variations in fetal fat deposition and body composition. Recently, the resolution of ultrasonography has remarkably improved, which enables better tissue characterization and quantification of fetal fat accumulation. In addition, fetal fractional limb volume has been introduced as a novel measure to quantify fetal soft tissue volume, including fat mass and lean mass. Detecting extreme variations in fetal fat deposition may provide further insights into the origins of altered fetal body composition in pathophysiological conditions (i.e., fetal growth restriction or fetal macrosomia), which are predisposed to the metabolic syndrome in later life. Further studies are warranted to determine the maternal or placental factors that affect fetal fat deposition and body composition. Elucidating these factors may help develop clinical interventions for altered fetal growth and body composition, which could potentially lead to primary prevention of the future risk of metabolic dysfunction.


2008 ◽  
Vol 42 (1) ◽  
pp. 10-18 ◽  
Author(s):  
Vera Maria Freitas da Silveira ◽  
Bernardo Lessa Horta

OBJETIVO: Analisar as evidências na literatura do efeito do peso ao nascer sobre a ocorrência de síndrome metabólica em adultos. MÉTODOS: Foram pesquisados nas bases PubMed and LILACS, no período de 1966 a maio de 2006, artigos publicados usando os seguintes descritores: "birth weight" , "birthweight" , "intra-uterine growth restriction (IUGR)", "fetal growth retardation", "metabolic syndrome", "syndrome X", "Reaven's X syndrome". Foram selecionados 224 estudos considerados elegíveis que relatavam estimativas de associação entre peso ao nascer e síndrome metabólica ou seus componentes. Desses, 11 apresentavam razões de odds e foram usados na meta-análise. RESULTADOS: Com exceção de dois estudos, os demais relataram associação inversa entre peso ao nascer e síndrome metabólica. Comparadas com pessoas de peso normal, a razão de odds do efeito combinado naquelas que nasceram com baixo peso foi de 2,53 (IC 95%: 1,57;4,08). O gráfico de funil sugere viés de publicação e o resultado permanece estatisticamente significativo mesmo em estudos com mais de 400 pessoas (efeito combinado 2,37; IC 95%: 1,15;4,90). CONCLUSÕES: Baixo peso ao nascer aumenta o risco de síndrome metabólica na idade adulta.


2011 ◽  
Vol 2011 ◽  
pp. 1-15 ◽  
Author(s):  
Jacqueline E. A. K. Bamfo ◽  
Anthony O. Odibo

Fetal growth restriction (FGR) remains a leading contributor to perinatal mortality and morbidity and metabolic syndrome in later life. Recent advances in ultrasound and Doppler have elucidated several mechanisms in the evolution of the disease. However, consistent classification and characterization regarding the severity of FGR is lacking. There is no cure, and management is reliant on a structured antenatal surveillance program with timely intervention. Hitherto, the time to deliver is an enigma. In this paper, the challenges in the diagnosis and management of FGR are discussed. The biophysical profile, Doppler, biochemical and molecular technologies that may refine management are reviewed. Finally, a model pathway for the clinical management of pregnancies complicated by FGR is presented.


2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Hisashi Masuyama ◽  
Takashi Mitsui ◽  
Eriko Eto ◽  
Kei Hayata

Abstract The links between obesity and metabolic syndrome in parents and their offspring and the role of genes and a shared environment are not completely understood. Adipocytokines play important roles in glucose and lipid metabolism. We have already developed the model mice for transgenerational effect of obesity and metabolic syndrome and demonstrated that exposure to a high fat diet in utero might cause a metabolic syndrome-like phenomenon through epigenetic modifications of adipocytokine, adiponectin and leptin gene expressions in offspring of the model mice. In this study, we examined whether poor circumstance in utero affected the adiponectin gene expression and epigenetic changes of this gene using samples from umbilical cord in patients with hypertensive disorder of pregnancy (HDP) and fetal growth restriction (FGR) or gestational diabetes mellitus (GDM) and heavy for date fetus (HFD) compared with normal pregnant women without HDP, GDM and abnormal fetal growth. We observed that the poor circumstance under HDP with HGR or GDM with HFD caused significantly lower adiponectin gene expression and higher methylation level of histone H3 at lysine 9 of the promoter of adiponectin gene compared with normal control. Thus, poor circumstance in utero affected adiponectin gene expressions through epigenetic modifications, which might result in the increased risk for metabolic syndrome of offspring.


1996 ◽  
Vol 22 (1) ◽  
pp. 37-53 ◽  
Author(s):  
E Petridou ◽  
D Trichopoulos ◽  
K Revinthi ◽  
D Tong ◽  
E Papathoma
Keyword(s):  

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