Patterns of Adiponectin Expression in Term Pregnancy: Impact of Obesity

Haghiac, Maricela; Basu, Subhabrata; Presley, Larraine; Serre, David; Catalano, Patrick M.; Mouzon, Sylvie Hauguel-de

doi:10.1210/jc.2013-4074

Cited by 59 publications

(54 citation statements)

References 42 publications

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“…We have proposed that lower maternal plasma adiponectin levels most likely reflect fluctuations in the synthesis and secretion by the maternal white adipose tissue. 58 Additionally, inflammatory stress and dietary factors such as a high-fat diet may act as epigenetic regulators of the adiponectin gene downregulating adiponectin synthesis. 58 The longitudinal modifications of adipokines in healthy pregnancy are further enhanced in the context of pregnancy associated with diabetes and obesity.…”

Section: Role Of Maternal Adipose Tissue: Metabolic and Endocrine Funmentioning

confidence: 99%

“…58 Additionally, inflammatory stress and dietary factors such as a high-fat diet may act as epigenetic regulators of the adiponectin gene downregulating adiponectin synthesis. 58 The longitudinal modifications of adipokines in healthy pregnancy are further enhanced in the context of pregnancy associated with diabetes and obesity. 59,60 Obesity in late pregnancy is associated with hypo-adiponectinemia which is inversely correlated to maternal insulin sensitivity and BMI but not GWG (Figure 5).…”

Section: Role Of Maternal Adipose Tissue: Metabolic and Endocrine Funmentioning

confidence: 99%

“…The hypoadiponectinemia reflects the decreased expression of adiponectin mRNA and methylation of the adipose adiponectin gene of obese women. 58 …”

Section: Role Of Maternal Adipose Tissue: Metabolic and Endocrine Funmentioning

confidence: 99%

“…67 In contrast, we and others have shown that the placenta is not a source of adiponectin. 58,68 However, the placenta may act as a functional target of maternal plasma adiponectin because there are a large amounts of adiponectin receptors expressed at the maternal placental surface. The metabolic actions of adiponectin are mediated via binding to specific adiponectin receptors.…”

Section: The Maternal–fetal Interface: Role Of the Placentamentioning

confidence: 99%

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Maternal obesity and metabolic risk to the offspring: why lifestyle interventions may have not achieved the desired outcomes

2015

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Obesity during pregnancy is associated with an increased risk of short- and long-term metabolic dysfunction in the mother and her offspring. Both higher maternal pregravid body mass index (kg m−2) and excessive gestational weight gain (GWG) have been associated with adverse pregnancy outcomes such as gestational diabetes, preeclampsia and fetal adiposity. Multiple lifestyle intervention trials consisting of weight management using various diets, increased physical activity and behavioral modification techniques have been employed to avoid excessive GWG and improve perinatal outcomes. These randomized controlled trials (RCTs) have achieved modest success in decreasing excessive GWG, although the decrease in GWG was often not within the current Institute of Medicine guidelines. RCTs have generally not had any success with decreasing the risk of maternal gestational diabetes (GDM), preeclampsia or excessive fetal growth often referred to as macrosomia. Although the lack of success for these trials has been attributed to lack of statistical power and poor compliance with study protocols, our own research suggests that maternal pregravid and early pregnancy metabolic condition programs early placenta function and gene expression. These alterations in maternal/placental function occur in the first trimester of pregnancy prior to when most intervention trials are initiated. For example, maternal accrural of adipose tissue relies on prior activation of genes controlling lipogenesis and low-grade inflammation in early pregnancy. These metabolic alterations occur prior to any changes in maternal phenotype. Therefore, trials of lifestyle interventions before pregnancy are needed to demonstrate the safety and efficacy for both the mother and her offspring.

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Section: Role Of Maternal Adipose Tissue: Metabolic and Endocrine Funmentioning

confidence: 99%

Section: Role Of Maternal Adipose Tissue: Metabolic and Endocrine Funmentioning

confidence: 99%

“…The hypoadiponectinemia reflects the decreased expression of adiponectin mRNA and methylation of the adipose adiponectin gene of obese women. 58 …”

Section: Role Of Maternal Adipose Tissue: Metabolic and Endocrine Funmentioning

confidence: 99%

Section: The Maternal–fetal Interface: Role Of the Placentamentioning

confidence: 99%

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Maternal obesity and metabolic risk to the offspring: why lifestyle interventions may have not achieved the desired outcomes

2015

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“…For instance, while several studies point to the possible association between lower adiponectin levels in obese women in different trimester of pregnancy compared to normal weight women at the same gestational age, [18][19][20] others refute these findings. [21][22][23] The aim of this review is to summarize the main findings of recently published studies on the circulating levels of inflammatory mediators in obese pregnant women.…”

Section: Pro-inflammatory Cytokines (Eg Interleukin (Il)-1 Tumour Nementioning

confidence: 99%

Maternal obesity and inflammatory mediators: A controversial association

Pendeloski

Ono

Torloni

et al. 2017

American J Rep Immunol

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The link between maternal obesity and inflammatory mediators is still unclear. Our aim was to summarize the main findings of recently published studies on this topic. We performed a search in Medline for studies published in the last years on obesity, human pregnancy, and inflammatory mediators. We report the findings of 30 studies.The characteristics and number of participants, study design, gestational age at sample collection, and type of sample varied widely. Approximately two-thirds of them investigated more than one mediator, and 50% included participants in only one trimester of pregnancy. The most frequently investigated mediators were leptin, tumour necrosis factor-alpha (TNF-α), and interleukin (IL)-6. Almost all studies reported an association between maternal obesity, leptin, and C-reactive protein (CRP) serum levels but not with IL-1β and IL-10. The association of IL-6, TNF-α, monocyte chemo-attractant protein-1 (MCP-1), adiponectin, and resistin with maternal obesity is still controversial.To clarify the physiopathological link between maternal obesity and inflammation, more high-quality studies are needed. K E Y W O R D Sadipokine, cytokine, inflammatory mediator, maternal obesity, pregnancy | INTRODUCTIONObesity has more than doubled in the last decades in the general population. Maternal obesity is also increasing. In the United Kingdom, nearly 20% of pregnant women are obese, 1 and in the United States, over 50% of all pregnant women are currently overweight or obese.2 Obesity in pregnancy is associated with both immediate and long term adverse events for both the mother and the offspring, including the risk of metabolic diseases years after delivery.

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Genetic determinants of adiponectin regulation revealed by pregnancy

Hivert

Scholtens

Allard

et al. 2017

Obesity

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ObjectiveWe investigated genetic determinants of adiponectin during pregnancy to reveal novel biology of adipocyte regulation.MethodsWe conducted a genome-wide association study in 1,322 pregnant women from the Hyperglycemia and Adverse Pregnancy Outcome (HAPO) Study with adiponectin measured at ~28 weeks of gestation. We selected variants reaching P<5x10−5 for de novo genotyping in two replication cohorts (Genetics of Glycemic regulation in Gestation and Growth (Gen3G) N=522; ECOGENE-21 N=174).ResultsIn the combined meta-analysis, the maternal T allele of rs900400 located on chr3q25 (near LEKR1/CCNL1) was associated with lower maternal adiponectin (β±SE= −0.18±0.03 SD of adiponectin per risk allele; P=1.5x10−8; N=2004; multivariable adjusted models). In contrast, rs900400 showed only nominal association with adiponectin in a large sample of non-pregnant women (β±SE= −0.012±0.006; P=0.05; N=16,678 women from the ADIPOgen consortium). Offspring rs900400 T risk allele was associated with greater neonatal skin fold thickness (β±SE=0.19±0.04 SD per risk allele; P=4.1x10−8; N=1489) and higher cord blood leptin (β±SE=0.28±0.05 log-leptin per risk allele; P=8.2x10−9; N=502), but not with cord blood adiponectin (P=0.23; N=495). T allele of rs900400 was associated with higher expression of TIPARP in adipocytes.ConclusionOur investigations of adipokines during pregnancy and early life suggest that rs900400 has a role in adipocyte function.

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Patterns of Adiponectin Expression in Term Pregnancy: Impact of Obesity

Cited by 59 publications

References 42 publications

Maternal obesity and metabolic risk to the offspring: why lifestyle interventions may have not achieved the desired outcomes

Maternal obesity and metabolic risk to the offspring: why lifestyle interventions may have not achieved the desired outcomes

Maternal obesity and inflammatory mediators: A controversial association

Genetic determinants of adiponectin regulation revealed by pregnancy

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