Mitochondrial content and hepcidin are increased in obese pregnant mothers

Anelli, Gaia Maria; Cardellicchio, Manuela; Novielli, Chiara; Antonazzo, Patrizio; Mazzocco, M.; Cetin, Irene; Mandò, Chiara

doi:10.1080/14767058.2017.1344209

Cited by 23 publications

(30 citation statements)

References 29 publications

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“…Few studies have evaluated the influence of obesity on hepcidin and iron status during pregnancy, but their results are inconclusive. While increased hepcidin in obese pregnant women was shown in previous studies,7 9 22 23 it has not been confirmed in another studies 25 26. Due to previous data, we expect to observe an increase in the serum hepcidin in obese pregnant women, consequentially increased soluble transferrin receptors as a marker for iron deficiency in cells and a lower level of Hb because of iron deficiency.…”

Section: Discussionmentioning

confidence: 63%

“…Obesity is a low-grade chronic inflammatory condition linked to the overexpression of hepcidin and secondarily to iron homeostasis. Increased hepcidin in obese pregnant women without GDM was shown in previous studies 7 9 22 23. Obesity-related inflammation may induce hepcidin biosynthesis with a consequent reduction of iron supply 7 24.…”

Section: Discussionmentioning

confidence: 69%

“…Anelli et al showed lower Hb concentration in obese pregnant women 22. Interestingly, anaemia was not related to the increase in hepcidin, while this was positively associated with maternal BMI 22…”

Section: Discussionmentioning

confidence: 96%

“…Obesity-related inflammation may induce hepcidin biosynthesis with a consequent reduction of iron supply 7 24. Anelli et al showed lower Hb concentration in obese pregnant women 22. Interestingly, anaemia was not related to the increase in hepcidin, while this was positively associated with maternal BMI 22…”

Section: Discussionmentioning

confidence: 99%

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Serum hepcidin and iron status parameters in pregnant women and the association with adverse maternal and fetal outcomes: a study protocol for a prospective cohort study

2019

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IntroductionHepcidin production is normally upregulated by iron stores, and in obesity has been shown to be overexpressed and correlated with low iron status. The increased hepcidin may restrain the iron release from the cells by affecting the expression of ferroportin, which probably associates with the development of diabetes complication. First, we investigate the difference of serum hepcidin and iron parameters between obese and non-obese pregnant women; second, we examine the correlation between serum hepcidin and adverse maternal and neonatal outcomes in pregnant women.Methods and analysisThis is a mono-centre, prospective cohort study with a study (obese) and a control group (non-obese women). In the first trimester, 188 singleton pregnancies will be recruited. Thereof, we expect 75 with a body mass index (BMI) ≥30 kg/m2 and 113 with a BMI 18.5–30 kg/m2. Serum hepcidin, iron and haematological parameters will be measured at 11–14, 24–28, 32–36 weeks of gestation and at time of delivery. Blood pressure, weight, BMI and smoking status will be examined at all visits. We will assess the composite endpoints adverse maternal outcomes (including pre-eclampsia, gestational hypertension, gestational diabetes mellitus, haemorrhage, placenta abruption) and adverse neonatal outcomes (preterm birth, intrauterine growth restriction, preterm premature rupture of membranes, Apgar score <7 at 5 min, stillbirth, neonatal death).Recruitment has started in April 2019.Ethics and disseminationThis study received ethical approval from the ethics committee in Basel. The results of the study will be published in a peer-reviewed journal, and presented at national scientific conferences.Trial registration number NCT03792464.

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Section: Discussionmentioning

confidence: 63%

Section: Discussionmentioning

confidence: 69%

Section: Discussionmentioning

confidence: 96%

Section: Discussionmentioning

confidence: 99%

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Serum hepcidin and iron status parameters in pregnant women and the association with adverse maternal and fetal outcomes: a study protocol for a prospective cohort study

2019

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“…Similarly, in pregnancies complicated by pre-existing diabetes, suppressed placental mitochondrial respiratory chain enzyme activity has been shown 40. Interestingly, in obese women without GDM, contrasting findings such as heightened mtDNA content in the placenta28 and peripheral blood,41 suggesting increased mitochondrial biogenesis, have been reported. Collectively, these data point toward reduced placental mitochondrial biogenesis and/or respiratory capacity in diabetic pregnancies.…”

Section: Discussionmentioning

confidence: 99%

Increased placental mitochondrial fusion in gestational diabetes mellitus: an adaptive mechanism to optimize feto-placental metabolic homeostasis?

Abbade

Klemetti

Farrell

et al. 2020

BMJ Open Diab Res Care

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IntroductionGestational diabetes mellitus (GDM), a common pregnancy disorder, increases the risk of fetal overgrowth and later metabolic morbidity in the offspring. The placenta likely mediates these sequelae, but the exact mechanisms remain elusive. Mitochondrial dynamics refers to the joining and division of these organelles, in attempts to maintain cellular homeostasis in stress conditions or alterations in oxygen and fuel availability. These remodeling processes are critical to optimize mitochondrial function, and their disturbances characterize diabetes and obesity.Methods and resultsHerein we show that placental mitochondrial dynamics are tilted toward fusion in GDM, as evidenced by transmission electron microscopy and changes in the expression of key mechanochemical enzymes such as OPA1 and active phosphorylated DRP1. In vitro experiments using choriocarcinoma JEG-3 cells demonstrated that increased exposure to insulin, which typifies GDM, promotes mitochondrial fusion. As placental ceramide induces mitochondrial fission in pre-eclampsia, we also examined ceramide content in GDM and control placentae and observed a reduction in placental ceramide enrichment in GDM, likely due to an insulin-dependent increase in ceramide-degrading ASAH1 expression.ConclusionsPlacental mitochondrial fusion is enhanced in GDM, possibly as a compensatory response to maternal and fetal metabolic derangements. Alterations in placental insulin exposure and sphingolipid metabolism are among potential contributing factors. Overall, our results suggest that GDM has profound impacts on placental mitochondrial dynamics and metabolism, with plausible implications for the short-term and long-term health of the offspring.

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The Influence of Obesity and Associated Fatty Acids on Placental Inflammation

Eastman

Moore

Townsend

et al. 2021

Clinical Therapeutics

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Purpose: Maternal obesity, affecting nearly 1 in 4 pregnancies, is associated with increased circulating saturated fatty acids, such as palmitate. These fatty acids are implicated in placental inflammation, which may in turn exacerbate both maternalefetal tolerance and responses to pathogens, such as group B Streptococcus. In this review, we address the question, "How do obesity and associated fatty acids influence placental inflammation?" Methods: In this narrative review, we searched PubMed and Google Scholar using combinations of the key words placental inflammation or pregnancy and lipids, fatty acids, obesity, palmitate, or other closely related search terms. We also used references found within these articles that may have been absent from our original search queries. We analyzed methods and key results of these articles to compare and contrast their findings, which were occasionally at odds with each other.Findings: Although obesity can be studied as a whole, complex phenomena with in vivo mouse models and human samples from patients with obesity, in vitro modeling often relies on the treatment of cells or tissues with 1 fatty acids and occasionally other compounds (eg, glucose and insulin). We found that palmitate, most commonly used in vitro to recreate hallmarks of obesity, induces apoptosis, oxidative stress, mitochondrial dysfunction, autophagy defects, and inflammasome activation in many placental cell types. We compare this to in vivo models of obesity wherever possible.We found that obesity as a whole may have more complex regulation of these phenomena (apoptosis, oxidative stress, mitochondrial dysfunction, autophagy defects, and inflammasome activation) compared with in vitro models of fatty acid treatment (primarily palmitate) because of the presence of unsaturated fatty acids (ie, oleate), which may have anti-inflammatory effects.Implications: The interaction of unsaturated fatty acids with saturated fatty acids may ameliorate many inflammatory effects of saturated fatty acids alone, which complicates interpretation of in vitro studies that focus on a particular fatty acid in isolation. This complication may explain why certain studies of obesity in vivo have differing outcomes from studies of specific fatty acids in vitro. (Clin Ther.

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Mitochondrial content and hepcidin are increased in obese pregnant mothers

Cited by 23 publications

References 29 publications

Serum hepcidin and iron status parameters in pregnant women and the association with adverse maternal and fetal outcomes: a study protocol for a prospective cohort study

Serum hepcidin and iron status parameters in pregnant women and the association with adverse maternal and fetal outcomes: a study protocol for a prospective cohort study

Increased placental mitochondrial fusion in gestational diabetes mellitus: an adaptive mechanism to optimize feto-placental metabolic homeostasis?

The Influence of Obesity and Associated Fatty Acids on Placental Inflammation

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