Maternal short and medium chain fatty acids supply during early pregnancy improves embryo survival through enhancing progesterone synthesis in rats

Ye, Qianhong; Cai, Shuang; Wang, Shuai; Zeng, Xiaoli; Ye, Changchuan; Chen, Meixia; Zeng, Xiangfang; Qiao, Shiyan

doi:10.1016/j.jnutbio.2019.03.015

Cited by 36 publications

(34 citation statements)

References 39 publications

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“…Pregnancy improves inflammatory markers in patients with IBD, which is associated with microbial alterations and normalization of the microbiome in these patients [53]. While data on butyrate levels during human pregnancy is scarce, butyrate enhances embryo survival in rats when given during early pregnancy [131]. Conversely, immunological alterations also affect the microbial composition.…”

Section: Microbial Changes As Cause or Consequence Of Metabolic Alterations In Pregnancymentioning

confidence: 99%

The immune system and microbiome in pregnancy

Fuhler

2020

Best Practice & Research Clinical Gastroenterology

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Hormonal changes during pregnancy instigate numerous physiological changes aimed at the growth and delivery of a healthy baby. A careful balance between immunological tolerance against fetal antigens and immunity against infectious agents needs to be maintained. A three-way interaction between pregnancy hormones, the immune system and our microbiota is now emerging. Recent evidence suggests that microbial alterations seen during pregnancy may help maintain homeostasis and aid the required physiological changes occurring in pregnancy. However, these same immunological and microbial alterations may also make women more vulnerable during pregnancy and the post-partum period, especially regarding immunological and infectious diseases. Thus, a further understanding of the hostmicrobial interactions taking place during pregnancy may improve identification of populations at risk for adverse pregnancy outcomes.

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Section: Microbial Changes As Cause or Consequence Of Metabolic Alterations In Pregnancymentioning

confidence: 99%

The immune system and microbiome in pregnancy

Fuhler

2020

Best Practice & Research Clinical Gastroenterology

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“…What is more, high and low fertility endometria display discrepancies in the lipid metabolism during middle and late luteal phases, indicating that lipid metabolism is involved in the luteal phase endometrial functionality [11,12]. Our group has proved that maternal short-and medium-chain fatty acid supply during early pregnancy enhances uterine phospholipid metabolism, leading to improved embryo survival [48]. Combined with the altered lipid metabolism observed in LRP proliferative endometria, it is deducible that lipid metabolism not only in the pregnancy period but also before pregnancy regulates the endometrium function for optimal pregnancy.…”

Section: Discussionmentioning

confidence: 85%

Uterine Insulin Sensitivity Defects Induced Embryo Implantation Loss Associated with Mitochondrial Dysfunction‐Triggered Oxidative Stress

Chen

Zhang

et al. 2021

Oxidative Medicine and Cellular Longevity

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Scope. Implantation loss is a considerable cause of early pregnancy loss in humans and mammalian animals. It is not addressed how proliferative uterine defects implicate in implantation loss. Methods and Results. Herein, a comprehensive proteomic analysis was conducted on proliferative endometria from sows with low and normal reproductive performance (LRP and NRP, respectively). Enrichment analysis of differentially expressed proteins revealed alterations in endometrial remodeling, substance metabolism (mainly lipid, nitrogen, and retinol metabolism), immunological modulation, and insulin signaling in LRP sows. Importantly, aberrant lipid metabolite accumulation and dysregulation of insulin signaling were coincidently confirmed in endometria of LPR sows, proving an impaired insulin sensitivity. Furthermore, established high-fat diet- (HFD-) induced insulin-resistant mouse models revealed that uterine insulin resistance beginning before pregnancy deteriorated uterine receptivity and decreased implantation sites and fetal numbers. Mitochondrial biogenesis and fusion were decreased, and reactive oxygen species was overproduced in uteri from the HFD group during the implantation period. Ishikawa and JAR cells directly demonstrated that oxidative stress compromised implantation in vitro. Conclusions. This study demonstrated that uterine insulin sensitivity impairment beginning before pregnancy resulted in implantation and fetal loss associated with oxidative stress induced by mitochondrial dysfunction.

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“…Approximately 15% of miscarriages occur during early pregnancy (7). During this time, female sex steroid hormones, particularly estrogen and/or progesterone, directly regulate the expression of several genes in the uterus to help maintain the pregnancy.…”

Section: Introductionmentioning

confidence: 99%

High-fat diet-induced obesity primes fatty acid β-oxidation impairment and consequent ovarian dysfunction during early pregnancy

Li¹,

Guo²,

Yang³

et al. 2021

Ann Transl Med

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Background: Obesity is associated with many adverse effects on female fertility. Obese women have a higher likelihood of developing ovulatory dysfunction due to dysregulation of the hypothalamic-pituitaryovarian axis. However, the effect of obesity on ovarian function during early pregnancy needs to be further assessed.Methods: C57BL6/J mice were given a high-fat diet (HFD) for 12 weeks to induce obesity. An in vitro high-fat model was established by treating the human ovarian granulosa cell line KGN with oleic acid and palmitic acid. Ovarian morphology of obese mice in early pregnancy was assessed by hematoxylin and eosin staining and ovarian function was assessed by enzyme-linked immunosorbent assay, western blotting, and immunohistochemistry. Oil Red O staining and transmission electron microscopy were used to detect fatty acid accumulation. Specific markers relating to the ovarian functional mechanism were assessed by real-time PCR, western blotting, lactate detection, adenosine triphosphate (ATP) detection, biochemical analyses, and enzyme-linked immunosorbent assay. Results:The results of this study showed that during early pregnancy, the number of corpus lutea, serum estradiol and progesterone levels, and the expression of the steroid biosynthesis-related protein CYP19A1 (aromatase), CYP11A1 (cholesterol side chain cleavage enzyme), and StAR (steroidogenic acute regulatory protein), were significantly increased in HFD mice. Mice fed an HFD also showed a significant increase in ovarian lipid accumulation on day 7 of pregnancy. Genes involved in fatty acid synthesis (Acsl4 and Elovl5), and fatty acid uptake and transport (Slc27a4), together with the β-oxidation rate-limiting enzyme Cpt1a, were significantly upregulated in HFD mice. Specifically, there was abnormal elevation of ATP and aberrant expression of tricarboxylic acid cycle (TCA)-and electron transport chain (ETC)-related genes in the ovaries of pregnant HFD mice. KGN cells treated with etomoxir targeting β-oxidation of fatty acid showed decreased TCA cycle and ETC related gene expression. The elevation of ATP and estradiol and progesterone levels was reversed.Conclusions: During early pregnancy, HFD-induced obesity increases fatty acid β-oxidation, which in turn increases TCA cycle and ETC related gene expression, leading to increased ATP production and ovarian dysfunction.

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Maternal short and medium chain fatty acids supply during early pregnancy improves embryo survival through enhancing progesterone synthesis in rats

Cited by 36 publications

References 39 publications

The immune system and microbiome in pregnancy

The immune system and microbiome in pregnancy

Uterine Insulin Sensitivity Defects Induced Embryo Implantation Loss Associated with Mitochondrial Dysfunction‐Triggered Oxidative Stress

High-fat diet-induced obesity primes fatty acid β-oxidation impairment and consequent ovarian dysfunction during early pregnancy

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