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How obesity and elevated androgen levels in women with polycystic ovary syndrome (PCOS) affect their offspring is unclear. In a Swedish nationwide register-based cohort and a clinical case–control study from Chile, we found that daughters of mothers with PCOS were more likely to be diagnosed with PCOS. Furthermore, female mice (F 0 ) with PCOS-like traits induced by late-gestation injection of dihydrotestosterone, with and without obesity, produced female F 1 –F 3 offspring with PCOS-like reproductive and metabolic phenotypes. Sequencing of single metaphase II oocytes from F 1 –F 3 offspring revealed common and unique altered gene expression across all generations. Notably, four genes were also differentially expressed in serum samples from daughters in the case–control study and unrelated women with PCOS. Our findings provide evidence of transgenerational effects in female offspring of mothers with PCOS and identify possible candidate genes for the prediction of a PCOS phenotype in future generations. Prenatal androgen exposure causes transgenerational increases in offspring susceptibility to polycystic ovary syndrome in adulthood.

Poor maternal mental health has been associated with a myriad of pregnancy and child health complications. Obesity in pregnancy is known to increase one’s risk of experiencing poor maternal mental health and associated physical and mental health complications. Probiotics may represent a novel approach to intervene in poor mental health and obesity. We conducted this pre-specified secondary analysis of the Healthy Mums and Babies (HUMBA) randomised controlled trial to investigate whether probiotics would improve maternal mental health outcomes up to 36 weeks of pregnancy. Two-hundred-and-thirty pregnant women with obesity (BMI ≥ 30.0 kg/m 2 ) were recruited and randomised to receive probiotic ( Lactobacillus rhamnosus GG and Bifidobacterium lactis BB12, minimum 6.5 × 10 9 CFU) or placebo capsules. Depression, anxiety, and functional health and well-being were assessed at baseline (12 0 −17 6 weeks’ gestation) and 36 weeks of pregnancy. Depression scores remained stable and did not differ between the probiotic ( M  = 7.18, SD  = 3.80) and placebo groups ( M  = 6.76, SD  = 4.65) at 36 weeks ( p -values > 0.05). Anxiety and physical well-being scores worsened over time irrespective of group allocation, and mental well-being scores did not differ between the two groups at 36 weeks. Probiotics did not improve mental health outcomes in this multi-ethnic cohort of pregnant women with obesity.

Purpose Obesity`s prevalence is rising in women of reproductive age worldwide and has become the most common medical condition at this age group. Besides, its occurrence is also rising during pregnancy. This condition not only increases the risk of noncommunicable diseases on the mother, such as cardiovascular disease and diabetes, but also transfers this risk to the offspring. Methods This is a narrative review based on scientific and review articles on the matter. Results Obesity is associated with an increased risk of gestational diabetes mellitus, gestational hypertension and preeclampsia, venous thromboembolism, infection, and mental health problems. Furthermore, it has an impact on the progress of labor and induction matters. Regarding offspring outcomes, it is related to higher incidence of congenital anomalies, perinatal mortality, and the occurrence of large for gestational age newborns. Still, it has implications on cardiometabolic risk and neurodevelopment in offspring. Conclusion It is, therefore, imperative to encourage the adoption of healthy lifestyles, especially in the peri-conception and interpregnancy periods. Likewise, there must be support in the multidisciplinary monitoring of these pregnant women to minimize associated complication rates.

Background Previous studies have reported a high prevalence of excessive gestational weight gain (GWG) in women with prepregnancy BMI classified as overweight and obese. However, the joint evidence regarding GWG and prepregnancy BMI in the worldwide population has not been synthesized. Thus, this systematic review and meta-analysis aimed to estimate global and regional mean GWG and the prevalence of GWG above, within and below 2009 Institute of Medicine (IOM) guidelines. Second, we aimed to estimate global and regional prepregnancy BMI and the prevalence of BMI categories according to World Health Organization (WHO) classification. Methods We searched Medline, Embase, the Cochrane Library and Web of Science to identify observational studies until 9 May 2018. We included studies published from 2009 that used 2009 IOM guidelines, reporting data from women in general population with singleton pregnancies. The 2009 IOM categories for GWG and the WHO categories for prepregnancy BMI were used. DerSimonian and Laird random effects methods were used to estimate the pooled and their respective 95% confidence intervals (95% CIs) of the mean and by category rates of GWG and prepregnancy BMI, calculated by global and regions. Results Sixty-three published studies from 29 countries with a total sample size of 1,416,915 women were included. The global prevalence of GWG above and below the 2009 IOM guidelines, was 27.8% (95% CI; 26.5, 29.1) and 39.4% (95% CI; 37.1, 41.7), respectively. Furthermore, meta-regression analyses showed that the mean GWG and the prevalence of GWG above guidelines have increased. The global prevalence of overweight and obesity, was 23.0% (95% CI; 22.3, 23.7) and 16.3% (95% CI; 15.4, 17.4), respectively. The highest mean GWG and prepregnancy BMI were in North America and the lowest were in Asia. Conclusions Considering the high prevalence of GWG above the 2009 IOM guidelines and women with overweight/obesity and their continuously increasing trend in most regions, clinicians should recommend lifestyle interventions to improve women’s weight during reproductive age. Due to regional variability, these interventions should be adapted to each cultural context. Trial registration Prospectively registered with PROSPERO ( CRD42018093562 ).

To address the intergenerational transmission of obesity and diabetes, strategies promoting the health of women of reproductive age appear to be urgently needed. In this narrative review, we summarise what has been learned from many prenatal clinical trials, discuss the emerging evidence from preconception clinical trials and highlight persistent gaps and critical future directions. Most trials tested prenatal interventions that resulted in a limited gestational weight gain of ~1 kg and reduced gestational diabetes by 20–30%. These interventions also reduced macrosomia by 20–40% but had little-to-no impact on other offspring outcomes at birth or beyond. Far fewer trials tested preconception interventions, with almost all designed to improve conception or live-birth rates in overweight or obese women with infertility rather than reduce intergenerational risks in diverse populations. Preconception trials have successfully reduced weight by 3–9 kg and improved markers of glucose homeostasis and insulin resistance by the end of the intervention but whether effects were sustained to conception is unclear. Very few studies have reported offspring outcomes at birth and beyond, with no evidence thus far of beneficial effects on offspring obesity or diabetes risks. Further efforts to develop effective and scalable strategies to reduce risk of obesity and diabetes before conception should be prioritised, especially for diverse and under-resourced populations at disparately high risk of obesity and diabetes. Future clinical trials should include interventions with high potential for dissemination, diverse populations, thorough maternal phenotyping from enrolment through to conception and pregnancy, and rigorous assessment of offspring obesity and diabetes risks from birth onwards, including into the third generation.

The prevalence of obesity is increasingly common in the United States, with ~25% of women of reproductive age being overweight or obese. Metaflammation, a chronic low grade inflammatory state caused by altered metabolism, is often present in pregnancies complicated by obesity. As a result, the fetuses of mothers who are obese are exposed to an in-utero environment that has altered nutrients and cytokines. Notably, both human and preclinical studies have shown that children born to mothers with obesity have higher risks of developing chronic illnesses affecting various organ systems. In this review, the authors sought to present the role of cytokines and inflammation during healthy pregnancy and determine how maternal obesity changes the inflammatory landscape of the mother, leading to fetal reprogramming. Next, the negative long-term impact on offspring’s health in numerous disease contexts, including offspring’s risk of developing neuropsychiatric disorders (autism, attention deficit and hyperactive disorder), metabolic diseases (obesity, type 2 diabetes), atopy, and malignancies will be discussed along with the potential of altered immune/inflammatory status in offspring as a contributor of these diseases. Finally, the authors will list critical knowledge gaps in the field of developmental programming of health and diseases in the context of offspring of mothers with obesity, particularly the understudied role of hematopoietic stem and progenitor cells.

Maternal obesity is associated with multiple adverse reproductive outcomes, whereas the underlying molecular mechanisms are still not fully understood. Here, we found the reduced nicotinamide phosphoribosyl transferase (NAMPT) expression and lowered nicotinamide adenine dinucleotide (NAD+) content in oocytes from obese mice. Next, by performing morpholino knockdown assay and pharmacological inhibition, we revealed that NAMPT deficiency not only severely disrupts maturational progression and meiotic apparatus, but also induces the metabolic dysfunction in oocytes. Furthermore, overexpression analysis demonstrated that NAMPT insufficiency induced NAD+ loss contributes to the compromised developmental potential of oocytes and early embryos from obese mice. Importantly, in vitro supplement and in vivo administration of nicotinic acid (NA) was able to ameliorate the obesity‐associated meiotic defects and oxidative stress in oocytes. Our results indicate a role of NAMPT in modulating oocyte meiosis and metabolism, and uncover the beneficial effects of NA treatment on oocyte quality from obese mice. This study reports that the potential pathway mediating the effects of NAD+ generation on the quality of HFD oocytes. Loss of NAD+ content and NAMPT protein results in the meiotic defects and oxidative stress in oocytes from obese mice. Nicotinic acid (NA) supplement could partly rescue the defective phenotype of these oocytes.

Maternal obesity has been shown to impair the oxidative status in the placenta and newborns, potentially leading to adverse pregnancy outcomes and long-term effects on the programming of offspring metabolic status. This study aimed to investigate the impact of maternal obesity on maternal and umbilical cord plasma oxidative status, as well as placental oxidative adaptation. Maternal obesity (n = 20), defined as a pre-pregnancy BMI ≥ 25 kg/m2, and maternal leanness (n = 20), defined as a pre-pregnancy BMI < 23 kg/m2, were the group categories used in this study. Both groups were matched according to gestational age at delivery. Maternal blood, umbilical cord blood, and placental tissue were collected to assess nutritional content (cholesterol, triglyceride, and protein), oxidative stress markers (MDA and protein carbonyl), and antioxidant activity (SOD and catalase). Placental protein expression (SOD2, catalase, UCP2, and Nrf2) was evaluated using Western blot analysis. Catalase activity in maternal plasma significantly increased in the maternal obesity group (p = 0.0200), with a trend toward increased MDA and protein carbonyl levels. In umbilical cord plasma, triglyceride, protein carbonyl, and catalase activity were significantly elevated in the maternal obesity group compared with the lean controls (p = 0.0482, 0.0291, and 0.0347, respectively). Placental protein expression analysis revealed significantly decreased SOD2 (p = 0.0011) and catalase (p < 0.0001), along with Nrf2 downregulation (p < 0.0001). An increase in mitochondrial antioxidant UCP2 expression was observed (p = 0.0117). The neonatal protein carbonyl levels positively correlated with placental protein carbonyl (r = 0.7405, p < 0.0001) and negatively correlated with maternal catalase activity (r = −0.4332, p = 0.0052). This study thus provides evidence that maternal obesity is associated with placental and fetal oxidative stress, alongside a concurrent increase in placental antioxidant UCP2 expression.

Maternal obesity increases the risk of health complications in offspring, but whether these effects are exacerbated by offspring exposure to unhealthy diets warrants further investigation. Female Sprague-Dawley rats were fed either standard chow (n = 15) or ‘cafeteria’ (Caf, n = 21) diets across pre-pregnancy, gestation, and lactation. Male and female offspring were weaned onto chow or Caf diet (2–3/sex/litter), forming four groups; behavioural and metabolic parameters were assessed. At weaning, offspring from Caf dams were smaller and lighter, but had more retroperitoneal (RP) fat, with a larger effect in males. Maternal Caf diet significantly increased relative expression of ACACA and Fasn in male and female weanling liver, but not CPT-1, SREBP and PGC1; PPARα was increased in males from Caf dams. Maternal obesity enhanced the impact of postweaning Caf exposure on adult body weight, RP fat, liver mass, and plasma leptin in males but not females. Offspring from Caf dams appeared to exhibit reduced anxiety-like behaviour on the elevated plus maze. Hepatic CPT-1 expression was reduced only in adult males from Caf fed dams. Post weaning Caf diet consumption did not alter liver gene expression in the adult offspring. Maternal obesity exacerbated the obesogenic phenotype produced by postweaning Caf diet in male, but not female offspring. Thus, the impact of maternal obesity on adiposity and liver gene expression appeared more marked in males. Our data underline the sex-specific detrimental effects of maternal obesity on offspring.

Obesity is prevalent among women of reproductive age and is associated with increased risk of developing multiple pregnancy disorders. Pregnancy must induce immune tolerance to avoid fetal rejection, while obesity can cause chronic inflammation through activating the immune system. Impaired maternal immuno-tolerance leads to pregnancy failure, such as recurrent spontaneous abortion (RSA), one of the most common complications during early pregnancy. How does maternal immune response change under obesity stress in normal pregnancy and RSA? In turn, is obesity affected by different gestational statuses? Limited information is presently available now. Our study investigated pregnancy outcomes and maternal immune responses in two murine models (normal pregnancy and spontaneous abortion models) after obesity challenge with a high-fat diet (HFD). Abortion-prone mice fed HFD had significantly higher weight gains during pregnancy than normal pregnant mice with HFD feeding. Nonetheless, the embryo implantation and resorption rates were comparable between HFD and normal chow diet (NCD)-fed mice in each model. Evaluation of immune cell subsets showed HFD-induced obesity drove the upregulation of activated NK cell-activating receptor (NKp46) + NK cells and pro-inflammatory macrophages (MHCII high M φ ) as well as CD4 + and CD8 + T cells in the normal pregnancy group. However, in the abortion-prone group, relative more immature NK cells with decreased activity phenotypes were found in obese mice. Moreover, there were increased DCreg (CD11b high DC) cells and decreased CD4 + and CD8 + T cells detected in the HFD abortion-prone mice relative to those fed the NCD diet. Our findings reveal how pregnancy obesity and maternal immune regulation are mutually influenced. It is worth noting that the abortion-prone model where active maternal immune status was intensified by obesity, in turn stimulated an overcompensation response, leading to an over-tolerized immune status, and predisposing to potential risks of perinatal complications.