Abstract

SummaryAltered gut microbiota (dysbiosis), inflammation and weight gain are pivotal to the success of normal pregnancy. These are features of metabolic syndrome that ordinarily increase the risk of type 2 diabetes in non-pregnant individuals. Though gut microbiota influences host energy metabolism and homeostasis, the outcome (healthy or unhealthy) varies depending on pregnancy status. In a healthy pregnancy, the gut microbiota is altered to promote metabolic and immunological changes beneficial to the mother and foetus but could connote a disease state in non-pregnant individuals. During the later stages of gestation, metabolic syndrome-like features, that is, obesity-related gut dysbiotic microbiota, increased insulin resistance, and elevated pro-inflammatory cytokines, promote energy storage in adipose tissue for rapid foetal growth and development, and in preparation for energy-consuming processes such as parturition and lactation. The origin of this gestation-associated host–microbial interaction is still elusive. Therefore, this review critically examined the host–microbial interactions in the gastrointestinal tract of pregnant women at late gestation (third trimester) that shift host metabolism in favour of a diabetogenic or metabolic syndrome-like phenotype. Whether the diabetogenic effects of such interactions are indeed beneficial to both mother and foetus was also discussed with plausible mechanistic pathways and associations highlighted.Lay summaryIn non-pregnant women, increased blood glucose, fat accumulation, and prolonged immune response lead to obesity and diabetes. However, during the later stages of pregnancy, the changes in the body’s metabolism described previously do not lead to disease, instead pregnancy facilitates the storage of sufficient energy in fat cells for rapid growth and development of the foetus. The excess energy stores also prepares the mother for labour and breastfeeding. This review examines the role of the normal bacteria in the digestive tract in this beneficial energy accumulation and transfer between the mother and foetus without leading to obesity, diabetes and hypertension in pregnancy.

Highlights

  • Metabolic syndrome (MetS) is characterised by a spectrum of clinical findings including hyperglycaemia, insulin resistance, increased adiposity, and chronic subclinical inflammation, that aggravate an individual’s risk of type 2 diabetes mellitus (T2DM) (Koren et al 2012)

  • This review examines the role of the normal bacteria in the digestive tract in this beneficial energy accumulation and transfer between the mother and foetus without leading to obesity, diabetes and hypertension in pregnancy

  • High bifidobacteria and A. muciniphila correlate with reduced inflammation, improved glucose tolerance and insulin sensitivity (Vyas et al 2019, Amabebe et al 2020, Xu et al 2020). Low amounts of these butyrate-producing species as observed with increased maternal weight gain towards the third trimester may contribute to the inflammatory processes and MetS-like phenotype associated with this stage of pregnancy (Fig. 2) (Collado et al 2008)

Read more

Summary

Introduction

Metabolic syndrome (MetS) is characterised by a spectrum of clinical findings (phenotypes) including hyperglycaemia, insulin resistance, increased adiposity, and chronic subclinical inflammation, that aggravate an individual’s risk of type 2 diabetes mellitus (T2DM) (Koren et al 2012). Even though the Firmicutes:Bacteroidetes ratio remains high in the later stages of gestation as seen in obesity, a low F. prausnitzii abundance could promote a pro-inflammatory state similar to MetS (Koren et al 2012, Garcia-Mantrana & Collado 2016, Nuriel-Ohayon et al 2016, Ferrocino et al 2018).

Results
Conclusion
Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call