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Basak, S.;  Das, R.K.;  Banerjee, A.;  Paul, S.;  Pathak, S.;  Duttaroy, A.K. Maternal Obesity and Gut Microbiota. Encyclopedia. Available online: https://encyclopedia.pub/entry/32262 (accessed on 16 June 2024).
Basak S,  Das RK,  Banerjee A,  Paul S,  Pathak S,  Duttaroy AK. Maternal Obesity and Gut Microbiota. Encyclopedia. Available at: https://encyclopedia.pub/entry/32262. Accessed June 16, 2024.
Basak, Sanjay, Ranjit K. Das, Antara Banerjee, Sujay Paul, Surajit Pathak, Asim K. Duttaroy. "Maternal Obesity and Gut Microbiota" Encyclopedia, https://encyclopedia.pub/entry/32262 (accessed June 16, 2024).
Basak, S.,  Das, R.K.,  Banerjee, A.,  Paul, S.,  Pathak, S., & Duttaroy, A.K. (2022, November 01). Maternal Obesity and Gut Microbiota. In Encyclopedia. https://encyclopedia.pub/entry/32262
Basak, Sanjay, et al. "Maternal Obesity and Gut Microbiota." Encyclopedia. Web. 01 November, 2022.
Maternal Obesity and Gut Microbiota
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Obesity in pregnancy induces metabolic syndrome, low-grade inflammation, altered endocrine factors, placental function, and the maternal gut microbiome. All these factors impact fetal growth and development, including brain development. The lipid metabolic transporters of the maternal-fetal-placental unit are dysregulated in obesity. Consequently, the transport of essential long-chain PUFAs for fetal brain development is disturbed. The mother’s gut microbiota is vital in maintaining postnatal energy homeostasis and maternal-fetal immune competence. Obesity during pregnancy changes the gut microbiota, affecting fetal brain development. Obesity in pregnancy can induce placental and intrauterine inflammation and thus influence the neurodevelopmental outcomes of the offspring.

obesity pregnancy microbiota placenta brain development fetal development

1. Introduction

Obesity during pregnancy is a rising public health concern rapidly increasing worldwide [1][2][3]. Excessive maternal weight gain during pregnancy is consistently associated with many adverse impacts, including neurocognitive outcomes in the offspring [1][4]. Recently, the effect of obesity in pregnancy on maternal and fetal health has been reviewed [5][6]. The adverse effect of maternal obesity on the fetal programming of adult diseases extends beyond non-communicable diseases to brain diseases [7][8]. Obesity and a high-fat diet predispose offspring to adverse cardiometabolic and neurodevelopmental outcomes [9]. In addition, maternal high-fat intake during pregnancy was associated with an elevated risk of neuropsychiatric disorders such as hyperactivity/attention-deficit disorder/anxiety and depressive-like behaviours later in life in offspring [10][11][12][13][14][15][16][17][18]. Both obesity and a high-fat diet can impact maternal lipid metabolic state and gut microbial composition and affect offspring’s metabolic health and brain development [19][20]. Available data from extensive epidemiologic studies indicate an association between maternal obesity and adverse neurodevelopmental outcomes in human offspring. Maternal diet, adiposity, peripheral inflammation, and gut microbiota are the potential mechanisms for underlying changes in offspring brains and behaviour [20][21][22][23].
The diversity of intestinal microbiota during pregnancy has emerged as an essential factor as their metabolites can affect the host’s health in multiple ways, from lipid metabolism to brain development and function. The microbiota-gut axis can regulate maternal obesity, diet, lifestyle and physical activity. Gut microbiota produces neurotransmitters and neuromodulators (e.g., serotonin, GABA, SCFAs and their metabolites) and their derivatives in the circulation. These bioactive factors are transported to the brain via blood vessels after crossing the BBB and modulate the neonate’s cognitive development and brain-mediated performance activities. A steady-state microbiota of the mother is determined by several extrinsic (environment, geography, lifestyle) and intrinsic (genetics, mode of delivery, eating habits, age, infection, stress, medication) factors. While one-third of the gut microbial composition is common in most individuals, the remaining two-thirds are specific to the individual [24]. Despite these, not much data is available on maternal obesity during pregnancy and the modulation of gut microbial composition and diversity on the brain development of the offspring.

2. Impacts of Obesity on Maternal Endocrine Factors and Fetal Brain Development

In pregnancy, the maternal metabolism changes dramatically to support fetal growth and meet maternal additional energy requirements. However, maternal obesity in pregnancy increases maternal complications and enhances the risk of developing obesity, cardiovascular disease, diabetes, and cognitive dysfunction in offspring in adult life [25][26]. Obesity-induced metaflammation results in aberrant changes at the cellular and humoral levels that contribute to pregnancy complications. However, the physiological inflammatory process favours implantation, placental development, and parturition [27]. Complex interactions mediate adverse effects of obesity between metabolic, inflammatory, and oxidative stress homeostasis. Obesity in pregnancy is associated with elevated levels of pro-inflammatory cytokines such as interleukin 6 (IL-6), IL-1β, IL-8, and monocyte chemotactic protein-1 (MCP-1) in both the placenta and in maternal plasma [28][29]. The maternal obesity-induced swing toward a pro-inflammatory state can affect the neurometabolic state of the fetus.
Obesity-induced changes in maternal hormone levels can affect gene expression involved in fetal brain growth and development [30][31]. Obese pregnant women possess an increased risk of developing thyroid dysfunction during gestation. Maternal hormones such as thyroid and glucocorticoids affect fetal brain development. The hormones’ effects on brain development are time- and concentration-dependent [32]. Since obesity is associated with hypothyroidism and consequently affects brain development [33]. Maternal thyroid metabolism is also disturbed by maternal iodine deficiency, environmental endocrine modifiers, and other intrinsic factors associated with thyroid diseases [34].
In early pregnancy, thyroid hormones are needed for brain developmental processes such as neuronal migration, differentiation of neurons, glial cells, neurogenesis, and synaptogenesis [35][36]. Thyroid hormones regulate gene expression in the cell cycle and intracellular signalling, cytoskeleton organization, extracellular matrix proteins and several cellular adhesion factors involved in neuronal migration and neurogenesis [35][37]. In addition, thyroid hormones are also involved in neuronal migration and neuron development by regulating reelin and neurogenin 2 genes [37]. Therefore, optimum maternal thyroid function is critically required for fetal neurodevelopment.
The altered thyroid hormone levels result in severe neurological deficiency and mental disability [38]. In addition, thyroid deficiency during pregnancy may drive offspring to the later onset of neurodevelopmental disorders [34][39][40]. Several neurodevelopmental deficits are observed in offspring born from mothers with thyroid dysfunction during the first half of gestation [41][42]. Even babies of the mother with asymptomatic thyroid dysfunction are at increased risk of impaired brain development [43]. The adverse subclinical hypothyroidism on fetal neurocognitive development is less specific. Maternal hypothyroxinemia occurs in mild iodine deficiency and may result in neurodevelopmental problems.
Corticosteroids in late gestation are indispensable for fetal brain maturation [44]. The developing brain is susceptible to corticosteroid-induced stress [45]. A study showed that prenatal maternal stress increased glucocorticoids, and a high-fat diet, increased the risk of developing obesity in offspring in later life [46]. Chronic activation of glucocorticoid receptors alters the levels of glucocorticoid in hippocampal and hypothalamic regions, thus modifying feedback regulation of the hypothalamic-pituitary-adrenal (HPA) axis [47]. Corticosteroid effects are also mediated via epigenetic changes in genes associated with synaptic plasticity [48].
Stress hormones such as catecholamines, vasopressin, and oxytocin affect fetal brain development and functionalities [49]. Chronically increased cortisol levels in maternal stress result in lower levels of maternal T4 available for the fetal brain, thus affecting fetal brain development [50].
In addition to thyroid and glucocorticoid, several other hormones play roles in fetal neurodevelopment [51]. Maternal obesity and abnormal hormone levels affect fetal programming beyond the endocrine and cardiovascular systems to the brain. Several studies showed an association between high maternal BMI and adverse neurodevelopmental functions in their progenies (Table 1).
Table 1. Epidemiological studies on maternal obesity and neurodevelopment of the offspring.
Observations References
Increased odds of developing autism spectrum disorders in offspring of obese. [52][53][54][55]
Increases odds of cognitive deficits in children of obese women observed in cohorts. [55][56][57][58][59][60]
Obese mothers have twice as likely to have a child with mental developmental delay. [58][61]
An increase in autism in children was reported in prospective pregnancy cohorts [62]
The maternal obesity was associated with schizophrenia in adult offspring in a large retrospective cohort study but other studies could not confirm this association. [63][64]
A dose-dependent increase in relative risk of cerebral palsy as maternal BMI was observed. [13][65][66][67]

3. The Placenta of an Obese Mother and Its Impact on Fetal Brain Development

An increase in total lipid content characterizes the placentas of obese women at term, infiltrated neutrophils, foam-loaded macrophages and increased levels of pro-inflammatory mediators [68][69]. The maternal obesity induced-metabolic changes affect early placental growth, gene expression, and subsequent placental structure and function, which becomes clinically manifest in late pregnancy [70]. Placental dysfunctions may adversely affect fetal development [71]. In early pregnancy, the human placenta also responds to elevated maternal insulin in obese women. Obesity in pregnancy affects human placental structure and function in many ways. The cellular signalling system may mediate these effects by modulating inflammation, metabolism, and oxidative stress pathways. These placental alterations affect pregnancy outcomes independently and synergistically with other risk factors [6][72]. The placenta is enriched with a complex vascularization for fetal blood supply that requires extensive angiogenesis. Sub-optimal angiogenesis leads to abnormal placental size and vasculature. Dysregulated angiogenesis in the placenta may directly or indirectly involve pregnancies, including pre-eclampsia, pre-term birth [73], GDM [74], and IUGR [75]. The n-3 fatty acids deficiency reduced the placental transfer of fatty acids in pre-eclampsia and GDM -associated fetuses [76]. Abnormal placental vasculature is present in several pathological conditions, such as pre-term birth, intrauterine growth restriction (IUGR), and pre-eclampsia. Suboptimal placental angiogenesis is contributed by genetics, dietary and lifestyle factors [77]. Optimal placentation is facilitated by several angiogenic factors such as vascular endothelial growth factor A (VEGFA), angiopoietin-like 4 (ANGPTL4), fibroblast growth factor (FGF), and placental growth factor (PlGF), as well as docosahexaenoic acid, 22:6 n-3 (DHA) [78][79].
High-fat diets and maternal obesity alter the metabolome and early changes in the placental transcriptome and decrease placenta vascularity [80]. During pregnancy, a maternal high-fat diet promotes ectopic lipid deposition, leading to lipotoxicity and chronic inflammation in the placenta [81]. Further, the high-fat diet enforces the placenta to adapt its metabolic response and structural change (thickness) by altering angiogenesis. Animal studies showed reduced placental labyrinth depth and elevated expression of insulin-like growth factor 2 (IGF2) and its receptor genes in the fetuses of high-fat diet dams [82]. The n-3 polyunsaturated fatty acids (n-3 PUFA) deficiency resembles high-fat diet-induced impaired placental phenotypes. The maternal n-3 PUFA deficiency affected the vascular development of decidua; the feto-placental unit suggests impacts of maternal fatty acid status on placental vascularity [83].
The lipid accumulation in the obese placenta results from altered activities of fatty acid transporter expression, lipoprotein lipase, and alterations to mitochondrial oxidative metabolism [84][85]. A recent analysis of the genome-wide transcriptome, epigenetics, and proteomics showed the effects of maternal obesity on placental lipid transport and metabolism [86][87]. Altered lipid transport and metabolism of the obese placenta, as reflected by the changes in fatty acid transporters expression, had adverse effects on smooth placental functioning in transport and the metabolism of lipids across the feto-placental unit [88][89][90]. The obese placenta had high total lipids, triglycerides, free fatty acids, and cholesterol levels. Obese placental phenotype favours excess lipid storage with reduced lipid transport to the developing fetus, including long-chain polyunsaturated fatty acids (LCPUFAs) essentially required for fetal brain development [85]. Optimal PUFA is critical for feto-placental development, and any changes, as in obesity, can have adverse effects on fetal brain development [91][92].
The pro-inflammatory cascade is favoured by an increased ratio of pro-inflammatory M1 over anti-inflammatory M2 macrophages during maternal obesity. In addition, obesity may further enhance pathological pregnancies, such as pre-eclampsia, by reducing the uterine natural killer (uNK) cell populations [93]. Furthermore, maternal obesity was associated with epigenetic dysregulations in leptin and adiponectin secretions [94]. Thus, dysregulated endocrine controls in the term placenta deprive protective effects of these adipokines on placental development, indicating the placenta’s adaptation to a harmful maternal environment. Maternal obesity and gestational diabetes mellitus (GDM) also affect fatty acid transport across the placenta. Increased placental fatty acid binding protein 4 (FABP4) and endothelial lipase expression were observed in obese women with diabetes [95][96]. In contrast, reduced levels of FABP5 and lowered uptake of n-6 LCPUFAs were reported in obese placentas [68][87][97]. Both low and high expressions of fatty acid translocase CD36/FAT were observed in the placenta of obese women [90][97].
Inflammation and metabolic dysfunction, as observed in obesity, increase placental oxidative, endoplasmic reticulum stress and downstream activation of the placental unfolded protein response, all of which have been associated with pregnancy complications, such as fetal growth restriction, pre-eclampsia, and gestational diabetes. Amounts of estradiol and progesterone concentrations in plasma and placenta are reduced in obese women than in lean women [98]. The obese placenta is exposed to high insulin in early pregnancy, which produces altered steroid hormones in mitochondria and affects energy metabolism.
Maternal lipid transport and metabolism regulate fetal adiposity via placental function. The placental transport of maternal lipids is compromised during pathological states such as IUGR and GDM. The inefficient placental LCPUFAs transfers and fat-soluble vitamins may induce metabolic dysfunction and decreased fetal growth. In GDM, the interplay of the placental ANGPTL4-lipoprotein lipase is responsible for fetal adiposity [99].

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