Metabolic and feeding adjustments during pregnancy

Haddad-Tóvolli, Roberta; Claret, Marc

doi:10.1038/s41574-023-00871-y

Cited by 4 publications

(3 citation statements)

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“…The maternal metabolic environment influences fetal growth and development through several pathways that include maternal glucose production and nutrient availability to the developing fetus [13,34,35]. Intrauterine undernutrition can disrupt the development of fetal organ structure and function, including organs responsible for insulin secretion and insulin sensitivity, prompting fetal favoring metabolically thrifty pathways to survive (i.e., thrifty phenotype) [36].…”

Section: Discussionmentioning

confidence: 99%

“…Overweight women may also have adipose tissue that secretes adipokines which have the potential to induce metabolic programming through several pathways, including fetal exposure to circulating adipokines. For example, leptin controls the development of hypothalamic neurocircuits and can lead to permanent changes in diet and exercise preferences [35]. Adiponectin can regulate fetal exposure to nutrients and, as a result, to fetal growth as well [13].…”

Section: Discussionmentioning

confidence: 99%

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Pancreatic Beta Cell Function in Infants Varies by Maternal Weight

Staimez,

Dutta,

Beyh

et al. 2024

Metabolites

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Background: The Asian Indian Beta Cell function (ABCs) in Infants Study examined the associations of maternal weight on infant pancreatic beta cell function across 7 months postpartum. Methods: Pregnant women aged 18–35 years were recruited in Hyderabad, India. Women were classified by first trimester weight as underweight (UW), BMI < 18.5 kg/m2; normal weight (NW), BMI 18.5–22.9 kg/m2; or overweight (OW), BMI 23.0 through <28.5 kg/m2. At age > 7 months, infants had an oral glucose tolerance test (OGTT, 1.75 g glucose/kg bodyweight) following a 3 h fast. Infant blood samples were assayed for C-peptide and glucose. Infant beta cell function (HOMA2-B; disposition index, DI) and insulin resistance (HOMA2-IR) were compared across maternal weight groups. Results: Mothers (UW n = 63; NW n = 43; OW n = 29) had similar age at delivery and second trimester 50 g glucose challenge test results. Cord HOMA2-B values were 51% greater for IUW (83.5, SD 55.2) and 44% greater for IOW (79.9, SD 60.8) vs. INW (55.4, SD 51.5), forming a U-shaped relationship between maternal weight and HOMA2-B. No qualitative differences in HOMA2-IR were found at birth. However, at 7 months postpartum, HOMA2-IR changed most within IUW (−64% median reduction) and changed the least in IOW (−7% median reduction). At seven months postpartum, DI was higher in IUW vs. the other groups (geometric mean IUW 1.9 SD 2.5; INW 1.3 SD 2.6 or vs. IOW mean 1.2 SD 3.7), reflecting a +49% difference in DI. Conclusions: Evidence from this study illustrates adaptations in the pancreatic functional response of infants associated with the maternal nutritional environment.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Pancreatic Beta Cell Function in Infants Varies by Maternal Weight

Staimez,

Dutta,

Beyh

et al. 2024

Metabolites

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“…During pregnancy, sensory functions such as smell [ 1 , 2 ], taste [ 3 , 4 ], skin pain [ 5 , 6 ] and itching [ 7 , 8 ] are altered. In particular, alterations in the senses of smell are associated with hyperemesis gravidarum experienced by many women in early and mid-pregnancy [ 9 , 10 ].…”

Section: Introductionmentioning

confidence: 99%

Histological analysis of neuronal changes in the olfactory cortex during pregnancy

Matsuda,

Takahashi,

Morishita

et al. 2024

Heliyon

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Interaction of the pre- and postnatal environment in the maternal immune activation model

Gundacker,

Cuenca Rico,

Stoehrmann

et al. 2023

Discov Ment Health

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Adverse influences during pregnancy are associated with a range of unfavorable outcomes for the developing offspring. Maternal psychosocial stress, exposure to infections and nutritional imbalances are known risk factors for neurodevelopmental derangements and according psychiatric and neurological manifestations later in offspring life. In this context, the maternal immune activation (MIA) model has been extensively used in preclinical research to study how stimulation of the maternal immune system during gestation derails the tightly coordinated sequence of fetal neurodevelopment. The ensuing consequence of MIA for offspring brain structure and function are majorly manifested in behavioral and cognitive abnormalities, phenotypically presenting during the periods of adolescence and adulthood. These observations have been interpreted within the framework of the “double-hit-hypothesis” suggesting that an elevated risk for neurodevelopmental disorders results from an individual being subjected to two adverse environmental influences at distinct periods of life, jointly leading to the emergence of pathology. The early postnatal period, during which the caregiving parent is the major determinant of the newborn´s environment, constitutes a window of vulnerability to external stimuli. Considering that MIA not only affects the developing fetus, but also impinges on the mother´s brain, which is in a state of heightened malleability during pregnancy, the impact of MIA on maternal brain function and behavior postpartum may importantly contribute to the detrimental consequences for her progeny. Here we review current information on the interaction between the prenatal and postnatal maternal environments in the modulation of offspring development and their relevance for the pathophysiology of the MIA model.

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Metabolic and feeding adjustments during pregnancy

Cited by 4 publications

References 205 publications

Pancreatic Beta Cell Function in Infants Varies by Maternal Weight

Pancreatic Beta Cell Function in Infants Varies by Maternal Weight

Histological analysis of neuronal changes in the olfactory cortex during pregnancy

Interaction of the pre- and postnatal environment in the maternal immune activation model

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