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Dietary intake of glucoraphanin during pregnancy and lactation prevents the behavioral abnormalities in the offspring after maternal immune activation.

ABSTRACT: Aim: Epidemiological data suggest that maternal immune activation (MIA) plays a role in the etiology of neuropsychiatric disorders including autism spectrum disorder (ASD) and schizophrenia. However, there is no prophylactic nutrition that can prevent the onset of neurodevelopmental disorders in offspring after MIA. The aim of this study was undertaken to examine whether dietary intake of glucoraphanin (GF: the precursor of a natural anti-inflammatory compound sulforaphane) can prevent the onset of behavioral abnormalities in offspring after MIA.

Methods: One percent of GF food pellet or normal food pellet was given into female mice during pregnancy and lactation (from E5 to P21). Saline (5 mL/kg/d) or poly(I:C) (5 mg/kg/d) was injected into pregnant mice from E12 to E17. Behavioral tests and immunohistochemistry of parvalbumin (PV) were performed in male offspring.

Results: Dietary intake of GF during pregnancy and lactation prevented cognitive deficits and social interaction deficits in the juvenile offspring after MIA. Furthermore, dietary intake of GF during pregnancy and lactation prevented cognitive deficits in the adult offspring after MIA. Moreover, dietary intake of GF prevented the reduction of PV immunoreactivity in the medial prefrontal cortex of adult offspring after MIA.

Conclusion: These data suggest that dietary intake of GF during pregnancy and lactation could prevent behavioral abnormalities in offspring after MIA.

SUBMITTER: Fujita Y

PROVIDER: S-EPMC7722647 | biostudies-literature | 2020 Sep

REPOSITORIES: biostudies-literature

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Dietary intake of glucoraphanin during pregnancy and lactation prevents the behavioral abnormalities in the offspring after maternal immune activation.

Fujita Yuko Y Fujita Atsuhiro A Ishima Tamaki T Hirai Ayumi A Suzuki Shigenori S Suganuma Hiroyuki H Hashimoto Kenji K

Neuropsychopharmacology reports 20200528 3

<h4>Aim</h4>Epidemiological data suggest that maternal immune activation (MIA) plays a role in the etiology of neuropsychiatric disorders including autism spectrum disorder (ASD) and schizophrenia. However, there is no prophylactic nutrition that can prevent the onset of neurodevelopmental disorders in offspring after MIA. The aim of this study was undertaken to examine whether dietary intake of glucoraphanin (GF: the precursor of a natural anti-inflammatory compound sulforaphane) can prevent th ...[more]

PMID: 32463181

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Project description:BACKGROUND:Consistent evidence of an influence of maternal dietary intake during pregnancy on infant body size and composition in human populations is lacking, despite robust evidence in animal models. OBJECTIVE:We sought to evaluate the influence of maternal macronutrient intake and balance during pregnancy on neonatal body size and composition, including fat mass and fat-free mass. STUDY DESIGN:The analysis was conducted among 1040 mother-offspring pairs enrolled in the prospective prebirth observational cohort: the Healthy Start Study. Diet during pregnancy was collected using repeated 24-hour dietary recalls (up to 8). Direct measures of body composition were obtained using air displacement plethysmography. The National Cancer Institute measurement error model was used to estimate usual dietary intake during pregnancy. Multivariable partition (nonisocaloric) and nutrient density (isocaloric) linear regression models were used to test the associations between maternal dietary intake and neonatal body composition. RESULTS:The median macronutrient composition during pregnancy was 32.2% from fat, 15.0% from protein, and 47.8% from carbohydrates. In the partition multivariate regression model, individual macronutrient intake values were not associated with birthweight or fat-free mass, but were associated with fat mass. Respectively, 418 kJ increases in total fat, saturated fat, unsaturated fat, and total carbohydrates were associated with 4.2-g (P = .03), 11.1-g (P = .003), 5.9-g (P = .04), and 2.9-g (P = .02) increases in neonatal fat mass, independent of prepregnancy body mass index. In the nutrient density multivariate regression model, macronutrient balance was not associated with fat mass, fat-free mass, or birthweight after adjustment for prepregnancy body mass index. CONCLUSION:Neonatal adiposity, but not birthweight, is independently associated with increased maternal intake of total fat, saturated fat, unsaturated fat, and total carbohydrates, but not protein, suggesting that most forms of increased caloric intake contribute to fetal fat accretion.

Project description:BackgroundObservational and experimental evidence demonstrates that protein intake in infancy programs linear growth. To our knowledge, few studies have examined prenatal maternal protein intake.ObjectiveOur objective was to examine associations of maternal protein intake during pregnancy with offspring linear growth.DesignWe analyzed data from 1961 mother-child pairs in Project Viva. We assessed first- and second-trimester diet with the use of food-frequency questionnaires and analyzed protein intake as grams per kilogram prepregnancy weight per day. We used research measures of offspring length at birth and in infancy (∼6 mo), early childhood (∼3 y), and midchildhood (∼7 y), as well as clinical growth measures obtained from after birth through midchildhood. We calculated sex-specific birth length z scores for gestational age with the use of international reference data. We used mixed models with repeated length measures to predict individual length gain velocities for birth to <6 mo and 6 mo to 7 y of age, then used these velocities as outcomes in adjusted linear regression models with maternal protein intake as the main predictor.ResultsMean (range) second-trimester protein intake was 1.4 g · kg-1 · d-1 (0.3-3.1 g · kg-1 · d-1). After adjusting for maternal sociodemographics, gestational weight gain, maternal and paternal height, and (for postdelivery outcomes) child sex, gestational age, and breastfeeding duration, each 1-SD (0.36 g · kg-1 · d-1) increment in second-trimester protein intake corresponded to a -0.10 (95% CI: -0.18, -0.03) change in birth length z score, a -0.03 cm/mo (95% CI: -0.05, -0.01 cm/mo) change in slope of length growth from birth to <6mo, and a -0.09 cm/y (95% CI: -0.14, -0.05 cm/y) change in slope of length growth from 6 mo to midchildhood. Results were similar for first-trimester intake.ConclusionsIn a population with relatively high protein intake during pregnancy, higher protein intake was associated with shorter offspring birth length and slower linear growth into midchildhood. Results suggest that higher protein intake during pregnancy does not increase fetal and child growth and may even reduce early length growth. Project Viva was registered at clinicaltrials.gov as NCT02820402.

Dataset Information

Dietary intake of glucoraphanin during pregnancy and lactation prevents the behavioral abnormalities in the offspring after maternal immune activation.

Publications

Dietary intake of glucoraphanin during pregnancy and lactation prevents the behavioral abnormalities in the offspring after maternal immune activation.

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