• Journal of the Korean Academy of Child and Adolescent Psychiatry
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• v.32 no.2
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• pp.63-70
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• 2021

Objectives: Adverse childhood experiences (ACEs) of mothers may negatively affect the mental health of their offspring. Little is known about the intergenerational effect of maternal ACE on post-traumatic stress disorder (PTSD) in the offspring. This study investigated the impact of maternal ACEs on PTSD in the offspring. Methods: A total of 156 mothers with children aged 13-18 years completed the Diagnostic Interview Schedule for Children (DISC) Predictive Scales to determine the presence of psychiatric disorders in their offspring. The subjects completed the ACE questionnaire and the Early Trauma Inventory Self-Report-Short Form. Multivariable logistic regression was used to analyze the relationship between maternal ACEs and PTSD in the offspring. Results: Of the mothers, 23.7% had at least one ACE, and PTSD was reported in 21.8% of the offspring. The offspring of the mothers in the ACE group had a significantly higher rates of traumatic experiences and PTSD than the offspring of the mothers in the no ACE group. Maternal household dysfunction independently predicted offspring PTSD [odds ratio (OR)=3.008, p=0.05), and three or more maternal ACEs were significantly related to PTSD in the offspring (OR=10.613, p=0.025). Conclusion: Maternal ACEs have a significant impact on the risk of traumatic experiences and PTSD in the offspring. These findings suggest the presence of intergenerational transmissions by which maternal ACEs affect the mental health of the offspring.

• Journal of Ecology and Environment
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• v.32 no.3
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• pp.177-182
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• 2009

The optimal strategy for semelparous females may involve adjustments in the relative investment in two fitness components, the number of offspring and the post-hatching investment per capita. To determine the pattern of maternal resource allocation to offspring in the matriphagous spider, Amaurobius ferox (Amaurobiidae), I investigated the relationship between maternal body-mass and the number of offspring, and quantified the transfer of maternal body-mass to the offspring via different forms of maternal provisioning (trophic egg-laying and matriphagy). There was a positive relationship between female body-mass and the number of offspring. However, Amaurobius mothers did not produce more trophic eggs when they had larger broods. Rather, spiderlings in larger A. ferox broods consumed larger quantities of maternal body-mass via matriphagy. Mothers transferred $28.8{\pm}6.5%$ of their body-mass to the spiderlings via trophic egg-laying, and an estimated $39.0{\pm}12.5%$ of their body-mass was transferred to the spiderlings via matriphagy.

• Journal of the Korean Academy of Child and Adolescent Psychiatry
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• v.32 no.1
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• pp.28-34
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• 2021

Objectives: This study aimed to examine the effect of maternal adverse childhood experiences (ACEs) on the attention-deficit/hyperactivity disorder (ADHD) symptoms in the offspring and to examine the mediating role of antepartum health risk on the intergenerational transmission of maternal ACEs. Methods: The participants consisted of 461 mother-child dyads. Mothers completed the ACEs questionnaire and Diagnostic Predictive Scales. Multivariate logistic regression analysis was used to estimate the risk of ADHD symptoms in the offspring of mothers with ACEs and the mediating effect of antepartum health risks by path analysis. Results: In all, 35.4% (n=163) had at least one maternal ACE, and 11.1% (n=51) had three or more. Compared to the non-ADHD symptom group, the group of offspring with ADHD symptoms showed a significant association with maternal ACE score (p<0.001) and antepartum health risks (p<0.001). Multivariate analysis further showed a significant association between the sum of maternal ACEs [odds ratio (OR)=1.264, 95% confidence interval (CI)= 1.060-1.516, p=0.009], antepartum health risks (OR=1.236, 95% CI=1.036-1.475, p=0.019), and ADHD symptoms in the offspring. In the mediation model in which the mother's ACE score affected the offspring's ADHD symptoms, partial mediation through antepartum health risks was found to be significant (B=0.041, 95% CI=0.011-0.124). Conclusion: Maternal ACEs are significantly related to the incidence of ADHD symptoms in the offspring and antepartum health risks exert an indirect effect. These findings suggest that maternal ACEs have a negative impact on the offspring's brain development through intergenerational transmission, resulting in neurodevelopmental disorders such as ADHD.

• Asian-Australasian Journal of Animal Sciences
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• v.33 no.9
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• pp.1463-1469
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• 2020

Objective: The effects of maternal and offspring dietary vitamin A (VA) supplementation on early body weight, digestive tract function and immune function in goslings were studied. Methods: Yangzhou geese (180 d old) were randomly divided into 5 experimental groups of 15 females and 3 males (the males were kept until slaughter). Eggs were collected for hatching during the peak laying period. A total of 96 goslings were selected from each treatment group (each fed a basic diet supplemented with 0, 4,000, 8,000, 12,000 or 16,000 IU/kg VA) and randomly divided into 2 groups, with 6 replicates in each group and 8 goslings in each replicate. The gosling diet was supplemented with 0 or 9,000 IU/kg VA. Results: i) Villus length, villus width and the muscle thickness of the duodenum, jejunum and ileum were increased and the crypt depth was reduced after adding 12,000 IU/kg VA to the goslings' diet (p<0.05). Adding 9,000 IU/kg VA to the offspring diet increased the length of the duodenal villi and width of the ileum and decreased the crypt depth of the ileum (p<0.05). ii) Supplementing the maternal diet with 12,000 IU/kg VA increased immune organ weight, the immune organ index and immunoglobulin content in goslings (p<0.05). The bursa weight and immunoglobulin G content of offspring were higher in the 9,000 IU/kg VA supplementation group than in the group with no supplementation (p<0.05). Conclusion: Offspring growth and development were affected by the amount of VA added into maternal diet. The negative effect of maternal VA deficiency on offspring can be compensated by adding VA to the offspring diet. Continued VA supplementation in the offspring diet after excessive VA supplementation in the maternal diet is unfavorable for gosling growth and development.

• Toxicological Research
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• v.32 no.4
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• pp.275-280
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• 2016

Prenatal nicotine exposure over an entire pregnancy has been associated with an increased prevalence of hyperactivity, anxiety-like behavior and depression-like behavior in mature rats. However, the effects of maternal nicotine exposure in late gestation and lactation on the psychology and behavior of adolescent rat offspring are unclear. Thus, we investigated the effect of nicotine exposure during late gestation and lactation on anxiety-like and impulsive decision-making behavior in adolescent offspring of rat. Female rats were orally exposed to nicotine which is within range of plasma level of human chronic smokers during the period of third last period of gestation and lactation. When the offspring were weaned, we observed alterations in the anxiety-like behavior and decision-making ability of adolescent rat offspring using light/dark box test and T-maze delay-based cost-benefit decision-making task. The maternal consumption of nicotine reduced both the time spent in the light compartment and the number of transitions compared to nicotine-free rats. Moreover, such nicotine exposed adolescent offspring rats showed impulsive decision making which chose the instant reward in a decision-making situation. We found that nicotine exposure during late gestation and lactation induces an increase in anxiety-like and impulsive decision-making behavior at this developmental stage. These findings suggest that maternal nicotine-exposed offspring are at an increased risk of developing anxious and impulsive behavior.

• Journal of Nutrition and Health
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• v.40 no.2
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• pp.130-137
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• 2007

Myelin basic protein (MBP), a major structural protein of the myelin, is thought to be important for the maintenance of myelin in the central nervous system (CNS). We investigated the effect of maternal folic acid nutritional status on the folate level and the synthesis of MBP in the offspring. In order to test this hypothesis, female Sprague-Dawley rats were fed either folic acid sufficient (8 mg/kg diet) or deficient (0 mg/kg diet) diet from 2 wks prior to the mating throughout the entire pregnancy, lactation and weaning period. We examined plasma folate level by the radioimmunoassay and homocysteine level by HPLC, respectively. The MBP expression was measured by the western blot analysis. The maternal folic acid deficiency decreased plasma folate level with a concomitant increase in plasma homocysteine level in their offspring. The maternal folic acid deficiency decreased hepatic levels of SAM and SAM/SAH ratio with a concomitant increase in hepatic levels of SAH and the MBP expression of spinal cord in their offspring at 7 wks of age. These results suggest that maternal folic acid nutritional status affect plasma folate and homocysteine level in their offspring. Moreover, the maternal folic acid deficiency mi호t inhibit the MBP expression of the spinal cord and disrupt many other vital CNS reactions in their offspring.

• Nutrition Research and Practice
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• v.17 no.6
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• pp.1084-1098
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• 2023

BACKGROUND/OBJECTIVES: Previous research has shown maternal betaine supplementation alleviates fetal-derived hepatic steatosis. Therefore, this study examined the anti-inflammatory effect of maternal betaine intake in offspring mice and its mechanism. MATERIALS/METHODS: Female C57BL/6J mice and their offspring were randomly divided into 3 groups according to the treatment received during gestation and lactation: control diet (CD), fatty liver disease (FLD), and fatty liver disease + 1% betaine (FLD-BET). The FLD group was given a high-fat diet and streptozotocin (HFD + STZ), and the FLD-BET group was treated with HFD + STZ + 1% betaine. After weaning, the offspring mice were given a normal diet for 5 weeks and then dissected to measure the relevant indexes. RESULTS: Compared to the CD group, the offspring mice in the FLD group revealed obvious hepatic steatosis and increased serum levels of alanine aminotransferase, interleukin (IL)-6, and tumor necrosis factor (TNF)-α; maternal betaine supplementation reversed these changes. The hepatic mRNA expression levels of IL-6, IL-18, and Caspase-1 were significantly higher in the FLD group than in the CD group. Maternal betaine supplementation reduced the expression of IL-1β, IL-6, IL-18, and apoptosis-associated speck-like protein containing C-terminal caspase recruitment domain (ASC). Maternal betaine supplementation also reversed the increasing protein expressions of nitric oxide dioxygenase-like receptor family pyrin domain containing 3 (NLRP3), ASC, Caspase-1, IL-1β, and IL-18 in offspring mice exposed to HFD + STZ. Maternal betaine supplementation decreased the homocysteine (Hcy) and s-adenosine homocysteine (SAH) levels significantly in the livers. Furthermore, the hepatic Hcy concentrations showed significant inverse relationships with the mRNA expression of TNF-α, NLRP3, ASC, and IL-18. The hepatic SAH concentration was inversely associated with the IL-1β mRNA expression. CONCLUSIONS: The lipotropic and anti-inflammatory effect of maternal betaine supplementation may be associated with the inhibition of NLRP3 inflammasome in the livers of the offspring mice.

• Nutrition Research and Practice
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• v.10 no.4
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• pp.386-392
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• 2016

BACKGROUND/OBJECTIVES: Changes in nutritional status during gestation and lactation have detrimental effects on offspring metabolism. Several animal studies have shown that maternal high-fat diet (HFD) can predispose the offspring to development of obesity and metabolic diseases, however the mechanisms underlying these transgenerational effects are poorly understood. Therefore, we examined the effect of maternal HFD consumption on metabolic phenotype and hepatic expression of involved genes in dams to determine whether any of these parameters were associated with the metabolic outcomes in the offspring. MATERIALS/METHODS: Female C57BL/6 mice were fed a low-fat diet (LFD: 10% calories from fat) or a high-fat diet (HFD: 45% calories from fat) for three weeks before mating, and during pregnancy and lactation. Dams and their male offspring were studied at weaning. RESULTS: Dams fed an HFD had significantly higher body and adipose tissue weights and higher serum triglyceride and cholesterol levels than dams fed an LFD. Hepatic lipid levels and mRNA levels of genes involved in lipid metabolism, including $LXR{\alpha}$, SREBP-2, FXR, LDLR, and ABCG8 were significantly changed by maternal HFD intake. Significantly lower total liver DNA and protein contents were observed in dams fed an HFD, implicating the disturbed liver adaptation in the pregnancy-related metabolic demand. HFD feeding also induced significant oxidative stress in serum and liver of dams. Offspring of dams fed an HFD had significantly higher serum cholesterol levels, which were negatively correlated with liver weights of dams and positively correlated with hepatic lipid peroxide levels in dams. CONCLUSIONS: Maternal HFD consumption induced metabolic dysfunction, including altered liver growth and oxidative stress in dams, which may contribute to the disturbed cholesterol homeostasis in the early life of male mice offspring.

• Nutrition Research and Practice
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• v.15 no.2
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• pp.160-172
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• 2021

BACKGROUND/OBJECTIVES: Nutritional status and food intake during pregnancy and lactation can affect fetal programming. In the current metabolic syndrome epidemic, high-fructose diets have been strongly implicated. This study investigated the effect of maternal high-fructose intake during pregnancy and lactation on the development of metabolic syndrome in adult offspring. SUBJECTS/METHODS: Drinking water with or without 20% fructose was administered to female C57BL/6J mice over the course of their pregnancy and lactation periods. After weaning, pups ate regular chow. Accu-Chek Performa was used to measure glucose levels, and a tail-cuff method was used to examine systolic blood pressure. Animals were sacrificed at 7 months, their livers were excised, and sections were stained with Oil Red O and hematoxylin and eosin (H&E) staining. Kidneys were collected for gene expression analysis using quantitative real-time Polymerase chain reaction. RESULTS: Adult offspring exposed to maternal high-fructose intake during pregnancy and lactation presented with heavier body weights, fattier livers, and broader areas under the curve in glucose tolerance test values than control offspring. Serum levels of alanine aminotransferase, aspartate aminotransferase, glucose, triglycerides, and total cholesterol and systolic blood pressure in the maternal high-fructose group were higher than that in controls. However, there were no significant differences in mRNA expressions of renin-angiotensin-aldosterone system genes and sodium transporter genes. CONCLUSIONS: These results suggest that maternal high-fructose intake during pregnancy and lactation induces metabolic syndrome with hyperglycemia, hypertension, and dyslipidemia in adult offspring.

• Clinical and Experimental Reproductive Medicine
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• v.39 no.4
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• pp.144-152
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• 2012

Objective: Concerns are growing about the decrease in male reproductive health. Caffeine is one of the popular nutrients that has been implicated as a risk factor for infertility. In the present study, we examined whether in utero and lactational exposure to caffeine affects the reproductive function of the offspring of rats. Methods: Pregnant rats received caffeine via drinking water during gestation (26 and 45 mg/kg) and lactation (25 and 35 mg/kg). Body and reproductive organ weight, seminiferous tubule diameter, germinal epithelium height, sperm parameters, fertility rate, number of implantations, and testosterone level of the offspring were assessed from birth to adulthood. Results: Significant dose-related decreases were observed in the body and reproductive organ weight, seminiferous tubule diameter, and germinal epithelium height of the offspring. Sperm density had declined significantly in offspring of the low-dose and high-dose groups, by 8.81% and 19.97%, respectively, by postnatal day 150. The number of viable fetuses had decreased significantly in females mated with male offspring of the high-dose group at postnatal days 60, 90, 120, and 150. There were also significant reductions in testosterone levels of high-dose group offspring from birth to postnatal day 150. Conclusion: It is concluded that maternal caffeine consumption impairs gonadal development and has long-term adverse effects on the reproductive efficiency of male offspring rats.