Body Weight Of Male Offspring Research Articles

Effect of high-fat diet on the fatty acid profiles of brain in offspring mice exposed to maternal gestational diabetes mellitus.

Fatty acids play a critical role in the proper functioning of the brain. This study investigated the effects of a high-fat (HF) diet on brain fatty acid profiles of offspring exposed to maternal gestational diabetes mellitus (GDM). Insulin receptor antagonist (S961) and HF diet were used to establish the GDM animal model. Brain fatty acid profiles of the offspring mice were measured by gas chromatography at weaning and adulthood. Protein expressions of the fatty acid transport pathway Wnt3/β-catenin and the target protein major facilitator superfamily domain-containing 2a (MFSD2a) were measured in the offspring brain by Western blot. Maternal GDM increased the body weight of male offspring (P < 0.05). In weaning offspring, factorial analysis showed that maternal GDM increased the monounsaturated fatty acid (MUFA) percentage of the weaning offspring's brain (P < 0.05). Maternal GDM decreased offspring brain arachidonic acid (AA), but HF diet increased brain linoleic acid (LA) (P < 0.05). Maternal GDM and HF diet reduced offspring brain docosahexaenoic acid (DHA), and the male offspring had higher DHA than the female offspring (P < 0.05). In adult offspring, factorial analysis showed that HF diet increased brain MUFA in offspring, and male offspring had higher brain MUFA than female offspring (P < 0.05). The HF diet increased brain LA in the offspring. Male offspring had higher level of AA than female offspring (P < 0.05). HF diet reduced DHA in the brains of female offspring. The brain protein expression of β-catenin and MFSD2a in both weaning and adult female offspring was lower in the HF + GDM group than in the CON group (P < 0.05). Maternal GDM increased the susceptibility of male offspring to HF diet-induced obesity. HF diet-induced adverse brain fatty acid profiles in both male and female offspring exposed to GDM.

IDENTIFICATION OF CRITICAL LACTATION STAGE FOR THE BODY COMPOSITION IN MALE OFFSPRING OF HIGH-FAT FED DAMS

Each stage (early, middle and late) of lactation is a critical period during which maternalmalnutritional can negatively effects on the offspring&amp;#39;s body development. We investigatedthe effects of a maternal high fat diet (HF) during the different stages of lactation on bodyweight of male offspring at weaning. Female Wistar rats were fed either a HF diet only duringthe first week (HF1-7 group), second week (HF7-14 group), third week (HF14-21 group) andthroughout lactation (group HF1-21) or standard diet during all lactation. Biometricparameters of dams and male offspring were evaluated. HF fed dams did not have a differencein body weight, food intake and fat pad compared with the control dams. Regarding theoffspring, a higher final body weight was observed in males from the HF7-14 and HF14-21and HF21 groups compared to the control. There was an increase in retroperitoneal andmesenteric fat in HF21 and HF14-21 compared with control groups. Higher perigonadal fatpat was only observed in HF21. Consumption of maternal HF diet throughout lactation causeshigh body weight in male offspring. Interestingly, each isolated phase also causes importantbody weight accumulation, mainly the second and third week.

LncRNA‑miRNA‑mRNA network in female offspring born from obese dams.

Maternal obesity is associated with disturbance of lipid metabolism and obesity in offspring; however, the pathogenesis is still unclear. The present study elucidated the role of potential lipid metabolism-associated long non-coding RNA (lncRNA) and identified the pathways involved in mice born to obese dams. In the present study, maternal obesity was induced by feeding a high-fat diet for 10 weeks in female C57/BL6 mice, whereas control mice were fed a standard diet. All female mice mated with healthy male mice and were allowed to deliver spontaneously. The results demonstrated that female offspring from obese dams presented a tendency to become overweight in the first 8 weeks after birth; however, maternal obesity did not significantly alter the body weight of male offspring. RNA-sequencing analysis was performed on female offspring liver at 3 weeks old. Significantly dysregulated lncRNAs and downstream targets in female offspring liver were identified using bioinformatics analysis. lncRNA, microRNA (miRNA or miR) and mRNA expression levels in liver and AML12 cells were assessed using reverse transcription-quantitative PCR. A total of 8 upregulated and 17 downregulated lncRNAs were demonstrated in offspring from obese dams and lncRNA Lockd was indicated to be a key dysregulated lncRNA. Competing endogenous RNA (ceRNA) models suggested that the lncRNA Lockd/miR-582-5p/Elovl5 pathway was key for lipid metabolism in the liver of offspring from obese dams. Finally, small interfering RNA and miRNA inhibitor transfection was used to evaluate the ceRNA models in AML12 cells. Taken together, the results of the present study indicated that lncRNA Lockd-miR-582-5p-Elovl5 network may be disrupted in lipid metabolism and lead to obesity in the offspring of obese dams. This research will provide new insights into the molecular mechanism of obesity and lipid metabolism disorder.

Effects of maternal urban particulate matter SRM 1648a exposure on birth outcomes and offspring growth in mice.

The association between exposure to particulate matter (PM) during pregnancy and abnormal birth outcomes is still inconclusive. This study aims to provide more evidence for this public health concern by investigating birth outcomes and the growth of offspring in mice exposed to PM during pregnancy. C57BL/6J pregnant mice were exposed to PM via nasal drip at three doses or solvent control. The dam weight gain was recorded during pregnancy. The number of pups, pup weight, and placental weight were recorded at embryonic day 18.5 (E18.5) necropsy. For mice that gave birth naturally, we calculated the gestation length and measured the body weight of offspring once a week from the 1st to the 6th week after birth. The results showed that there were no significant differences in maternal body weight gain, conception rate, pregnancy duration, and litter size among different groups. There were no significant differences in fetal weight, placental weight, and fetal/placental weight ratio at E18.5. Weight gain in offspring was reduced after birth. The average body weight of offspring in the high-dose group was significantly lower than that in the control group at weeks 5 in female pups. There were no significant differences in the body weight of male offspring among groups from 1st to the 6th. Together, our study indicated that maternal exposure to PM did not significantly impact birth outcomes of C57BL/6J mice but affected growth trajectories in offspring after birth in a dose- and fetal sex-dependent manner.

Maternal exercise and high-fat diet affect hypothalamic neural projections in rat offspring in a sex-specific manner

This study aimed to investigate the effect of maternal high-fat (HF) diet and exercise during gestation and lactation on hypothalamic neural projection development in the offspring. Pregnant Sprague-Dawley rats were fed a CHOW or HF diet during gestation and lactation, and further divided into two subgroups: voluntary exercised and sedentary. Offspring's brains and tissue were collected at weaning and 16 weeks of age. Maternal exercise downregulated dams’ body weight and food intake during lactation, but failed to normalize increased fat weight, plasma and milk leptin levels of HF dams at weaning. Maternal HF diet significantly increased offspring's body weight, adipose depots, plasma insulin, and leptin at weaning and had long-term effect on body weight of male offspring, while maternal exercise decreased offspring's body weight from 3 to 5 weeks of age in both sexes. At weaning, maternal exercise decreased αMSH fiber density and maternal HF diet impaired agouti-related peptide fiber density in the paraventricular nucleus of hypothalamus of male pups, while maternal HF diet disrupted αMSH fiber density in the paraventricular nucleus of hypothalamus of female pups. The impaired αMSH fiber density was consistent with reduced STAT3 signaling in the arcuate nucleus of hypothalamus, while the reduced agouti-related peptide fiber density was consistent with reduced ERK1/2 signaling in the arcuate nucleus of hypothalamus. The impaired hypothalamic projections were compensated in adulthood in both sexes. Our findings suggest that maternal HF diet and exercise exerts different effects on hypothalamic neural projections development through distinct signaling pathways in a sex-specific manner.

Transgenerational Evaluation of Elateriospermum tapos Extracts on the Male Offspring of Obesity-Induced Sprague Dawley Rats

Obesity has been considered as a great public health concern, that has spread in both economic and poor resources countries. This study aimed to investigate the effect of Elateriospermum tapos supplementation on the male offspring of female obesity-induced Sprague Dawley (SD) rats at weaning and adult age. A total of thirty (30) female and fifteen (15) male Sprague Dawley rats (N=45) were purchased for this study. Of the 30 female rats, six (n=6) were randomly selected as the control group (CG) and fed separately with male on standard chow diet, while the remaining rats (n=24) were fed on a high-fat diet for 5 weeks. The obese group were further randomly divided into 4 groups, positive control group (PG), orlistat treatment (DG) at 200 mg/kg, treatment 1 (TX1, 200 mg/kg E. tapos seed) and treatment 2 (TX2, 200 mg/kg E. tapos shell) for 6 weeks. One male pup from each dam was culled at weaning (postnatal day 21 (PND21)) and adulthood (12 weeks). The liver, kidney, retroperitoneal white adipose tissue (RpWAT) and brown adipose tissue (BAT) were collected for histopathological study. Serum lipid profiles, liver enzyme activities and creatinine were measured. The bodyweight of male offspring from treatment 1 (MTX1) and 2 (MTX2) was significantly lower (P&lt;0.05) compare to MNG group. The RpWAT weight in MTX1 and MTX2 for adult offspring also were significantly lower (P&lt;0.05) compared to MPG. The histopathological examination of liver in MCG, MDG, MTX1, and MTX2 showed normal hepatocytes while the MPG group showed the presence of ballooning cell and hypertrophy of adipocytes was also observed in MPG group compared to another group’s rat. The E. tapos extracts from the shell have greater therapeutic potential on maternal obesity in short and long term treatment.

Maternal Chronodisruption Throughout Pregnancy Impairs Glucose Homeostasis and Adipose Tissue Physiology in the Male Rat Offspring

Compelling evidence in rats support the idea that gestational chronodisruption induces major changes in maternal circadian rhythms and fetal development and that these changes impact adult life at many physiological levels. Using a model of chronic photoperiod shifting throughout gestation (CPS), in which pregnant female rats (Sprague–Dawley strain; n = 16 per group) were exposed to lighting schedule manipulation every 3–4 days reversing the photoperiod completely or light/dark photoperiod (12/12; LD), we explored in the adult rat male offspring body weight gain, glucose homeostasis, adipose tissue content, adipose tissue response to norepinephrine (NE), and adipose tissue proteomic in the basal condition with standard diet (SD) and in response to high-fat diet (HFD). In adult CPS male (100–200 days old; n = 8 per group), we found increasing body weight, under SD and adiposity. Also, we found an increased response to intraperitoneal glucose (IGTT). After 12 weeks of HFD, white adipose tissue depots in CPS offspring were increased further, and higher IGTT and lower intraperitoneal insulin tolerance response were found, despite the lack of changes in food intake. In in vitro experiments, we observed that adipose tissue (WAT and BAT) glycerol response to NE from CPS offspring was decreased, and it was completely abolished by HFD. At the proteomic level, in CPS adipose tissue, 275 proteins displayed differential expression, compared with LD animals fed with a standard diet. Interestingly, CPS offspring and LD fed with HFD showed 20 proteins in common (2 upregulated and 18 downregulated). Based on these common proteins, the IPA analysis found that two functional pathways were significantly altered by CPS: network 1 (AKT/ERK) and network 2 (TNF/IL4; data are available via ProteomeXchange with identifier PXD026315). The present data show that gestational chronodisruption induced deleterious effects in adipose tissue recruitment and function, supporting the idea that adipose tissue function was programmed in utero by gestational chronodisruption, inducing deficient metabolic responses that persist into adulthood.

Biomarker Identification of Maternal Genistein Exposure Induced Obesity by Metabonomics Analysis.

The objective of this study was to confirm the effect of maternal genistein exposure on body weight of male offspring and the metabolic alterations associated with maternal genistein-induced obesity. Pregnant female Sprague-Dawley (SD) rats were supplemented with 300 mg/kg diet of genistein (GEN) or no genistein (CON) throughout pregnancy and lactation. The growth of male offspring was investigated until 12 week age and the mechanism of obesity was studied using metabonomics by ultra performance liquid chromatography and quadrupole time-of-flight (UPLC Q-TOF) MS with electrospray ionization in positive ESI mode (ESI+). Compared with the CON group, body weight, fat pad and food intake of male offspring in GEN group were increased significantly at the age of weeks 10 to 12 (p<0.05). Ten urine principal metabolites contributing to the clusters were identified, including increased 8-Isoprostaglandin F2a, and decreased L-Proline, Betaine, L-Acetylcarnitine, Norsalsolinol, Indoleacrylic acid, L-Tryptophan, Lysophosphatidylcholines (LysoPC) (20 : 4), Lysophosphatidylethanolamines (LysoPE) (18 : 1) and LysoPC (O-18 : 0). Our results confirmed weight-increasing effects of maternal genistein exposure, accompanied by favorable changes in metabolites in the male offspring' urine. Therefore, this research enables us to better understand obesity and predict risk of obesity-related disease by studying metabolites present in the urine.

Effects of Maternal Exposure to Piperonyl Butoxide (PBO) on Behavioral Development in F1-Generation Mice.

Female mice were exposed maternally to piperonyl butoxide (PBO) through diet to provide dietary levels of 0% (control), 0.01%, 0.03%, and 0.09% during gestation and lactation periods, and selected reproductive and neurobehavioral parameters were measured in the F1 generation. There was no adverse effect of PBO on litter size, litter weight, or sex ratio at birth. The average body weights of male offspring decreased significantly in dose-related manners on postnatal days (PNDs) 0, 4, 7, and 14 (p = 0.0019, 0.0096, 0.033, and 0.038, respectively) during the lactation period. In female offspring, the average body weights decreased in dose-related manners on PNDs 0, 4, 7, and 14 (p = 0.0027, 0.0104, 0.0193, and 0.0062, respectively). The survival of dams slightly decreased (p = 0.0209) in the high-dose group during the lactation period. With respect to behavioral developmental parameters, surface righting on PND 7 of male and female offspring was delayed significantly in a dose-related manner (p < 0.001 in each). Swimming direction on PND 7 of male offspring was delayed significantly in a dose-related manner (p < 0.01), and for female offspring it was delayed significantly in the high-dose group (p < 0.05). Swimming head angle on PND 7 of male offspring was delayed significantly in a dose-related manner (p < 0.05). Spontaneous behavior examination in males indicated that rearing increased in the high-dose group in the F1 generation. The dose levels of PBO in the present study produced some adverse effects in neurobehavioral parameters in mice.

Safety assessment of Hibiscus sabdariffa after maternal exposure on male reproductive parameters in rats

Context: Hibiscus sabdariffa L. (Malvaceae) is a species widely used in folk medicine for the treatment of some disorders. Objective: This study evaluated the effects of H. sabdariffa (HS) on the development of the male reproductive tract in rats following in utero exposure. Materials and methods: Pregnant rats received 250 or 500 mg/kg of HS extract or vehicle from gestational day 12 until day 21 of lactation. Results and discussion: Both doses of HS increased the body weight of male offspring at weaning, without compromising the puberty onset parameters. At puberty, there was a significant increase in the vas deferens absolute weight and a significant reduction in the relative weight of kidney at higher dose. These animals also presented a significant reduction in the sperm number in the caput/corpus of epididymis after exposure to both doses and a reduction in the sperm number in the cauda epididymis for the lower dose. At adulthood, the highest dose significantly reduced the sperm production in relation to controls and both doses provoked a reduction in the relative sperm number in the epididymis without affecting the sperm morphology. Conclusion: These findings demonstrated that maternal exposure to H. sabdariffa can adversely influence the male reproductive system in rats.

Multigeneration Reproduction and Male Developmental Toxicity Studies on Atrazine in Rats

BACKGROUNDReproductive toxicity of Atrazine (ATR) was evaluated in two rat multigenerational studies. Development of male reproductive parameters was evaluated in separate studies after prenatal or postnatal exposure.METHODSIn multigenerational studies, rats received dietary concentrations of 0, 10, 50, 100 or 500 ppm ATR. In separate studies in female rats, ATR was administered by gavage at 0, 1, 5, 25 or 125 mg/kg/day during pregnancy (GD6–21) or lactation (LD2–21). Plasma testosterone concentration, testicular and epididymal weights, and sperm counts were measured in male offspring on PND70 and 170.RESULTSIn the multigenerational studies, parental systemic toxicity occurred at 500 ppm (38.7 mg/kg/day), but reproductive endpoints were unaffected. In the prenatal study, maternal toxicity and embryo-fetal mortality occurred at 125 mg/kg/day. In male offspring, testosterone levels and sperm counts were unaffected, although the percentage of abnormal sperm increased at 125 mg/kg/day (PND 70) and 25 mg/kg/day (PND170). In the postnatal study, maternal toxicity and reduced body weights of male offspring occurred at 125 mg/kg/day. Additionally, reduced testicular (PND70, PND170) and epididymal (PND70) weights and increased numbers of abnormal sperm (PND70, PND170) were seen, but no changes in plasma testosterone or sperm counts.CONCLUSIONSDietary administration of ATR did not affect rat reproduction up to a parentally toxic dose of 38.7 mg/kg/day. Some effects on male reproductive system development occurred after high dose, bolus administration to dams, but doses were much higher than expected under normal use conditions. Thus, oral RfDs for ATR would be protective for reproductive effects

Exposure to a maternal n-3 fatty acid-deficient diet during brain development provokes excessive hypothalamic–pituitary–adrenal axis responses to stress and behavioral indices of depression and anxiety in male rat offspring later in life

Brain docosahexaenoic acid (DHA, 22:6n-3) accumulates rapidly during brain development and is essential for normal neurological function. The aim of this study was to evaluate whether brain development was the critical period in which DHA deficiency leads to dysregulation of the hypothalamic–pituitary–adrenal (HPA) axis in response to stress later in life. Rats were exposed to an n-3 fatty acid-deficient diet or the same diet supplemented with fish oil as an n-3 fatty acid-adequate diet either throughout the preweaning period from embryo to weaning at 3 weeks old or during the postweaning period from 3 to 10 weeks old. Exposure to the n-3 fatty acid-deficient diet during the preweaning period resulted, at weaning, in a significant decrease in hypothalamic DHA levels and a reduced male offspring body weight. DHA deficiency during the preweaning period significantly increased and prolonged restraint stress-induced changes in colonic temperature and serum corticosterone levels, caused a significant increase in GABAA antagonist-induced heart rate changes and enhanced depressive-like behavior in the forced swimming test and anxiety-like behavior in the plus-maze test in later life. These effects were not seen in male rats fed the n-3 fatty acid-deficient diet during the postweaning period. These results suggest that brain development is the critical period in which DHA deficiency leads to excessive HPA responses to stress and elevated behavioral indices of depression and anxiety in adulthood. We propose that these effects of hypothalamic DHA deficiency during brain development may involve a GABAA receptor-mediated mechanism.

A cross-fostering study in a genetic animal model of depression: Maternal behavior and depression-like symptoms

Connections between maternal behavior and childhood depression were examined by using a “genetic animal model”; Flinder Sensitive Line — (FSL) rats, and cross-fostering the offspring with the control strain, Sprague Dawley (SD) rats. The control procedure was “in-fostering”, where the foster dam and her pups were from the same strain. Contribution of pups' characteristics/genotype to maternal behavior was examined. After weaning, we measured male offspring's body weight, immobility in the swim test, and basal corticosterone (CORT) and adrenocorticotropin (ACTH) levels at the prepubertal age of 35 days. While maternal behavior (of “depressive-like” dams and their controls) was not altered significantly by the pups' strain, the adoption procedure per se appeared to have more adverse effects on “depressive-like” symptoms of the SD prepubertal rats than on the FSL pups. Nevertheless, the combination between abnormal maternal behavior and genetic predisposition affected the hormonal stress responses of the offspring in a more severe manner than genetic predisposition or abnormal maternal behavior per se.

Two low protein diets differentially affect food consumption and reproductive performance in pregnant and lactating rats and long-term growth in their offspring.

We fed 2 low protein diets (LPD) to rats during pregnancy and lactation, and compared food intake and reproductive performance in the dams, and long-term growth in their offspring. The L93 and LM76 LPDs were derived from the American Society of Nutrition's recommended AIN93G and a modified version of the AIN76A purified control diets, respectively. The LPDs contained 8% crude protein in the form of casein and differed in their fat and carbohydrate sources. The purified control diets contained 19% crude protein. A regular cereal-based diet was also included, therefore, a total of 5 groups were tested. Blood urea nitrogen concentrations in dams of both LPD groups were lower than their respective controls, confirming decreased protein intake. The LM76 diet lowered food consumption of dams and produced energy malnourishment during pregnancy that persisted throughout lactation. In contrast, the L93 diet produced energy malnourishment only during lactation. Offspring of both LPD groups exhibited lower birth weights than their respective controls. Despite initiating nutritional rehabilitation at weaning (d 28), perinatal administration of both low protein diets produced long-term reductions in the body weight of male offspring. Interestingly, in the female offspring, the LM76 diet reduced birth weight for the entire duration of the study (180 d), whereas the L93 diet produced a relatively short-term (up to 58 d) reduction in body weight. This suggests that the imprinting effect of the perinatal nutritional environment on body weight is diet and gender dependent. The performance of the purified control diet groups were similar to the nonpurified diet group in most measured biochemical indices, with the notable exception of a decrease in the body-weight normalized kidney weight of the dams.

The effects of maternal exposure to 2,3,7,8‐tetrachlorodibenzo‐p‐dioxin on testicular steroidogenesis in infantile male rats

Exposure of adult male animals to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) decreases serum androgen concentrations. Reduction in androgen levels after maternal exposure has also been reported, but these results have not been reproduced. We have earlier shown that TCDD stimulates rather than inhibits testosterone synthesis in the prenatal rat testis. The aim of the present study was to elucidate in utero-induced effects of TCDD on testicular steroidogenesis in the 14-day-old infant rats. At that time the foetal Leydig cell population is still the prevailing source of androgens. Pregnant Sprague-Dawley dams were given a single oral dose of TCDD (0, 0.04, 0.2, or 1.0 microg/kg) on day 13 of pregnancy. On postnatal day 14, the body weight of male offspring was reduced after exposure to 1.0 microg/kg TCDD (from 33.9 +/- 1.66 g to 31.6 +/- 2.67 g). Relative testis weight, plasma testosterone, luteinizing hormone and follicle-stimulating hormone levels remained unaltered in all exposure groups. Moreover, in ex vivo incubations, testosterone and cAMP production was not affected. StAR protein level in the freshly isolated testes was increased in the 0.2 microg/kg group, and seminiferous cord diameter in the 0.04 microg/kg group. The present study confirms our earlier findings in in utero TCDD-exposed foetal testis indicating that maternal TCDD exposure does not negatively influence the developmental testosterone production of foetal type Leydig cells in rats.

Reproductive and neurobehavioural toxicity study of tartrazine administered to mice in the diet

Tartrazine was given in the diet to provide levels of 0% (control), 0.05%, 0.15%, and 0.45% (approximately 83, 259, 773 mg/kg/day, respectively) from five weeks of age of the F 0 generation to nine weeks of age of the F 1 generation in mice, and selected reproductive and neurobehavioural parameters were measured. In movement activity of exploratory behaviour in the F 0 generation, number of vertical activity was significantly increased in the middle-dose group in males. There were no adverse effects of tartrazine on either litter size, litter weight and sex ratio at birth. The average body weight of male offspring was significantly increased in the high-dose group and that of female offspring was significantly increased in the middle-dose group at birth. In behavioural developmental parameters, surface righting at PND 4 was significantly accelerated in the high-dose group in male offspring, and those effects were significantly dose-related in a trend test ( P < 0.01). Cliff avoidance at PND 7 was significantly accelerated in the middle-dose group in male offspring. Negative geotaxis at PND 4 was significantly delayed in the high-dose group in female offspring. Other variables measured showed no significant adverse effects in either sex in the lactation period. In movement activity of exploratory behaviour in the F 1 generation, number of movement showed a significant tendency to be affected in the treatment groups in male offspring in a trend test ( P < 0.05). The dose level of tartrazine in the present study produced a few adverse effects in neurobehavioural parameters during the lactation period in mice. Nevertheless, the high-dose level were in excess of the ADI of tartrazine (0–7.5 mg/kg bw), and the actual dietary intake of tartrazine is presumed to be much lower. It would therefore appear that the levels of actual dietary intake of tartrazine is unlikely to produce any adverse effects in humans.

Effect of prenatal or perinatal nicotine exposure on neonatal thyroid status and offspring growth in rats

Smoking during pregnancy causes intrauterine growth retardation and low birth weight of the offspring. However, it is unclear whether nicotine, rather than other compounds from a cigarette, would mediate long-term growth retardation. There is a body of evidence suggesting that optimal thyroid status is important for the normal development of the fetus. Therefore, these studies examined whether developmental nicotine exposure would interfere with the growth of the offspring and alter the thyroid status of neonates. Pregnant Sprague-Dawley rats were given 0, 15 or 25 mg nicotine pellets throughout pregnancy. Some offspring continued to receive 1 or 2 mg/kg/day nicotine during early postnatal period. The remaining offspring received no further treatment after birth. The body weight of all offspring was monitored until adulthood. Additionally, the neonatal thyroid status from all treatment groups was assessed from the serum of 10-day-old pups. Regardless of the timing of nicotine exposure, the nicotine treatment significantly increased the body weight in female offspring starting on postnatal day (PD) 35 and such an increase persisted into adulthood (PD 91). However, this nicotine exposure paradigm led to a transient increase in male offspring body weight on PD 35. Furthermore, current nicotine exposure regimens did not alter the total T4 level, T3 uptake and the calculated Free T4 index. The present findings are in agreement with some clinical studies reporting a higher body weight among children born to mothers who smoked during pregnancy. Furthermore, the data on thyroid status suggest that cigarette smoking-induced alterations in thyroid status might be mediated through compounds in cigarettes other than nicotine.

Effect of the Age of Pregnant Females on Brain Development in the Offspring

We examined offspring of 9-10 and 3.5-4 month-old female rats. Female offspring (14, 21, 28, 35, and 40 days) of old rats had higher body weight than offspring of young animals. No intergroup differences were revealed in the body weight of male offspring. At the age of 40 days the offspring of old females differed from the offspring of young rats by higher absolute weight of the brain (females), lower size of ganglionic neurons in the parietal lobe (males and females), and lower blood testosterone concentration (males). Thirty-day-old offspring of old rats exhibited higher locomotor activity and lower degree of anxiety compared to the offspring of young animals.

Prenatal immune challenge affects growth, behavior, and brain dopamine in offspring.

It is known that the development and plasticity of the neuroendocrine system can be affected by many factors, and that adverse events during the prenatal period can result in long-lasting changes in adulthood. This study was aimed at evaluating the possible consequences for offspring from chronic inflammation during pregnancy. Chronic inflammation was simulated by treatment with increasing doses of lipopolysaccharide (LPS) to dams on days 15 through 19 of pregnancy. Attempts were made to prevent possible negative alterations by keeping animals in an enriched environment (EE). Maternal exposure to LPS resulted in a significant reduction of body weight of male offspring during the weaning period. This difference remained until the age of 63 days in controls (C), but not in animals reared in EE. The content of dopamine in the nucleus accumbens was found to be lower in prenatally stressed (PS) adult males. Furthermore, prenatal exposure to maternal immune challenge was associated with lower locomotor activity in elevated plus maze and increased number of skips in the beam-walking test, as observed in female offspring. No differences in ACTH and corticosterone concentrations with regard to prenatal treatment were found; however, both groups kept in EE showed increased levels of corticosterone as well as enlarged adrenal glands. Thus, immune activation during pregnancy may induce long-term changes in brain catecholamines and behavior, but it is not harmful to basal hormone secretion in the offspring.

Effects of bis(2-ethylhexyl) phthalate (DEHP) on secondary sex ratio of mice in a cross-mating study

Bis(2-ethylhexyl) phthalate (DEHP) was given in the diet to provide levels of 0 (C) or 0.03% (T) from 5 weeks of age of the F 0 generation to birth of the F 1 generation in mice. At 9 weeks of age, each female was paired with one male from the same or another treatment groups (cross-mating: C/C, T/C, C/T, T/T), for a period of 5 days. The males were removed from females after 5 days, and the females were allowed to carry their litters to term and deliver. There were no adverse effects of DEHP on either litter size, litter weight and sex ratio at birth. The average body weight of male offspring was significantly increased in all treatment groups at birth. There were no adverse effects of DEHP on female offspring weight at birth. The dose level of DEHP in the present study produced no adverse effects on secondary sex ratio, which meant sex ratio at birth, in mice.