Influence of maternal dietary calcium levels on milk zinc, calcium and phosphorus contents and milk production in rats

The aim of this study was to analyze zinc (Zn), calcium (Ca) and phosphorus (P) contents in milk and the lactational performance in rats fed different Ca levels. Female Wistar rats were fed during pregnancy and lactation with experimental diets containing 20% protein and high (0.90%, HCa), normal (0.60%, NCa) or low (0.20%, LCa) Ca levels. Milk samples were collected after 15 days to determine the milk mineral composition. Pup weight was recorded from birth to weaning (litter size: 6-8 pups) to determine weight gain and calculate milk production. At delivery there were no significant differences in the body weight of the pups between the groups, but at day 15, the LCa group showed lower values than both NCa and HCa groups (p<0.05). The weight gain of the LCa group was significantly lower than of the HCa and NCa groups, between delivery and day 5 (p<0.05). This reduced rate of weight gain led to the LCa group reaching weaning weight later than the other groups. Milk production (g/pup/day) was significantly lower when dams were fed the LCa than the NCa and HCa diets (p<0.05). There were no significant differences among the groups in milk Ca, P and Zn levels and Ca/P ratio. The body mineral composition of the pups at birth did not differ between the groups; at weaning, however, both LCa and HCa groups had lower element contents than the NCa group (p<0.05). In conclusion, dams fed with a diet containing low Ca levels produced smaller volumes of milk and their pups reached weaning weights later than the other groups. As the milk mineral composition was not affected, it can be hypothesized that in dams fed low dietary Ca, the smaller milk yield might have been a way of maintaining milk quality. High Ca levels affected neither pregnancy outcome nor lactational performance.     

Effects of feeding endophyte infected tall fescue seed on reproductive performance of female CD-1 mice via competitive breeding

This study was conducted to determine the effects of feeding endophyte-infected (Acremonium coenophialum ) tall fescue (Festuca arundinacea ) seed on the growth and reproductive performance of female CD-1 mice via competitive breeding. One hundred sixty female mice were randomly allocated to groups of ten and fed one of two diets. Diet 1 consisted of 50% mouse chow and 50% noninfected Ky-31 tall fescue seed (w/w). Diet 2 contained 50% chow and 50% tall fescue seed that was 80% infected with A. coenophialum . After 50 d of preconditioning on their respective diets, a single male was introduced into each group of 10 females and allowed to cohabitate for 96 h. The males were removed after the cohabitation period and the females continued through gestation on their respective diets. Body weight of dams and litter weights were recorded at parturition. There were no differences (P>0.05) in pregnancy rates between dietary Treatments 1 and 2 (50% vs 48.8%, respectively). However, the average number of pups born per litter (11.10 pups) and average total litter weight (17.21 g) was greater for those females consuming Diet 1 than for females consuming Diet 2 (9.33 pups per litter and 13.97 g total litter weight). The incidence of dead and cannibalized pups was more frequent with Diet 2 than Diet 1 (0.13 vs 0.0 dead; 0.21 vs 0.03 cannibalized, respectively). The obtained data suggest that although the pregnancy rate was similar between the two dietary treatments, the reproductive capacity (litter size and litter weight) of female CD-1 mice was affected by the consumption of endophyte infected fescue seed.     

Long-term consequences of maternal high-fat feeding on hypothalamic leptin sensitivity and diet-induced obesity in the offspring

Epidemiological and animal studies suggest that the alteration of hormonal and metabolic environment during fetal and neonatal development can contribute to development of metabolic syndrome in adulthood. In this paper, we investigated the impact of maternal high-fat (HF) diet on hypothalamic leptin sensitivity and body weight gain of offspring. Adult Wistar female rats received a HF or a control normal-fat (C) diet for 6 wk before gestation until the end of the suckling period. After weaning, pups received either C or HF diet during 6 wk. Body weight gain and metabolic and endocrine parameters were measured in the eight groups of rats formed according to a postweaning diet, maternal diet, and gender. To evaluate hypothalamic leptin sensitivity in each group, STAT-3 phosphorylation was measured in response to leptin or saline intraperitoneal bolus. Pups exhibited similar body weights at birth, but at weaning, those born to HF dams weighed significantly less (-12%) than those born to C dams. When given the HF diet, males and females born to HF dams exhibited smaller body weight and feed efficiency than those born to C dams, suggesting increased energy expenditure programmed by the maternal HF diet. Thus, maternal HF feeding could be protective against adverse effects of the HF diet as observed in male offspring of control dams: overweight (+17%) with hyperleptinemia and hyperinsulinemia. Furthermore, offspring of HF dams fed either C or HF diet exhibited an alteration in hypothalamic leptin-dependent STAT-3 phosphorylation. We conclude that maternal high-fat diet programs a hypothalamic leptin resistance in offspring, which, however, fails to increase the body weight gain until adulthood.     

Offspring metabolomic response to maternal protein restriction in a rat model of intrauterine growth restriction (IUGR)

Intrauterine growth restriction (IUGR), along with postnatal growth trajectory, is closely linked with metabolic diseases and obesity at adulthood. The present study reports the time-dependent metabolomic response of male offspring of rat dams exposed to maternal adequate protein diet during pregnancy and lactation (CC) or protein deprivation during pregnancy only (IUGR with rapid catch-up growth, RC) or through pregnancy and lactation (IUGR with slow postnatal growth, RR). Plasma LC-HRMS metabolomic fingerprints for 8 male rats per group, combined with multivariate statistical analysis (PLS-DA and HCA), were used to study the impact of IUGR and postnatal growth velocity on the offspring metabolism in early life (until weaning) and once they reached adulthood (8 months). Compared with CC rats, RR pups had clear-cut alterations in plasma metabolome during suckling, but none at adulthood; in contrast, in RC pups, alterations in metabolome were minimal in early life but more pronounced in the long run. In particular, our results pinpoint transient alterations in proline, arginine, and histidine in RR rats, compared to CC rats, and persistent differences in tyrosine and carnitine, compared to RC rats at adulthood. These findings suggest that the long-term deregulation in feeding behavior and fatty acid metabolism in IUGR rats depends on postnatal growth velocity.     

Pregnancy in adolescent rats, growth and neurodevelopment in their offspring

Pregnancy, lactation and the relationship between mother and their offspring in adolescence was studied in terms of pups neurosomatic development. The frequency of conception and birth rate were reduced in adolescent dams. Their body weight gain was accelerated during the first two weeks of pregnancy, while a significant delay occurred in the third week. At birth, plasma corticosterone level in the neonates was increased. Adolescent dams ingested less food during the first week of gestation. Following that, till the second week of lactation, the food consumption was equal to that of control group. Although adolescent pups were heavier at birth, the reduction of their number and of their body weight occurred during lactation. Judging by appearance of grasping, righting, placing and of negative geotaxis reflexes, the delay in their neurological maturation was also present. The reason for the growth and neurodevelopmental delay during lactation is probably the result of malnutrition and stress of disturbed mother - infant relationship in adolescent litters, which lasted at least during the two postnatal weeks. It was indicated by the resting plasma corticosterone levels during the first two postnatal weeks. This finding suggests that the pregnancy in adolescent rats induces delay in physical and neurological development, as well as in the increased rate of postnatal mortality of their offspring.     

Long-term effects of postovulatory aging of mouse oocytes on offspring: a two-generational study.

Aims of this study were to analyze the long-term effects of postovulatory aging of mouse oocytes on 1) reproductive traits of parental (F(0)) and first (F(1))-generation females (pregnancy rate, gestation length, litter size, perinatal death, and sex ratio of offspring) and 2) developmental and behavioral variables of F(1) and second-generation (F(2)) offspring (birth weight and weight gain during preweaning development, postnatal day of attainment of immediate righting, spontaneous motor activity, and passive and active conditioned learning ability). Hybrid (C57BL/6JIco x CBA/JIco) females were artificially inseminated at 13 h (control group) or 22 h (oocyte-aged group) after GnRH injection. Experimental (oocyte-aged group) F(0) females exhibited lower pregnancy rate, shortened gestation length, decreased litter size, higher perinatal death of their pups, and increased percentage of male offspring compared to control F(0) females. Postovulatory aging of oocytes was also associated with increased number of growth-retarded pups, delayed development of the righting reflex, and higher spontaneous motor activity and emotionality of F(1) offspring. Postovulatory aging of F(0) oocytes did not affect birth weight, weight gain during preweaning development, passive and active conditioned learning ability of F(1) offspring, or reproductive traits of F(1) females or developmental and behavior variables of F(2) offspring.     

Onset of puberty in CD-1 mouse pups exposed prenatally through weaning to endophyte-infected tall fescue seed

This study was undertaken to investigate the effects of feeding endophyte - infected (Acremonium coenophialum ) tall fescue seed to CD-1 mouse dams (P(1)) during gestation and lactation, and on the subsequent growth and sexual maturity (onset of puberty) of their male and female offspring (F(1)). Forty-eight 21 d old pups (24 male and 24 female F(1) mice) were weaned from dams fed one of two diets containing 50% rodent chow (w/w) and 50% KY-31 tall fescue (Festuca arundinacea ) seed. The seed in Diet 1 was noninfected, while the seed in Diet 2 was 80% endophyte-infected. At weaning (21 d), the F(1) pups were fed rodent chow, ad libitum throughout the remaining experimental period. At 24 d, they were paired with sexually mature non-treated virgin CD-1 mice (fed 100% rodent chow) for one parturition cycle. Male F(1) mice were sacrificed at 84 d to determine testicular development. The age at the birth of the first litter for Diet 2 F(1) male (76.8 +/- 2.2 d) and female (58.4 +/- 2.1 d) was significantly greater (P<0.05) than the age at parturition for Diet 1 male and female F(1) test mice (64.1 +/- 1.8 and 51.9 +/- 1.2 d, respectively). At parturition, the female F(1) mice showed no significant differences (P>0.05) in either mean parturition weight or number of F(2) pups born per litter. However, total F(2) litter wight (11.38 +/- 1.14 g) and mean weight per F(2) pup (1.40 +/- 0.04 g) for Diet 2 female F(1) mice litters were lower (P<0.05) when compared with Diet 1 females (14.53 +/- 0.57 g and 1.66 +/- 0.02 g, respectively). No significant differences were observed between the two male F(1) treatment groups, for total F(2) litter weight or the number of pups born per F(2) litter. Although Diet 2 F(1) males weighed significantly less (P<0.05) at weaning and at pairing, final body weights at sacrifice (84 d) were not different (P>0.05) from the Diet 1 males.     

Kin Recognition and Maternal Care under Restricted Feeding in House Mice (Mus domesticus)

This study tests the hypothesis that female house mice (F1 generation of wild caught Mus domesticus) should preferentially invest in own offspring if confronted with young of different degrees of relatedness. The maternal behaviour of females with litters of 4 own and 4 unrelated alien young (cross-fostered at day 1 of lactation) was analysed during a lactation period of 22 days both under ad libitum and under restricted feeding (food was restricted by 20%). Cross-fostering and restricted feeding had no effect on the amount of time spent nursing until weaning. Under both feeding conditions the females did not differ in their maternal behaviour towards own and alien young: there were no significant differences either in the amount of time spent nursing own versus alien pups or in the time spent licking own versus alien young. Weight gain of own and alien = wild littermates did not differ significantly in mixed litters and was similar both under ad libitum and under restricted feeding. Such indiscriminate behaviour might be adaptive if female house mice prefer to communally nest with a relative and thus improve their inclusive fitness by investing in own and related offspring in a communal nest. Under moderate restricted feeding females could not wean the entire litter but reduced litter size by cannibalizing on average 2.7 pups (75% of the pups were killed when they were 4–8 days old). Females with cross-fostered litters killed as many own as alien young. This suggests that females cannot discriminate between own and unrelated young if cross-fostering takes place at day 1 of lactation. Besides testing kin recognition abilities, the experiments also allow analysis of the weaning strategy of females under food shortage. Under restricted feeding, body weight of the females was significantly lower during middle lactation than under ad libitum feeding. Weaning weight of young in reduced litters under food restriction (9–10 g) did not differ significantly from weaning weight of young in litters of 7–10 young, but was lower than that of young in similar sized litters (litter size 6), under ad libitum feeding. The maternal behaviour of cannibalizing some young under food shortage can be interpreted as a weaning strategy which results in the largest number of offspring that can be raised to a minimal weaning weight of 9–10 g. Such a weaning strategy might represent a favourable trade-off between number and size of young produced.     

Offspring growth, survival and reproductive success in the bank vole: a litter size manipulation experiment

To estimate the optimality of brood size, it is essential to study the effects of brood size manipulation on offspring survival and reproductive success. Moreover, testing the generality of the hypothesis of reproductive costs requires experimental data from a diversity of organisms. Here I present data on the growth, survival and reproductive success of bank vole Clethrionomys glareolus individuals from manipulated litters. Furthermore, the survival of mothers whose litter size was manipulated was studied. At weaning, the mean weight of pups from enlarged litters was lower and from reduced litters higher compared to control litters. After winter, at the start of the breeding season, individuals from enlarged litters, especially males, were still lighter than individuals from the other two treatments. Litter enlargements did not increase the number of reproducing female offspring per mother, nor did the litter sizes of female offspring differ between treatments. There were no differences between treatments in winter survival of offspring after weaning, but among female offspring, weaning weight explained the survival probabilities over winter. A higher weight of females at winter determined the probability of starting to reproduce in spring. The survival of mothers did not seem to be influenced by litter manipulation performed the previous year. According to the results, mothers nursing enlarged or reduced litters do not gain any fitness benefits in terms of number of offspring surviving to breeding. The results are consistent with the majority of experiments conducted in birds, which have found costs of enlarged brood appearing as offspring trade-offs rather than parent trade-offs. Received: 14 December 1997 / Accepted: 1 March 1998     

Changes in Blood-Brain Barrier Nutrient Transport in the Offspring of Iodine-Deficient Rats and Their Preventability

Thyroid hormones affect the structure and function of biological membranes. Whether or not they affect the Blood-Brain Barrier nutrient transport, the rate limiting membrane transport regulating nutrient supply to brain is to be established yet. That the impaired brain development and function seen in iodine deficiency could be due to such an effect has been assessed in situ by the brain uptake index (BUI) method in Wistar/NIN rat pups born to dams subjected to dietary iodine deficiency/rehabilitation for different times. Compared to controls (C), there was a significant decrease in the BUI values of 2-Deoxy-D-Glucose (2-DG) and L-leucine (Leu) in the pups (D1) born to dams chronically fed low iodine test (LIT) diet through their active growth and subsequent pregnancy and lactation. Surprisingly transport of L-Tyrosine (Tyr) and sucrose (the background marker) was not altered, nor was the BBB transport of all these nutrients affected by feeding LIT diet during the mothers' gestation (D2) and lactation (D3) only. The hypothyroidism in D1 pups was only moderate and preventable by rehabilitation of mothers with control diet from conception (R1) or parturition (R2), as were the changes in BBB nutrient transport. The results suggest that chronic material dietary iodine deficiency impairs BBB nutrient transport in the offspring and this could be prevented by their rehabilitation with iodine.     

Long-term effects of maternal magnesium restriction on adiposity and insulin resistance in rat pups

Objective: We investigated the long‐term effects of maternal/postnatal magnesium (Mg) restriction on adiposity, glucose tolerance, and insulin secretion in the offspring and the probable biochemical mechanisms associated with them. Methods and Procedures: Female weanling Wistar/NIN (WNIN) rats received a control diet or 70% Mg‐restricted (MgR) diet for 9 weeks and mated with control males. A third of the restricted dams were shifted to control diet from parturition. Half of the pups born to the remaining restricted dams were weaned on to control diet, while the other half continued on MgR diet. Various parameters were determined in the offspring at 18 months of age. Results: The percentage of body fat increased, lean body mass (LBM) and fat free mass (FFM) decreased in restricted offspring and were irreversible by rehabilitation. While glucose tolerance and insulin resistance (IR) were comparable among groups, glucose‐stimulated insulin secretion and basal glucose uptake by the diaphragm were significantly decreased in restricted offspring and not corrected by rehabilitation. Plasma leptin was lower, and tumor necrosis factor‐α (TNF‐α) was higher in restricted offspring, whereas expression of fatty acid synthase (FAS) and fatty acyl transport protein 1 (FATP 1) was higher in liver and adipose tissue. While changes in FAS and FATP 1 were not correctible by rehabilitation, those in leptin and TNF‐α were corrected by rehabilitation from parturition but not from weaning. Tissue oxidative stress and antioxidant status were comparable among groups. Discussion: Results indicate that maternal and postnatal Mg status is important in the long‐term programming of body adiposity and insulin secretion in rat offspring.     

Effects of maternal and grandmaternal flea infestation on offspring quality and quantity in a desert rodent: evidence for parasite-mediated transgenerational phenotypic plasticity

Parasites can cause a broad range of sublethal fitness effects across a wide variety of host taxa. However, a host’s efforts to compensate for possible parasite-induced fitness effects are less well-known. Parental effects may beneficially alter the offspring phenotype if parental environments sufficiently predict the offspring environment. Parasitism is a common stressor across generations; therefore, parental infestation could reliably predict the likelihood of infestation for offspring. However, little is known about relationships between parasitism and transgenerational phenotypic plasticity. Thus, we investigated how maternal and grandmaternal infestation with fleas (Xenopsylla ramesis) affected offspring quality and quantity in a desert rodent (Meriones crassus). We used a fully-crossed design with control and infested treatments to examine litter size, pup body mass at birth, and pup mass gain before weaning for combinations of maternal and grandmaternal infestation status. No effect of treatment on litter size or pup body mass at birth was found. However, maternal and grandmaternal infestation status significantly affected pre-weaning body mass gain, a proxy for the rate of maturation, in male pups. Pups gained significantly more weight before weaning if maternal and grandmaternal infestation statuses matched, regardless of the treatment. Thus, pups whose mothers and grandmothers experienced similar risks of parasitism, either both non-parasitized or both infested, would reach sexual maturity more quickly than those pups whose mothers’ infestation status did not match that of their grandmothers. These results support the contention that parents can receive external cues such as the risk of parasitism, that prompt them to alter offspring provisioning. Therefore, parasites could be a mediator of environmentally-induced maternal effects and could affect host reproductive fitness across multiple generations.     

Involvement of the GHSR in the developmental programming and metabolic disturbances induced by maternal undernutrition

The mismatch between maternal undernutrition and adequate nutrition after birth increases the risk of developing metabolic diseases. We aimed to investigate whether the hyperghrelinemia during maternal undernourishment rewires the hypothalamic development of the offspring and contributes to the conversion to an obese phenotype when fed a high-fat diet (HFD). Pregnant C57BL/6 J, wild type (WT) and ghrelin receptor (GHSR)^−/− mice were assigned to either a normal nourished (NN) group, or an undernutrition (UN) (30% food restricted) group. All pups were fostered by NN Swiss mice. After weaning, pups were fed a normal diet, followed by a HFD from week 9. Plasma ghrelin levels peaked at postnatal day 15 (P15) in both C57BL/6 J UN and NN pups. Hypothalamic Ghsr mRNA expression was upregulated at P15 in UN pups compared to NN pups and inhibited agouti-related peptide (AgRP) projections. Adequate lactation increased body weight of UN WT but not of GHSR^−/− pups compared to NN littermates. After weaning with a HFD, body weight and food intake was higher in WT UN pups but lower in GHSR^−/− UN pups than in NN controls. The GHSR prevented a decrease in ambulatory activity and oxygen consumption in UN offspring during ad libitum feeding. Maternal undernutrition triggers developmental changes in the hypothalamus in utero which were further affected by adequate feeding after birth during the postnatal period by affecting GHSR signaling. The GHSR contributes to the hyperphagia and the increase in body weight when maternal undernutrition is followed by an obesity prone life environment.     

Chronic hypoxia exposure during pregnancy is associated with a decreased active nursing activity in mother and an abnormal birth weight and postnatal growth in offspring of rats

Stress during pregnancy is known to have a significant impact on animal's behavior and offspring development. The effects of gestational hypoxia on maternal behavior have not been studied. In the present study, we investigated the effects of gestational hypoxia exposure on dam's maternal behavior, offspring's growth and plasma corticosterone levels after parturition in rats. Altitude hypoxia (3 and 5 km) was simulated in the hypobaric chambers during the last week of pregnancy and the effects were compared to those found in controls exposed at sea level. We found that gestational hypoxia significantly decreased dam's arched-back nursing activity across the lactation period. The effect was more profound in 5 km group. Gestational hypoxia also altered other maternal behaviors such as blanket and passive nursing. Hypoxia exposure was associated with abnormal birth weight and postnatal growth in pups, with a significantly higher and lower birth weight than control found in 3 and 5 km groups, respectively, and accelerated growth in both stressed groups. Gestational hypoxia exposure significantly elevated plasma corticosterone levels in dams at the time of weaning and in pups across the measurement days. Taken together, the present results indicate that hypoxia, particularly severe hypoxia during the late phase of pregnancy has a significantly adverse impact on animal's behavior, endocrine function and offspring development. The higher birth weight found in the offspring of 3 km group suggests a compensatory system counteracting with the inhibitory effects of hypoxia on fetus growth at this altitude.     

Hormonal manipulation of offspring number: maternal effort and reproductive costs

We used exogenous gonadotropin hormones to physiologically enlarge litter size in the bank vole (Clethrionomys glareolus). This method allowed the study design to include possible production costs of reproduction and a trade-off between offspring number and body size at birth. Furthermore, progeny rearing and survival and postpartum survival of the females took place in outdoor enclosures to capture salient naturalistic effects that might be present during the fall and early winter. The aim of the study was to assess the effects of the manipulation on the growth and survival of the offspring and on the reproductive effort, survival, and future fecundity of the mothers. Mean offspring body size was smaller in enlarged litters compared to control litters at weaning, but the differences disappeared by the winter. Differences in litter sizes disappeared before weaning age due to higher mortality in enlarged litters. In addition to the effects of the litter size, offspring performance was probably also influenced by the ability of the mother to support the litter. Experimental females had higher reproductive effort at birth, and they also tended to have higher mortality during nursing. Combined effects of high reproductive effort at birth and high investment in nursing the litter entailed costs for the experimental females in terms of decreased probability of producing a second litter and a decreased body mass gain. Thus, enlarged litter size had both survival and fecundity costs for the mothers. Our results suggest that the evolution of litter size and reproductive effort is determined by reproductive costs for the mothers as well as by a trade-off between offspring number and quality.     

Experimental manipulation of breeding density and litter size: effects on reproductive success in the bank vole

1. Reproductive success of individual females may be determined by density-dependent effects, especially in species where territory provides the resources for a reproducing female and territory size is inversely density-dependent.
2. We manipulated simultaneously the reproductive effort (litter size manipulation: ± 0 and + 2 pups) and breeding density (low and high) of nursing female bank voles Clethrionomys glareolus in outdoor enclosures. We studied whether the reproductive success (number and quality of offspring) of individual females is density-dependent, and whether females can compensate for increased reproductive effort when not limited by saturated breeding density.
3. The females nursing their young in the low density weaned significantly more offspring than females in the high density, independent of litter manipulation.
4. Litter enlargements did not increase the number of weanlings per female, but offspring from enlarged litters had lower weight than control litters.
5. In the reduced density females increased the size of their home range, but litter manipulation had no significant effect on spacing behaviour of females. Increased home range size did not result in heavier weanlings.
6. Mother's failure to successfully wean any offspring was more common in the high density treatment, whereas litter manipulation or mother's weight did not affect weaning success.
7. We conclude that reproductive success of bank vole females is negatively density-dependent in terms of number, but not in the quality of weanlings.
8. The nursing effort of females (i.e. the ability to provide enough food for pups) seems not to be limited by density-dependent factors.     

Suckling ability and maternal prolactin levels in hypothyroid rats

Long-Evans rats and their offspring were made hypothyroid by addition of the antithyroid goitrogen 6-N-propylthiouracil (PTU) to the drinking water (0.1%) from the day of parturition. Serum concentrations of prolactin (PRL), thyroid-stimulating hormone (TSH) and thyroxine (T4) were determined by double radioimmunoassay (RIA). From the fifth postnatal day, body weight of PTU-treated pups was significantly lower than that of control rats, and a strikingly elevated serum TSH level and nondetectable amount of T4 were measured both in PTU-exposed mothers and their offspring at Day 10 postpartum. To test the youngs' suckling capability and the amount of maternal milk production, 10- and 15-day-old normal and PTU-treated pups were separated from their mothers for 4 hr in the morning and then reunited and allowed to suckle. Normal pups gained body weight at the end of both the first and second hour postreunion, while PTU pups gained only during the first hour and lost weight in the second hour of testing. When the pups were exchanged between normal and PTU mothers, opposite results were obtained, indicating that the reduced gain in hypothyroid rats was not due to impaired suckling capability, or insufficient sensory stimulation for milk secretion but to a decreased milk production of PTU mothers. In accordance with this, in lactating hypothyroid rats both the basal (presuckling) level and the suckling-induced rise of serum PRL were found significantly depressed.     

Pyrroloquinoline quinone improves growth and reproductive performance in mice fed chemically defined diets

Growth, reproductive performance, and indices of collagen maturation and expression were investigated in Balb/c mice fed chemically defined, amino acid-based diets with or without the addition 6 micro Mpyrroloquinoline quinone (PQQ)/kg diet. The diets were fed to virgin mice for 8 weeks before breeding. At weaning, the pups from successful pregnancies were fed the same diet as their respective dams. Reproductive performance was compromised in mice fed diets devoid of PQQ, and their offspring grew at slower rates than offspring from mice fed diets supplemented with PQQ. Successful mating (confirmed vaginal plugs) was not affected by the presence or absence of PQQ; however, pup viability (number of pups at parturition/number of pups at Day 4 of lactation) was decreased in PQQ-deprived mice. Conception (percentage of females giving live births) and fertility (percentage of births) were also decreased in PQQ-deprived mice. The slower rates of growth in offspring from PQQ-deprived mice were associated with decreased steady-state mRNA levels for Type I procollagen alpha(1)-chains in skin and lungs from neonatal mice. Values for lysyl oxidase accumulation as protein in PQQ-deficient mice also tended to be lower than corresponding values from PQQ-supplemented or -replete mice. Skin collagen solubility was increased in PQQ-deprived mice. These results indicate that PQQ supplementation can improve reproductive performance, growth, and may modulate indices of neonatal extracellular matrix production and maturation in mice fed chemically defined, but otherwise nutritionally complete diets.     

Chronic Maternal Vitamin B12 Restriction Induced Changes in Body Composition & Glucose Metabolism in the Wistar Rat Offspring Are Partly Correctable by Rehabilitation

Maternal under-nutrition increases the risk of developing metabolic diseases. We studied the effects of chronic maternal dietary vitamin B12 restriction on lean body mass (LBM), fat free mass (FFM), muscle function, glucose tolerance and metabolism in Wistar rat offspring. Prevention/reversibility of changes by rehabilitating restricted mothers from conception or parturition and their offspring from weaning was assessed. Female weaning Wistar rats (n = 30) were fed ad libitum for 12 weeks, a control diet (n = 6) or the same with 40% restriction of vitamin B12 (B12R) (n = 24); after confirming deficiency, were mated with control males. Six each of pregnant B12R dams were rehabilitated from conception and parturition and their offspring weaned to control diet. While offspring of six B12R dams were weaned to control diet, those of the remaining six B12R dams continued on B12R diet. Biochemical parameters and body composition were determined in dams before mating and in male offspring at 3, 6, 9 and 12 months of their age. Dietary vitamin B12 restriction increased body weight but decreased LBM% and FFM% but not the percent of tissue associated fat (TAF%) in dams. Maternal B12R decreased LBM% and FFM% in the male offspring, but their TAF%, basal and insulin stimulated glucose uptake by diaphragm were unaltered. At 12 months age, B12R offspring had higher (than controls) fasting plasma glucose, insulin, HOMA-IR and impaired glucose tolerance. Their hepatic gluconeogenic enzyme activities were increased. B12R offspring had increased oxidative stress and decreased antioxidant status. Changes in body composition, glucose metabolism and stress were reversed by rehabilitating B12R dams from conception, whereas rehabilitation from parturition and weaning corrected them partially, highlighting the importance of vitamin B12 during pregnancy and lactation on growth, muscle development, glucose tolerance and metabolism in the offspring.     

Brain serotonin determines maternal behavior and offspring survival

Maternal care is an indispensable component of offspring survival and development in all mammals and necessary for reproductive success. Although brain areas regulating maternal behaviors are innervated by serotonergic afferents, very little is known about the role of this neurotransmitter in these behaviors. To evaluate the contribution of serotonin to maternal care, we used mice with a null mutation in the gene for tryptophan hydroxylase‐2 (TPH2), which results in a genetic depletion of brain serotonin, and tested them in a wide range of maternal behavior paradigms. We found that litters born to and reared by TPH2^?/? mothers showed decreased survival, lower weaning weights and increased cannibalization. In addition, TPH2^?/? mothers performed poorly in pup retrieval, huddling, nest construction and high‐arched back nursing. Aggression in TPH2^?/? dams was not triggered by lactation and was steadily high. Survival and weaning weight deficits of TPH2^?/? pups were rescued by cross‐fostering and in litters of mixed genotype (TPH2^?/? and TPH2^?/+). However, the maternal behaviors of TPH2^?/? dams did not improve when rearing either TPH2^+/+ pups or mixed‐genotype litters. In addition, TPH2^?/? pups significantly worsened the behavior of TPH2^+/+ dams with respect to cannibalism, weaning weight and latency to attack. Olfactory and auditory functions of TPH2^?/? females or anxiety‐like behaviors did not account for these maternal alterations as they were equal to their TPH2^+/+ counterparts. These findings illustrate a profound influence of brain serotonin on virtually all elements of maternal behavior and establish that TPH2^?/? pups can engender maladaptive mothering in dams of both genotypes.