scholarly journals Neonatal mice exposed to a high-fat dietin uteroinfluence the behaviour of their nursing dam

2018 ◽  
Vol 285 (1891) ◽  
pp. 20181237 ◽  
Author(s):  
Marine Baptissart ◽  
Harold E. Lamb ◽  
Kimberly To ◽  
Christine Bradish ◽  
Jesse Tehrani ◽  
...  

The behaviour of a nursing dam influences the development, physiology, and behaviour of her offspring. Maternal behaviours can be modulated both by environmental factors, including diet, and by physical or behavioural characteristics of the offspring. In most studies of the effects of the environment on maternal behaviour, F0dams nurse their own F1offspring. Because the F1are indirectly exposed to the environmental stressorin uteroin these studies, it is not possible to differentiate between effects on maternal behaviour from direct exposure of the dam and those mediated by changes in the F1as a consequence ofin uteroexposure. In this study, we used a mouse model of high-fat (HF) diet feeding, which has been shown to influence maternal behaviours, combined with cross-fostering to discriminate between these effects. We tested whether the diet of the F0dam or the exposure experienced by the F1pupsin uterois the most significant predictor of maternal behaviour. Neither factor significantly influenced pup retrieval behaviours. However, strikingly, F1in uteroexposure was a significant predictor of maternal behaviour in the 15 min immediately following pup retrieval while F0diet had no discernable effect. Our findings suggest thatin uteroexposure to HF diet programmes physiological changes in the offspring which influence the maternal behaviours of their dam after birth.

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Showall Moazzam ◽  
Noshin Noorjahan ◽  
Jessica S Jarmasz ◽  
Yan Jin ◽  
Tabrez J Siddiqui ◽  
...  

Abstract Background: About a third of pregnant women of age 20-39 are obese, which carries significant risks for the mother and fetus, and adversely impacts pregnancy outcome. Specifically, women with obesity are at increased risk for peripartum depression. Maternal behaviour in mice is influenced by changes in hormone signaling in pregnancy, which is associated with effects on adult neurogenesis in the brain. Thus, we used mouse as a model system to gain further insight into the possible relationship between overeating/obesity and brain physiology and maternal behaviour. Objective: To assess the ability of a high-fat diet (HFD) versus a regular chow diet (CD), starting up to 10 weeks pre-pregnancy, to modify glucose clearance before and during pregnancy and affect maternal behaviour in the CD1 mouse. Study Design: Two groups of 3-4 week-old female CD1 mice were fed a HFD (fat=60 kcal%; carbohydrate=20 kcal%; protein=20 kcal%) or CD (fat=14 kcal%; carbohydrate=60 kcal%; protein=26 kcal%) and maintained on their respective diets throughout the study and weighed periodically. After at least 4 weeks of feeding on their diets, mice were allowed to breed. Glucose tolerance was tested using 2 g/kg of i.p. glucose at gestational day (GD) -1) after fasting (16 hours-overnight) as well as during pregnancy at GD16.5. An even number of pregnant and non-pregnant females were selected for each diet for maternal behaviour testing. Tests include an assessment of nest building at GD16.5-17 (use of nesting material and nest quality), and after birth pup retrieval at postpartum day (PD) 3, 4 and 5 (time of retrieval of each of the four pups within six minutes) using video capture. Results: The HFD led to a significant increase in weight relative to mice fed a CD. HFD impaired glucose-load clearances at GD -1 and 16.5 (p<0.05) compared to mice fed a CD. Mice fed on HFD performed poorly in the nest building task (p<0.01) as well as demonstrated a reduced completion rate on the pup retrieval test on PD3 (CD=8/10 vs. HFD 2/9 mice) but their retrieval response latency was improved by PD4 (CD=8/10 vs. HFD 8/9 mice) and PD5 (CD=7/10 vs. HFD 7/9 mice). Conclusions: Initial observations suggest that a HFD for at least 4 weeks before and during pregnancy results in overweight CD1 mice with impaired glucose clearance, and a negative effect on maternal behaviour as assessed by nest-building during pregnancy and pup retrieval postpartum; however, with regard to the latter, mice on the HFD show the ability to learn. Additional behavioural tests for locomotion, anxiety, risk avoidance and object recognition memory during or after pregnancy, as well as associated changes in hormonal signaling and adult neurogenesis are also currently under investigation.


1985 ◽  
Vol 59 (2) ◽  
pp. 408-412 ◽  
Author(s):  
A. R. Gwosdow ◽  
E. L. Besch ◽  
C. L. Chen

The physiological changes in male rats during acclimation were studied following direct or stepwise exposure to heat (32.5 degrees C) in a controlled-environment room. The animals were exposed to each temperature for 10 days beginning at 24.5 degrees C and returning to 24.5 degrees C in the reverse order of initial exposure. Relative humidity of 50 +/- 2% and a 12-h light-dark photoperiod (light from 0900 to 2100 h) were maintained. Physiological changes in metabolic rate (MR), evaporative water loss (EWL), plasma corticosterone, body water turnover, and food and water intake were measured. The results indicate a significantly (P less than 0.001) elevated plasma corticosterone and MR in rats exposed directly to heat from control temperature (24.5 degrees C) but not in those animals exposed stepwise via 29.0 degrees C. All kinetic parameters of water pool changed (P less than 0.01) on direct exposure to heat, whereas rats exposed in a stepwise manner increased only pool turnover. In addition, exposure to experimental temperatures resulted in reduced (P less than 0.05) relative food intake and increased (P less than 0.05) water intake. Compared with the control condition of 24.5 degrees C, EWL was significantly (P less than 0.05) elevated when the animals were exposed either directly or in a stepwise fashion to 32.5 degrees C. These data suggest that the response to elevated temperatures is influenced by the temperature to which the rat is acclimated.


Reproduction ◽  
1963 ◽  
Vol 5 (2) ◽  
pp. 133-141 ◽  
Author(s):  
V. H. DENENBERG ◽  
L. J. GROTA ◽  
M. X. ZARROW

2008 ◽  
Vol 22 (S1) ◽  
Author(s):  
Torsten Plosch ◽  
Esther M.E. Straten ◽  
Nicolette C.A. Huijkman ◽  
Juul F.W. Baller ◽  
Folkert Kuipers

2015 ◽  
Vol 46 (4) ◽  
pp. 855-863 ◽  
Author(s):  
S. Z. Levine ◽  
I. Levav ◽  
Y. Goldberg ◽  
I. Pugachova ◽  
Y. Becher ◽  
...  

BackgroundNo evidence exists on the association between genocide and the incidence of schizophrenia. This study aims to identify critical periods of exposure to genocide on the risk of schizophrenia.MethodThis population-based study comprised of all subjects born in European nations where the Holocaust occurred from 1928 to 1945, who immigrated to Israel by 1965 and were indexed in the Population Register (N = 113 932). Subjects were followed for schizophrenia disorder in the National Psychiatric Case Registry from 1950 to 2014. The population was disaggregated to compare groups that immigrated before (indirect exposure: n = 8886, 7.8%) or after (direct exposure: n = 105 046, 92.2%) the Nazi or fascist era of persecutions began. The latter group was further disaggregated to examine likely initial prenatal or postnatal genocide exposures. Cox regression modelling was computed to compare the risk of schizophrenia between the groups, adjusting for confounders.ResultsThe likely direct group was at a statistically (p < 0.05) greater risk of schizophrenia (hazard ratio = 1.27, 95% confidence interval 1.06–1.51) than the indirect group. Also, the likely combined in utero and postnatal, and late postnatal (over age 2 years) exposure subgroups were statistically at greater risk of schizophrenia than the indirect group (p < 0.05). The likely in utero only and early postnatal (up to age 2 years) exposure subgroups compared with the indirect exposure group did not significantly differ. These results were replicated across three sensitivity analyses.ConclusionsThis study showed that genocide exposure elevated the risk of schizophrenia, and identified in utero and postnatal (combined) and late postnatal (age over 2 years) exposures as critical periods of risk.


2014 ◽  
Vol 210 (1) ◽  
pp. S42-S43
Author(s):  
Melissa Suter ◽  
Jun Ma ◽  
Patricia Vuguin ◽  
Kirsten Hartil ◽  
Ariana Fiallo ◽  
...  

2014 ◽  
Vol 46 (23) ◽  
pp. 841-850 ◽  
Author(s):  
Sarah J. Borengasser ◽  
Jennifer Faske ◽  
Ping Kang ◽  
Michael L. Blackburn ◽  
Thomas M. Badger ◽  
...  

The proportion of pregnant women who are obese at conception continues to rise. Compelling evidence suggests the intrauterine environment is an important determinant of offspring health. Maternal obesity and unhealthy diets are shown to promote metabolic programming in the offspring. Mitochondria are maternally inherited, and we have previously shown impaired mitochondrial function in rat offspring exposed to maternal obesity in utero. Mitochondrial health is maintained by mitochondrial dynamics, or the processes of fusion and fission, which serve to repair damaged mitochondria, remove irreparable mitochondria, and maintain mitochondrial morphology. An imbalance between fusion and fission has been associated with obesity, insulin resistance, and reproduction complications. In the present study, we examined the influence of maternal obesity and postweaning high-fat diet (HFD) on key regulators of mitochondrial fusion and fission in rat offspring at important developmental milestones which included postnatal day (PND)35 (2 wk HFD) and PND130 (∼16 wk HFD). Our results indicate HFD-fed offspring had reduced mRNA expression of presenilin-associated rhomboid-like (PARL), optic atrophy (OPA)1, mitofusin (Mfn)1, Mfn2, fission (Fis)1, and nuclear respiratory factor (Nrf)1 at PND35, while OPA1 and Mfn2 remained decreased at PND130. Putative transcriptional regulators of mitochondrial dynamics were reduced in rat placenta and offspring liver and skeletal muscle [peroxisome proliferator-activated receptor gamma coactivator (PGC1)α, PGC1β, and estrogen-related receptor (ERR)α], consistent with indirect calorimetry findings revealing reduced energy expenditure and impaired fat utilization. Overall, maternal obesity detrimentally alters mitochondrial targets that may contribute to impaired mitochondrial health and increased obesity susceptibility in later life.


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