scholarly journals Particulate Matter Exposure During Perinatal Life Results in Impaired Glucose Metabolism in Adult Male Rat Offspring

2018 ◽  
Vol 49 (1) ◽  
pp. 395-405 ◽  
Author(s):  
Rosiane Aparecida Miranda ◽  
Claudinéia Conationi da Silva Franco ◽  
Carina Previate ◽  
Vander Silva Alves ◽  
Flávio Andrade Francisco ◽  
...  
Keyword(s):  
Particulate Matter ◽  
Air Quality ◽  
Glucose Metabolism ◽  
Urban Area ◽  
Corn Oil ◽  
Disease Incidence ◽  
Later Life ◽  
Male Offspring ◽  
Male Rat ◽  
Rat Offspring

Background/Aims: Particulate matter (PM) is an important risk factor for immunological system imbalance due to its small size, which can reach more distal regions of the respiratory tract, independently of its chemical composition. Some studies have suggested that PM exposure is associated with an increased incidence of diabetes, especially in industrialized urban regions. However, studies regarding the effects of PM exposure during perinatal life on glucose metabolism are limited. We tested whether exposure to PM from an urban area with poor air quality during pregnancy and lactation could cause short- and long-term dysfunction in rat offspring. Methods: Samples of < 10 µm PM were collected in an urban area of Cotonou, Benin (West Africa), and reconstituted in corn oil. Pregnant Wistar rats received 50 µg PM/day by gavage until the end of lactation. After birth, we analyzed the dams’ biochemical parameters as well as those of their male offspring at 21 and 90 days of age. Results: The results showed that PM exposure did not lead to several consequences in dams; however, the male offspring of both ages presented an increase of approximately 15% in body weight. Although the blood glucose levels remained unchanged, the insulin levels were increased 2.5- and 2-fold in PM exposure groups of both ages, respectively. HOMA-IR and HOMA-β were also increased at both ages. We also demonstrated that the number, islet area and insulin immunodensity of pancreatic islets were significantly increased at both ages from PM exposure. Conclusion: Our data show that chronic PM exposure by the oral route during perinatal life in rats leads to glucose dyshomeostasis in male offspring both in early and later life. Thus, we suggest that an ambience with poor air quality, mainly where traffic is dense, can contribute to an increase in metabolic disease incidence.

Maternal exposure to low doses of bisphenol A affects learning and memory in male rat offspring with abnormal N-methyl-d-aspartate receptors in the hippocampus

2021 ◽  
pp. 074823372098462
Author(s):  
Chong Wang ◽  
Yao Shu ◽  
Li Xu ◽  
Qiling Liu ◽  
Bei Zhang ◽  
...  
Keyword(s):  
Bisphenol A ◽  
Learning And Memory ◽  
Maternal Exposure ◽  
Male Offspring ◽  
Male Rat ◽  
Control Group ◽  
Sprague Dawley ◽  
Expression Levels ◽  
Rat Offspring ◽  
Sprague Dawley Rats

Bisphenol A (BPA), a component of polycarbonate and epoxy resins, has been reported to induce learning and memory deficits. However, the mechanisms have not been fully elucidated. Growing evidence has suggested that N-methyl-d-aspartate receptors (NMDARs) are involved in cognitive impairments. In this study, BPA was administered to female Sprague–Dawley rats (six per dose group) at concentrations of 0 (control), 4, 40, and 400 μg/kg·body weight/day from gestation day 1 through lactation day 21. Spatial learning was evaluated using the Morris water maze on postnatal day 22. Expression levels of NMDARs were determined using real-time polymerase chain reaction and Western blot. The results showed that male offspring exposed to BPA exhibited increased latency in reaching the platform and reduced time in the target quadrant, and the number of crossing the platform was less, as compared with the control group. The mRNA and protein expression levels of NMDARs in the hippocampus were significantly downregulated when compared with the control group of male offspring. The data showed that maternal exposure to BPA at low dosage can cause cognitive deficits in male rat offspring, probably due to a decrease in NMDARs in the hippocampus.

scholarly journals Maternal Resveratrol Treatment Re-Programs and Maternal High-Fat Diet-Induced Retroperitoneal Adiposity in Male Offspring

2020 ◽  
Vol 17 (8) ◽  
pp. 2780
Author(s):  
Ti-An Tsai ◽  
Chang-Ku Tsai ◽  
Li-Tung Huang ◽  
Jiunn-Ming Sheen ◽  
Mao-Meng Tiao ◽  
...  
Keyword(s):  
Leptin Receptor ◽  
Control Diet ◽  
Male Offspring ◽  
Male Rat ◽  
High Fat ◽  
Negative Effects ◽  
Maternal Control ◽  
Rat Offspring ◽  
Resveratrol Treatment ◽  
R Ratio

Obesity during pregnancy increases the risk of cardiovascular problems, diabetes, asthma, and cognitive impairments, affecting the offspring. It is important to reduce the negative effects of obesity and high-fat (HF) diet during pregnancy. We employed a rat model of maternal HF diet to evaluate the possible de-programming effects of resveratrol in rodent male offspring with maternal HF diet/obesity. Male rat offspring were randomized into four groups: maternal control diet/postnatal control diet, maternal HF diet/postnatal control diet, maternal control diet plus maternal resveratrol treatment/postnatal control diet, and maternal HF diet plus maternal resveratrol treatment/postnatal control diet. Maternal HF diet during pregnancy plus lactation resulted in retroperitoneal adiposity in the male offspring. Maternal resveratrol treatment re-programmed maternal HF exposure-induced visceral adiposity. Offspring that received prenatal HF diet showed higher leptin/soluble leptin receptor (sOB-R) ratio than offspring that received prenatal control diet. Maternal resveratrol treatment ameliorated maternal HF exposure-induced increase in leptin/sOB-R ratio and altered the expression of genes for crucial fatty acid synthesis enzymes in the offspring. Thus, maternal resveratrol administration reduces retroperitoneal adiposity in rat offspring exposed to prenatal HF diet/obesity and could be used to ameliorate negative effects of maternal HF diet in the offspring.

scholarly journals Maternal High-Fat Diet Modulates Cnr1 Gene Expression in Male Rat Offspring

Nutrients ◽  
2021 ◽  
Vol 13 (8) ◽  
pp. 2885
Author(s):  
Dawid Gawliński ◽  
Kinga Gawlińska ◽  
Irena Smaga
Keyword(s):  
Gene Expression ◽  
High Fat Diet ◽  
Cpg Islands ◽  
Male Offspring ◽  
Epigenetic Mechanism ◽  
Male Rat ◽  
High Fat ◽  
Rat Offspring ◽  
Pregnancy And Lactation ◽  
Cnr1 Gene

In recent years, strong evidence has emerged that exposure to a maternal high-fat diet (HFD) provokes changes in the structure, function, and development of the offspring’s brain and may induce several neurodevelopmental and psychiatric illnesses. The aims of this study were to evaluate the effects of a maternal HFD during pregnancy and lactation on depressive-like behavior and Cnr1 gene expression (encoding the CB1 receptor) in brain structures of rat offspring and to investigate the epigenetic mechanism involved in this gene expression. We found that a maternal HFD during pregnancy and lactation induced a depressive-like phenotype at postnatal days (PNDs) 28 and 63. We found that a maternal HFD decreased the Cnr1 mRNA levels in the prefrontal cortex with the increased levels of miR-212-5p and methylation of CpG islands at the Cnr1 promoter and reduced the level of Cnr1 gene expression in the dorsal striatum with an increased level of miR-154-3p in adolescent male offspring. A contrasting effect of a maternal HFD was observed in the hippocampus, where upregulation of Cnr1 gene expression was accompanied by a decrease of miR-154-3p (at PNDs 28 and 63) and miR-212-5p (at PND 63) expression and methylation of CpG islands at the Cnr1 promoter in male offspring. In summary, we showed that a maternal HFD during pregnancy and lactation triggered several epigenetic mechanisms in the brains of rat offspring, which may be related to long-lasting alterations in the next generation and produce behavioral changes in offspring, including a depressive-like phenotype.

Reproductive effects of endosulfan on male offspring of rats exposed during pregnancy and lactation

1999 ◽  
Vol 18 (9) ◽  
pp. 583-589 ◽  
Author(s):  
P R Dalsenter ◽  
E Dallegrave ◽  
J Rb Mello ◽  
A Langeloh ◽  
R T Oliveira ◽  
...  
Keyword(s):  
Male Offspring ◽  
Male Rats ◽  
Male Rat ◽  
Seminiferous Tubules ◽  
Sperm Production ◽  
Rat Offspring ◽  
Stage Of Development ◽  
Reproductive Effects ◽  
Pregnancy And Lactation ◽  
Daily Sperm Production

1 The reproductive effects of endosulfan on the male offspring of rats were examined. Dams were treated orally with 0, 1.5 or 3.0 mg endosulfan/kg from day 15 of pregnancy to postnatal day (PND) 21 of lactation. The male offspring rats were investigated at PND 65 or 140, corresponding to the pubertal and adulthood stage of development. 2 The dose of 3.0 mg endosulfan/kg induced a decrease in maternal body weight during pregnancy, but litter size and mean birth weight were not affected. Similarly, the age at testis descent and preputial separation was not affected on the male offspring. 3 The daily sperm production (6106) was permanently decreased in the highest dose group when investigated at puberty and at adulthood. At the lowest dose, however, the daily sperm production was significantly reduced only at puberty. 4 Histologically, the percentage of seminiferous tubules showing complete spermatogenesis was significantly decreased at puberty. This finding may explain the decrease in daily sperm production observed in the endosulfan-exposed male rats. 5 The results of this study show that low doses of endosulfan have no apparent effect on developmental landmarks or on the weight of reproductive and accessory sex organ. Daily sperm production was the most susceptible endpoint in the male offspring exposed to endosulfan during pregnancy and lactation. To further understand the reproductive effects of endosulfan on male rat offspring, additional reproductive and toxicokinetic studies should be carried out to determine the extent of endosulfan exposure in male rat offspring in utero and during lactation.

Maternal conjugated linoleic acid consumption prevented TAG alterations induced by a high-fat diet in male adult rat offspring

2020 ◽  
Vol 124 (3) ◽  
pp. 286-295
Author(s):  
Marcela Aída González ◽  
Jimena Lavandera ◽  
Carolina Gerstner ◽  
Ana Clara Fariña ◽  
Juliana Saín ◽  
...  
Keyword(s):  
Linoleic Acid ◽  
Conjugated Linoleic Acid ◽  
Adult Male ◽  
Liver Steatosis ◽  
Male Offspring ◽  
Male Rat ◽  
High Fat ◽  
Male Adult ◽  
Hepatic Lipid ◽  
Rat Offspring

AbstractMaternal nutritional programming by a high-fat (HF) diet is related to hepatic lipid accumulation and steatosis in offspring. Conjugated linoleic acid (CLA) might ameliorate impaired hepatic lipid homoeostasis; therefore, the aim was to investigate the potential preventive effect of maternal CLA consumption on TAG metabolism alterations induced by HF diets in adult male rat offspring receiving or not receiving CLA. Female Wistar rats were fed a control (C) diet, HF diet or HF diet supplemented with CLA (HF+CLA) for 4 weeks before mating and throughout pregnancy and lactation. After weaning, for 9 weeks, male offspring of C or HF rats continued with the same diets as their mothers (C/C or HF/HF groups, respectively) and male offspring of HF+CLA rats were fed HF or HF+CLA diets (HF+CLA/HF or HF+CLA/HF+CLA groups, respectively). Nutritional parameters, serum and liver TAG levels, the TAG secretion rate (TAG-SR) and the activities as well as gene expression of key hepatic enzymes involved in TAG regulation were assessed. The most interesting results were that maternal CLA decreased epididymal white adipose tissue weight and prevented serum and liver TAG accumulation induced by a HF diet in adult male offspring receiving or not receiving CLA. The prevention of liver steatosis in HF+CLA/HF+CLA and HF+CLA/HF offspring was associated with an increased hepatic TAG-SR. Overall, this study provides evidence that maternal CLA consumption programmes TAG regulation and in this way contributes to lowering lipid levels in tissues and preventing liver steatosis in particular.

Assessment of three-dimensional, fine-granular measurement of particulate matter by a smart air quality network in urban area

2019 ◽  
Author(s):  
Johanna Redelstein ◽  
Matthias Budde ◽  
Josef Cyrys ◽  
Stefan Emeis ◽  
Thomas Gratza ◽  
...  
Keyword(s):  
Particulate Matter ◽  
Air Quality ◽  
Urban Area ◽  
Three Dimensional

Prenatal hypoxia increases blood pressure in male rat offspring and affects their response to artificial light at night

2020 ◽  
pp. 1-8
Author(s):  
Hana Sutovska ◽  
Lubos Molcan ◽  
Romana Koprdova ◽  
Michaela Piesova ◽  
Mojmír Mach ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cardiovascular System ◽  
Mature Male ◽  
Male Offspring ◽  
Prenatal Hypoxia ◽  
Male Rat ◽  
Artificial Light ◽  
Negative Consequences ◽  
Light At Night ◽  
Rat Offspring

Abstract Prenatal hypoxia (PH) has negative consequences on the cardiovascular system in adulthood and can affect the responses to additional insults later in life. We explored the effects of PH imposed during embryonic day 20 (10.5% O2 for 12 h) on circadian rhythms of systolic blood pressure (BP) and heart rate (HR) in mature male rat offspring measured by telemetry. We evaluated: (1) stability of BP and HR changes after PH; (2) circadian variability of BP and HR after 2 and 5 weeks of exposure to artificial light at night (ALAN; 1–2 lx); and (3) response of BP and HR to norepinephrine. PH increased BP in the dark (134 ± 2 mmHg vs. control 127 ± 2 mmHg; p = 0.05) and marginally in the light (125 ± 1 mmHg vs. control 120 ± 2 mmHg) phase of the day but not HR. The effect of PH was highly repeatable between 21- and 27-week-old PH male offspring. Two weeks of ALAN decreased the circadian variability of HR (p < 0.05) and BP more in control than PH rats. After 5 weeks of ALAN, the circadian variability of HR and BP were damped compared to LD and did not differ between control and PH rats (p < 0.05). Responses of BP and HR to norepinephrine did not differ between control and PH rats. Hypoxia at the end of the embryonic period increases BP and affects the functioning of the cardiovascular system in mature male offspring. ALAN in adulthood decreased the circadian variability of cardiovascular parameters, more in control than PH rats.

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