scholarly journals Long-Term Effects of Late Gestation in Utero Hypoxic Stress on Mood Disorders: Sex and Age Differences

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A751-A751
Author(s):  
Steve Mabry ◽  
E Nicole Wilson ◽  
Nataliya Rybalchenko ◽  
Rachel Engelland ◽  
Oluwadarasimi Fadeyibi ◽  
...  
Keyword(s):  
Food Intake ◽  
Anxiety Disorders ◽  
Young Adulthood ◽  
In Utero ◽  
Late Gestation ◽  
Hypoxic Stress ◽  
Long Term Effects ◽  
Female Progeny ◽  
Mood And Anxiety Disorders

Abstract Introduction: In utero insults have been linked with increased fear and anxiety in progeny. In utero hypoxic stress is associated with a multitude of gestational complications such as pregnancy-associated hypertensive disorders and intrauterine growth restriction. Maternal hypertension during pregnancy is also associated with increased mood and anxiety disorders in progeny. However, it is unknown if these associations are due to in utero hypoxic stress. We hypothesized that exposure to late gestational hypoxia will have a long-term impact on anxiety in progeny. Methods: Timed pregnant female Long-Evans rats were exposed to five days (gestational days: 15-20) of chronic intermittent hypoxia (CIH) or room air (normoxia - 21% O2) for 8 hours during their sleep phase. Each CIH cycle was 6 min of 3 min hypoxia (10% O2) and 3 min normoxia (21% O2) for a total of 10 CIH cycles/hour. At weaning (PND 28), progeny was pair-housed with a conspecific of same sex and similar weight. To examine mood and anxiety disorders, we quantified anxiety-related behaviors (time spent in the center of open field arena, marble burying test, social and anti-social behaviors with conspecifics) along with quantifying food intake and circulating sex hormone levels during puberty (postnatal day, PND 40-45) and young adulthood (PND 60-65) in male and female progeny. Results: Gestational CIH did not impact circulating sex hormones or food intake, regardless of sex or age of progeny. However, gestational CIH increased anxiety related behaviors in pubertal females. These effects of gestational CIH on anxiety in pubertal females were not maintained, as these behaviors resolved in young adulthood. Gestational CIH did not impact male progeny, regardless of age. Conclusion: Exposure to CIH during gestation resulted in increased anxiety related behaviors in pubertal female progeny. In utero hypoxia during late gestation may temporarily increase the risk for mood and anxiety disorders in pubertal females.

scholarly journals Long-Term Effects of Late Gestation in Utero Hypoxic Stress on Neurodegeneration: Sex and Age Differences

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A751-A752
Author(s):  
E Nicole Wilson ◽  
Steve Mabry ◽  
Nataliya Rybalchenko ◽  
Rachel Engelland ◽  
Oluwadarasimi Fadeyibi ◽  
...  
Keyword(s):  
Adult Male ◽  
In Utero ◽  
Ultrasonic Vocalizations ◽  
Late Gestation ◽  
Nigrostriatal Pathway ◽  
Open Field Activity ◽  
Female Progeny ◽  
Male Progeny ◽  
Field Activity

Abstract Introduction: In utero insults have been proposed to lead to the onset of neurodegenerative diseases later in life, such as Parkinson’s disease (PD). In utero hypoxia is associated with a multitude of conditions, such as maternal sleep apnea, preeclampsia, gestational diabetes, and maternal hypertension. Exposure to in utero hypoxia may impact male progeny more than female progeny, which may underlie the male biased sex differences in PD. It is currently unknown whether late gestational hypoxic stress has a long-term effect on brain regions associated with PD, such as the nigrostriatal pathway. We hypothesized that exposure to late gestational hypoxia will result in nigrostriatal impairment in adult male progeny compared to adult female progeny. Methods: Timed pregnant female Long-Evans rats were exposed to five days (gestational days: 15-20) of chronic intermittent hypoxia (CIH) or room air (normoxia - 21% O2) for 8 hours during their sleep phase. Each CIH cycle was 6 min of 3 min hypoxia (10% O2) and 3 min normoxia (21% O2) for a total of 10 CIH cycles/hour. Gestational age at delivery was recorded and neonate’s body weights were measured within 12-16 hours from birth. At weaning (postnatal day, PND 28), progeny was pair-housed with a conspecific of the same sex and similar weight. To examine PD, we focused on PD associated characteristics of oxidative stress in the nigrostriatal pathway and behavioral impairments of motor (open field activity and ultrasonic vocalizations) and cognitive (spatial memory) function during puberty (PND 40-45) and young adulthood (PND 60-65). Results: Gestational CIH had no effect on the duration of gestation, litter size, and neonatal weight at birth. Gestational CIH did not impact circulating oxidative stress, regardless of sex or age of progeny. Offspring gross motor function (open field activity) and cognitive (Morris Water maze) function were unaffected by gestational CIH. In contrast, gestational CIH impaired ultrasonic vocalizations in adult male progeny. Gestational CIH increased the latency to vocalize and decreased the loudness of the vocalizations in adult male progeny. Conclusion: Exposure to CIH during gestation resulted in nigrostriatal impairment in adult male progeny, as evidenced by impaired ultrasonic vocalizations that require a functional nigrostriatal pathway. In utero hypoxia during late gestation may increase the risk for PD in males.

Short-term and long-term effects of iron deficiency in utero

The Lancet ◽  
2000 ◽  
Vol 356 (9231) ◽  
pp. 696 ◽  
Author(s):  
Dimitrios Trichopoulos
Keyword(s):  
Iron Deficiency ◽  
In Utero ◽  
Long Term Effects ◽  
Short Term

scholarly journals Effect of pre- and postnatal growth and post-weaning activity on glucose metabolism in the offspring

2014 ◽  
Vol 224 (2) ◽  
pp. 171-182 ◽  
Author(s):  
Neele S Dellschaft ◽  
Marie-Cecile Alexandre-Gouabau ◽  
David S Gardner ◽  
Jean-Philippe Antignac ◽  
Duane H Keisler ◽  
...  
Keyword(s):  
Caloric Restriction ◽  
Young Adulthood ◽  
Postnatal Growth ◽  
Late Gestation ◽  
Leptin Resistance ◽  
Metabolic Phenotype ◽  
Obesogenic Environment ◽  
Appetite Control ◽  
Pregnant Sheep

Maternal caloric restriction during late gestation reduces birth weight, but whether long-term adverse metabolic outcomes of intra-uterine growth retardation (IUGR) are dependent on either accelerated postnatal growth or exposure to an obesogenic environment after weaning is not established. We induced IUGR in twin-pregnant sheep using a 40% maternal caloric restriction commencing from 110 days of gestation until term (∼147 days), compared with mothers fed to 100% of requirements. Offspring were reared either as singletons to accelerate postnatal growth or as twins to achieve standard growth. To promote an adverse phenotype in young adulthood, after weaning, offspring were reared under a low-activity obesogenic environment with the exception of a subgroup of IUGR offspring, reared as twins, maintained in a standard activity environment. We assessed glucose tolerance together with leptin and cortisol responses to feeding in young adulthood when the hypothalamus was sampled for assessment of genes regulating appetite control, energy and endocrine sensitivity. Caloric restriction reduced maternal plasma glucose, raised non-esterified fatty acids, and changed the metabolomic profile, but had no effect on insulin, leptin, or cortisol. IUGR offspring whose postnatal growth was enhanced and were obese showed insulin and leptin resistance plus raised cortisol. This was accompanied by increased hypothalamic gene expression for energy and glucocorticoid sensitivity. These long-term adaptations were reduced but not normalized in IUGR offspring whose postnatal growth was not accelerated and remained lean in a standard post-weaning environment. IUGR results in an adverse metabolic phenotype, especially when postnatal growth is enhanced and offspring progress to juvenile-onset obesity.

Gender-related long-term effects in adult rats by perinatal dietary ratio of n-6/n-3 fatty acids

2005 ◽  
Vol 288 (3) ◽  
pp. R575-R579 ◽  
Author(s):  
Marina Korotkova ◽  
Britt G. Gabrielsson ◽  
Agneta Holmäng ◽  
Britt-Marie Larsson ◽  
Lars Å. Hanson ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Linseed Oil ◽  
Maternal Diet ◽  
Perinatal Period ◽  
Late Gestation ◽  
Male Rats ◽  
Long Term Effects ◽  
Adult Rats ◽  
Serum Leptin

Epidemiological studies in humans have shown that perinatal nutrition affects health later in life. We have previously shown that the ratio of n-6 to n-3 polyunsaturated fatty acids (PUFA) in the maternal diet affects serum leptin levels and growth of the suckling pups. The aim of the present study was to investigate the long-term effects of various ratios of the dietary n-6 and n-3 PUFA during the perinatal period on serum leptin, insulin, and triacylglycerol, as well as body growth in the adult offspring. During late gestation and throughout lactation, rats were fed an isocaloric diet containing 7 wt% fat, either as linseed oil (n-3 diet), soybean oil (n-6/n-3 diet), or sunflower oil (n-6 diet). At 3 wk of age, the n-6/n-3 PUFA ratios in the serum phospholipids of the offspring were 2.5, 8.3, and 17.5, respectively. After weaning, all pups were given a standard chow. At the 28th postnatal wk, mean body weight and fasting insulin levels were significantly increased in the rats fed the n-6/n-3 diet perinatally compared with the other groups. The systolic blood pressure and serum triacylglycerol levels were only increased in adult male rats of the same group. These data suggest that the balance between n-6 and n-3 PUFA during perinatal development affects several metabolic parameters in adulthood, especially in the male animals.

Long-term effects of TRH administration on food intake and body weight in the rat

1986 ◽  
Vol 24 (6) ◽  
pp. 1817-1819 ◽  
Author(s):  
R. Iglesias ◽  
M. Llobera ◽  
E. Montoya
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Long Term Effects

LONG TERM EFFECTS OF IN-UTERO EXPOSURE TO PERFLUORINATED CHEMICALS ON FEMALE REPRODUCTION

2011 ◽  
Vol 2011 (1) ◽  
Author(s):  
Susanne Lund Kristensen ◽  
Cecilia Høst Ramlau-Hansen ◽  
Erik Ernst ◽  
Sjurdur Frodi Olsen ◽  
Jens Peter Bonde ◽  
...  
Keyword(s):  
In Utero ◽  
In Utero Exposure ◽  
Long Term Effects ◽  
Female Reproduction ◽  
Perfluorinated Chemicals

Prenatal programming of adult blood pressure: role of maternal corticosteroids

2005 ◽  
Vol 289 (4) ◽  
pp. R955-R962 ◽  
Author(s):  
Lori L. Woods ◽  
Douglas A. Weeks
Keyword(s):  
Blood Pressure ◽  
Food Intake ◽  
Female Offspring ◽  
Common Mechanism ◽  
Long Term Effects ◽  
Pregnant Rats ◽  
Body Weights ◽  
Glucocorticoid Administration ◽  
Blood Pressures

Both maternal glucocorticoid administration and maternal dietary protein or food restriction in pregnancy cause fewer nephrons and hypertension in the adult offspring. The purpose of these studies was to determine the extent to which nutritional factors contribute to programming of offspring hypertension by maternal glucocorticoids. Pregnant rats were treated with dexamethasone (100 μg·kg−1·d−1sc) on days 1–10 (ED) or days 15–20 (LD) of pregnancy. Additional groups of pregnant animals were pair fed to the early (EDPF) and late (LDPF) dexamethasone-treated groups, and another group was untreated or given vehicle (C). The dams treated with dexamethasone reduced their food intake and lost or failed to gain a normal amount of weight during treatment; body weights of ED dams caught up to normal after the treatment period, whereas those of LD dams did not. In adulthood (∼21 wks), chronically instrumented male offspring of ED had normal blood pressures (125 ± 2 mmHg vs. 126 ± 1 mmHg in C), whereas LD offspring were hypertensive (136 ± 3 mmHg). However, LDPF offspring were equally hypertensive (134 ± 2 mmHg). Glomerular filtration rates normalized to body weight were not significantly different among groups. Qualitatively similar results were found in female offspring. Thus the long-term effects of maternal glucocorticoid administration at this dose on offspring’s blood pressure may, in large part, be accounted for by the reduction in maternal food intake. These data suggest that maternal glucocorticoids and maternal food or protein restriction may, at least in part, share a common mechanism in programming offspring for hypertension. The window of sensitivity of future offspring blood pressure to either maternal insult coincides with nephrogenesis in the rat, suggesting that impaired renal development could play an important role in this programming.

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