Mechanical-tactile stimulation (MTS) intervention in a neonatal stress model alters adult adipose tissue deposition and prevents hyperinsulinemia in male rats

Haley, Shannon; Neff, Kimberly M.; Gulliver, Kristina; Gough, G.; Slater, Hillarie; Lane, Robert H.; Moyer‐Mileur, Laurie J.

doi:10.1016/j.earlhumdev.2012.12.005

Cited by 12 publications

(13 citation statements)

References 47 publications

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“…These effects were not seen in the female offspring. In male rats, abdominal obesity increases the risk of adverse metabolic sequelae such as hyperglycemia, hyperinsulinemia, and hypoadiponectinemia (29). Prenatal CIH may be a useful tool to study of potential mechanisms underlying abdominal visceral obesity with cardiovascular outcomes.…”

Section: Discussionmentioning

confidence: 99%

Intermittent hypoxia in utero damages postnatal growth and cardiovascular function in rats

Chen

Zadi

Jin

et al. 2018

Journal of Applied Physiology

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Obstructive sleep apnea (OSA) is common in pregnancy and may compromise fetal and even postnatal development. We developed an animal model to determine if maternal OSA could have lasting effects in offspring. Pregnant Sprague-Dawley rats were exposed to reduced ambient O from 21 to 4-5%, approximately once per minute [chronic intermittent hypoxia (CIH)] for 8 h/day during gestation days 3-19. Similarly handled animals exposed to ambient air served as controls (HC). Offspring were studied for body growth and cardiovascular function for 8 postnatal weeks. Compared with HC, prenatal CIH led to growth restriction, indicated by smaller body weight and tibial length, and higher arterial blood pressure in both male and female offspring. Compared with same-sex HC, CIH males showed abdominal obesity (greater ratio of abdominal fat weight to body weight or tibial length), left ventricular (LV) hypertrophy (greater heart weight-to-tibial length ratio and LV posterior wall diastolic thickness), elevated LV contractility (increases in LV ejection fraction, end-systolic pressure-volume relations, and preload recruitable stroke work), elevated LV and arterial stiffness (increased end-diastolic pressure-volume relationship and arterial elasticity), and LV oxidative stress (greater lipid peroxide content). Compared with female CIH offspring, male CIH offspring had more profound changes in blood pressure (BP), cardiac function, myocardial lipid peroxidase (LPO) content, and abdominal adiposity. Rodent prenatal CIH exposure, mimicking human maternal OSA, exerts detrimental morphological and cardiovascular effects on developing offspring; the model may provide useful insights of OSA effects in humans. NEW & NOTEWORTHY Obstructive sleep apnea is common in human pregnancy. Following maternal exposure to chronic intermittent hypoxia, a hallmark of sleep apnea, both sexes of rat offspring showed growth retardation, with males being more vulnerable to hypertension and dysfunctional left ventricular changes. This model is useful to study detrimental effects of maternal obstructive sleep apnea on developing offspring in humans.

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Section: Discussionmentioning

confidence: 99%

Intermittent hypoxia in utero damages postnatal growth and cardiovascular function in rats

Chen

Zadi

Jin

et al. 2018

Journal of Applied Physiology

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“…However, this relationship has not been observed in maternally separated Wistar rats [77]. In addition, GCs enhance fat storage and contribute to visceral fat accumulation [72,78], and ELS effectively increases the deposition of abdominal fat [77]; however, this can be prevented by neonatal stimulation [79]. The lack of association between CORT levels and body weight observed in the present study suggest that SIR-induced body weight gain in MS180 animals could be related to both hyperphagia and increased peripheral fat deposition, but is not directly modulated by GC.…”

Section: Discussionmentioning

confidence: 99%

Early Life Stress Increases Metabolic Risk, HPA Axis Reactivity, and Depressive-Like Behavior When Combined with Postweaning Social Isolation in Rats

et al. 2016

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Early-life stress is associated with depression and metabolic abnormalities that increase the risk of cardiovascular disease and diabetes. Such associations could be due to increased glucocorticoid levels. Periodic maternal separation in the neonate and rearing in social isolation are potent stressors that increase hypothalamus-pituitary-adrenal axis activity. Moreover, social isolation promotes feed intake and body weight gain in rats subjected to periodic maternal separation; however, its effects on metabolic risks have not been described. In the present study, we evaluated whether periodic maternal separation, social isolation rearing, and a combination of these two stressors (periodic maternal separation + social isolation rearing) impair glucose homeostasis and its relation to the hypothalamus-pituitary-adrenal axis and depressive-like behavior. Periodic maternal separation increased basal corticosterone levels, induced a passive coping strategy in the forced swimming test, and was associated with a mild (24%) increase in fasting glucose, insulin resistance, and dyslipidemia. Rearing in social isolation increased stress reactivity in comparison to both controls and in combination with periodic maternal separation, without affecting the coping strategy associated with the forced swimming test. However, social isolation also increased body weight gain, fasting glucose (120%), and insulin levels in rats subjected to periodic maternal separation. Correlation analyses showed that stress-induced effects on coping strategy on the forced swimming test (but not on metabolic risk markers) are associated with basal corticosterone levels. These findings suggest that maternal separation and postweaning social isolation affect stress and metabolic vulnerability differentially and that early-life stress-related effects on metabolism are not directly dependent on glucocorticoid levels. In conclusion, our study supports the cumulative stress hypothesis, which suggests that metabolic risk markers arise when vulnerable individuals are exposed to social challenges later in life.

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“…Studies that have investigated basal HPA axis functioning in adult rodents exposed to early life stress have reported mixed results. Attenuated basal corticosterone concentrations have been observed in adult rats exposed to early life stress in the forms of maternal separation/neonatal handling (Faure et al, 2006; Haley et al, 2013; Panagiotaropoulos et al, 2004; Papaioannou et al, 2002; Slotten et al, 2006), postnatal novelty exposure (Tang et al, 2003), and restraint given to pregnant dams (Belay et al, 2011). However, others have observed either no difference or increased basal corticosterone concentrations following early life stress (Kao et al, 2012; Lukkes et al, 2009; Tiba et al, 2008; Veenema and Neumann, 2009).…”

Section: Discussionmentioning

confidence: 99%

Transgenerational effects of social stress on social behavior, corticosterone, oxytocin, and prolactin in rats

Babb

Carini

Spears

et al. 2014

Hormones and Behavior

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Social stressors such as depressed maternal care and family conflict are robust challenges which can have long-term physiological and behavioral effects on offspring and future generations. The current study investigates the transgenerational effects of an ethologically relevant chronic social stress on the behavior and endocrinology of juvenile and adult rats. Exposure to chronic social stress during lactation impairs maternal care in F0 lactating dams and the maternal care of the F1 offspring of those stressed F0 dams. The overall hypothesis was that the male and female F2 offspring of stressed F1 dams would display decreased social behavior as both juveniles and adults and that these behavioral effects would be accompanied by changes in plasma corticosterone, prolactin, and oxytocin. Both the female and male F2 offspring of dams exposed to chronic social stress displayed decreased social behavior as juveniles and adults, and these behavioral effects were accompanied by decreases in basal concentrations of corticosterone in both sexes, as well as elevated juvenile oxytocin and decreased adult prolactin in the female offspring. The data support the conclusion that social stress has transgenerational effects on the social behavior of the female and male offspring which are mediated by changes in the hypothalamic–pituitary–adrenal axis and hypothalamic–pituitary–gonadal axis. Social stress models are valuable resources in the study of the transgenerational effects of stress on the behavioral endocrinology of disorders such as depression, anxiety, autism, and other disorders involving disrupted social behavior.

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Mechanical-tactile stimulation (MTS) intervention in a neonatal stress model alters adult adipose tissue deposition and prevents hyperinsulinemia in male rats

Cited by 12 publications

References 47 publications

Intermittent hypoxia in utero damages postnatal growth and cardiovascular function in rats

Intermittent hypoxia in utero damages postnatal growth and cardiovascular function in rats

Early Life Stress Increases Metabolic Risk, HPA Axis Reactivity, and Depressive-Like Behavior When Combined with Postweaning Social Isolation in Rats

Transgenerational effects of social stress on social behavior, corticosterone, oxytocin, and prolactin in rats

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