Neonatal anoxia impairs long‐term energy metabolism and somatic development of Wistar rats

Abstract

Background: Neonatal anoxia may cause neurological injuries, behavioral alterations and changes in somatic growth. Somatic developmental changes suggest a possible effect of anoxia on energy metabolism and/or feeding behavior. Short-term effects of oxygen deficit on energy homeostasis have been described. In contrast, just a few studies report long-term effects. This study investigated the effects of neonatal anoxia on energy metabolism and somatic development at adulthood of males and females Wistar rats. Method: Male (m) and female (f) rats were exposed, on postnatal day 2 (P2), to either 25-min of Anoxia or Control treatment. At P34 part of the subjects of each group was fasted for 18 h, refeed for 1 h and then perfused 30 min later, at P35; the remaining subjects were submitted to these treatments at P94 and perfused at P95. Therefore, there were 8 groups: AmP35, AmP95, AfP35, AfP95, CmP35, CmP95, CfP35 and CfP95. For subjects perfused at P95, body weight and food intake were recorded up to P90. For subjects perfused at P35 and P95, glycemia, leptin and insulin were assessed after fasting and refeed. After perfusion the encephalon and pancreas were collected for Fos immunohistochemistry and Hematoxylin-Eosin stain analyses. Results: Even though neonatal anoxia did not interfere with regular food intake, it reduced body weight gain along growing in both male and female subjects as compared to the corresponding controls. At P35 neonatal anoxia decreased post-prandial glycemia and increased insulin. While at P95 neonatal anoxia altered the pancreatic histomorphology and increased post-fasting weight loss, decreasing leptin, insulin and glycemia secretion, as well Fos immunoreactivity (IR) in ARC. Conclusion: Neonatal anoxia impairs long-term energy metabolism and somatic development in Wistar rats, with differences related to sex and age.

Neonatal Anoxia Impacts Rats’ Maternal Behavior and Offspring Development due to Ultrasonic Vocalization’s Impairment

“…The condition is aggravated in low-weight preterm newborns, which accounts for 60% of the incidence of HI, which leads to long-term negative effects on motor, sensory, and cognitive development due to brain injury [1, 2]. Previous studies of our research group revealed that the global and noninvasive NA model, validated by Takada et al [2], (1) triggered a decrease in total hippocampal volume [3, 4], (2) decreased performance in spatial memory [5, 6], (3) showed sex-dependent differences concerning sensorimotor deficits [7], and (4) further described long-term metabolic and somatic development impairments related to NA outcomes [8].…”

Sensorimotor development of male and female rats subjected to neonatal anoxia

“…Neonatal anoxia differently affects the body's energy metabolism, according to sex and age (Cruz‐Ochoa et al., 2019). This stimulus affects the development of both sexes differently: while anoxic male weighs more than their control, the female show no changes in the weight compared with their control group.…”

Indole‐3‐carbinol ameliorated the neurodevelopmental deficits in neonatal anoxic injury in rats

“…Short‐ and long‐term neurodevelopmental abnormalities by neonatal anoxia are reproduced in neurological reflexes and motor coordination, which can assess brain maturation during neonatal development (Cruz‐Ochoa et al, 2019; Lubics et al, 2005; Smart & Dobbing, 1971). We have induced the anoxia in full‐term (30 h age) pups by providing 100% nitrogen, which mimics the human neonatal anoxic conditions in preterm babies (6 gestational months) (Kumar et al, 2019).…”

“…We also noticed a significant decrease in cliff avoidance response in anoxic pups, suggesting that anoxic injury to pups resulted in the loss of coordination between vibrissae and locomotor output. Neurodevelopmental deficits following anoxic injury are proportional to a decline in somatic growth (Cruz‐Ochoa et al, 2019; Kumar et al, 2017). We found that I3C treatment increased the somatic growth of anoxic pups, implying body growth and brain development.…”

“…Therefore, novel targets and chemical entities are sought for anoxia treatment (van Bel & Groenendaal, 2016). Recent studies have shown that neonatal anoxia is exacerbated by mitochondrial dysfunction (Samaiya et al, 2016; Samaiya & Krishnamurthy, 2015) and oxidative stress, which induces cell death (Samaiya et al, 2018), resulting in short‐term and long‐term neurodevelopmental deficits (Cruz‐Ochoa et al, 2019; Samaiya et al, 2016). Therefore, these pathological abnormalities have to be minimized.…”