The growth and metabolic response of unweaned rats fed with honey were investigated. Ten day old Sprague-Dawley rats were gavaged with 50% honey solution (low dose 10 ml/kg or high dose 20 ml/kg) twice daily for ten days. All data were expressed as mean ± SEM and analyzed by one way ANOVA. Pups nourished with honey had 5.41-7.43% body weight gain than untreated rats. Tibial length was significantly increased (p < 0.05) in the honey-fed group than control (6-9%). The differences in growth could be attributed to circulating insulin-like growth factor-1 as the concentrations were also significantly higher in the honey-fed pups. There were no differences in the circulating and stored metabolic substrates (glucose, triglycerides, free fatty acid, cholesterol, lipid and glycogen) between the treatment and control groups. The plasma alanine transaminase was not affected by the treatments, however there was significantly increased plasma alkaline phosphatase activity in the male pups compared with female litter mates. Short term (10-day) oral administration of honey resulted in growth promotion and increased alkaline phosphatase in male rats, possibly in relation to bone growth and caused no liver pathology in neonatal rats. It was concluded that honey supplements administered orally to suckling rats have a positive effect on body weight and linear growth, and these effects are beneficial during weaning and development of fast growing animals.
BACKGROUND: Use of the synthetic opioid fentanyl increased ~300% in the last decade, including among women of reproductive ages. Adverse neonatal outcomes and long-term behavioral disruptions are associated with perinatal opioid exposure. Our previous work demonstrated that perinatal fentanyl exposed (PFE) mice displayed enhanced negative affect and somatosensory circuit and behavioral disruptions during adolescence. However, little is known about molecular adaptations across brain regions that underlie these outcomes. We performed RNA-sequencing across three reward and two sensory brain areas to study transcriptional programs in PFE juvenile mice. METHODS: C57BL/6 pregnant dams received 10ug/ml fentanyl in the drinking water from embryonic day 0 (E0) through gestational periods until weaning at postnatal day 21 (P21). RNA was extracted from nucleus accumbens (NAc), prelimbic cortex (PrL), ventral tegmental area (VTA), somatosensory cortex (S1) and ventrobasal thalamus (VBT) from PFE mice of both sexes at P35. RNA-sequencing was performed, followed by analysis of differentially expressed genes (DEGs) and gene co-expression networks. RESULTS: Transcriptome analysis revealed sex-specific DEGs and gene modules significantly associated with PFE. The VTA had the most DEGs, while pronounced gene enrichment occurred in NAc. Genes enriched in mitochondrial respiration were pronounced in NAc and VTA of PFE males, extracellular matrix (ECM) and neuronal migration enrichment were pronounced in NAc and VTA of PFE males, while genes associated with vesicular cycling and synaptic signaling were markedly altered in NAc of PFE female mice. In sensory areas from PFE females, we found alterations in mitochondrial respiration, synaptic and ciliary organization processes. CONCLUSION: Our findings demonstrate sex-specific neuroadaptations in PFE mice. Our studies identify distinct transcriptomes across reward and sensory brain regions that may underlie disrupted behavioral and circuit states in PFE mice.
Use of the synthetic opioid fentanyl increased ~300% in the last decade, including among women of reproductive ages. Adverse neonatal outcomes and long-term behavioral disruptions are associated with perinatal opioid exposure. Our previous work demonstrated that perinatal fentanyl exposed mice displayed enhanced negative affect and somatosensory circuit and behavioral disruptions during adolescence. However, little is known about molecular adaptations across brain regions that underlie these outcomes. We performed RNA-sequencing across three reward and two sensory brain areas to study transcriptional programs in perinatal fentanyl exposed juvenile mice. Pregnant dams received 10μg/ml fentanyl in the drinking water from embryonic day 0 (E0) through gestational periods until weaning at postnatal day 21 (P21). RNA was extracted from nucleus accumbens (NAc), prelimbic cortex (PrL), ventral tegmental area (VTA), somatosensory cortex (S1) and ventrobasal thalamus (VBT) from perinatal fentanyl exposed mice of both sexes at P35. RNA-sequencing was performed, followed by analysis of differentially expressed genes (DEGs) and gene co-expression networks. Transcriptome analysis revealed DEGs and gene modules significantly associated with exposure to perinatal fentanyl in a sex-wise manner. The VTA had the most DEGs, while robust gene enrichment occurred in NAc. Genes enriched in mitochondrial respiration were pronounced in NAc and VTA of perinatal fentanyl exposed males, extracellular matrix (ECM) and neuronal migration enrichment were pronounced in NAc and VTA of perinatal fentanyl exposed males, while genes associated with vesicular cycling and synaptic signaling were markedly altered in NAc of perinatal fentanyl exposed female mice. In sensory areas from perinatal fentanyl exposed females, we found alterations in mitochondrial respiration, synaptic and ciliary organization processes. Our findings demonstrate distinct transcriptomes across reward and sensory brain regions, with some showing discordance between sexes. These transcriptome adaptations may underlie structural, functional, and behavioral changes observed in perinatal fentanyl exposed mice.
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