THE ASSESSMENT OF GLUCOMETABOLIC HORMONES IN IMMATURE RATS AFTER HYPOXIC-ISCHEMIC INSULT

Neonatal hypoxic-ischemic encephalopathy (HIE) is one of the main devastating causes of morbidity and mortality in new-borns. Infants who survive such severe hypoxic-ischemic insult (HII) frequently develop neurological sequelae later in life, such as cerebral palsy, epilepsy, developmental delay, cognitive impairment, and behavioral.¹ Although the glucose metabolism in the adult brain has been studied extensively, there is still a lot more of unknown about neonatal glucose and energy metabolism.²  Thus, finding novel therapeutic approaches to reduce the severity of brain injury and its consequences is critical in neonatology. The main goal of this study was to investigate the alterations in glucose metabolites in immature rats after HII.

Lithium pilocarpine status epilepticus model (Li-Pilo SE) was induced in male Wistar rat pups by pre-treatment with lithium chloride (127 mg/kg, n=11) on the 11^th postnatal day. After 24 hours, the lithium pre-treated pups were administered either with pilocarpine (Li-Pilo) intraperitoneally (i.p.) (35 mg /kg b.w., n=6) or saline (0,9% NaCl, n=5) as for control group (Control). Serum was collected on the 19^th postnatal day.³ The serum levels of glucagon, glucagon-like peptide-1 (GLP-1), ghrelin, leptin, and plasminogen activator inhibitor 1 (PAI-1) were thoroughly assessed by magnetic bead-based immunoassays on Bio-Plex 200 systems (Bio-Rad, U.S.) and interpreted. The relevant changes in the set of five glucometabolic hormones were observed: the levels of GLP-1, glucagon, leptin, and PAI-1 were significantly elevated in Li-Pilo experimental group as compared to the Control.

Our data confirmed former observations that encephalopathy causes major modifications in glucose metabolism disposition in immature rats.⁴ Though different mechanisms interacting with seizures, such as the anticonvulsant impact of ghrelin, have already been reported, the relevance of these changes is still about to be elucidated.⁵ In conclusion, this work broadens knowledge of the alterations in glucose metabolism in immature rats after HII. The data demonstrated the significance of systemic glucose metabolism regulation in encephalopathy. Interactions with glucose metabolism thus represent a potential pharmaceutical target for future scientific research.