Prenatal Alcohol Exposure Inducing Insulin Resistance And Stress Injury In Mouse Hippocampi

With the social and economic prosperity and people’s living standards improving, the demanding forsocial exchange, the consumption of alcoholic drinks tends to go up, or even become a part of people’slives necessities. Toxicological effects of alcohol, especially the toxicological effects of alcohol on the fetushad be paid attention on by people began in1899, when German physician William Sullivan foundpregnant women drinking during pregnancy can affect fetal development. A large number of studies haveshown that alcohol exposure may result in adults with multiple organ damage, and drinking alcohol duringpregnancy can affect in addition to fetal normal growth and development, each organ malformations, andseriously affect the development of the fetus in the nervous system, and even the formation of the fetalalcohol syndrome. The pathway the alcohol play affection on central nervous system through ismultifaceted. Domestic related pregnancy alcohol exposure, inducing the neurons developmental apoptosisand even the development of fetal alcohol syndrome, limited to direct toxicological effects, such as theimpact of the neurotrophic factor signaling factor pathway and neuronal receptor function, activation ofendogenous sexual apoptotic pathway affect neurotransmitter function and inhibition pathway in neuronalapoptosis induced, but the IR as the entry point to explore the lack of IR research impact, as well as one ofthe signal transduction pathway of the CNS. Therefore, we have established pregnancy alcohol exposuremodel to explore the relationship between IR and CNS stress injury through the hippocampus oxidativestress injury observed IR and CNS, Contact, analysis of the molecular mechanisms of metabolic disordersinduced CNS injury FAS incidence the mechanism is further provided a new theoretical basis and FASgene diagnosis and gene therapy to provide a certain theoretical basis.Objective: Our aim is to investigate the relationship of prenatal alcohol exposure inducing insulinresistance and the stress injury in the mouse hippocampi. Method: Using C57BL/6J mice to establish themodels of prenatal alcohol exposure with control group, moderate ethanol group and high ethanol group.Then, the pups of different groups at P7, P14and P30were gathered for the measurements of fasting bloodglucose and blood insulin. In the meantime, the insulin resistance index (HOM-IR) to be calculated, and thestress injury in hippocampal CA1area was also observed as well. For instance, the expression of stress injury proteins, c-Fos and NF-κB, of hippocampus at P7and P14was tested with immunofluorescentlabeling and Western blot to analysis as well. Results:①After prenatal alcohol exposure, fasting glucoseand insulin resistance index increased with dose dependency and long term effect (P <0.05,n=10).②Afterprenatal alcohol exposure, c-Fos and NF-κB positive cells increased in hippocampi with dose dependencyand long term effect (P <0.05,n=10).③The expression of c-Fos and NF-κB protein with Western blottingin hippocampus was harmonized with the results of immunocytochemistry (P <0.05,n=5). Conclusion: Theprenatal alcohol exposure can induced pups insulin resistance, and the insulin resistance probably is causedby stress injury. In addition, the insulin resistance may be involved in the pathogenesis and brain injuries offetal alcohol syndrome, through c-Fos and NF-κB pathway.