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prenatal programing of motivated behaviors:can innate immunity prime behavior?

Neural Regeneration Research 2023年第2期18卷 280-283页

作者： Larisa Montalvo-Martínez Gabriela Cruz-Carrillo Roger Maldonado-Ruiz Luis ATrujillo-Villarreal Eduardo AGarza-Villarreal Alberto Camacho-Morales Universidad Autónoma de Nuevo León Department of BiochemistryCollege of MedicineMonterreyMéxico Universidad Autónoma de Nuevo León Neurometabolism UnitCenter for Research and Development in Health SciencesMonterreyMéxico Universidad Nacional Autónoma de México Campus Juriquilla Instituto de NeurobiologíaQueretaroMéxico

prenatal programming during pregnancy sets physiological outcomes in the offspring by integrating external or internal stimuli.Accordingly,pregnancy is an important stage of physiological adaptations to the environment where the fetus becomes exposed and adapted to the maternal milieu.Maternal exposure to high-energy dense diets can affect motivated behavior in the offs p ring leading to addiction and impaired sociability.A high-energy dense exposure also increases the pro-inflammatory cytokines profile in plasma and brain and favors microglia activation in the offspring.While still under investigation,prenatal exposure to high-energy dense diets promotes structural abnormalities in selective brain regions regulating motivation and social behavior in the offspring.The current review addresses the role of energy-dense foods programming central and peripheral inflammatory profiles during embryonic development and its effect on motivated behavior in the offspring.We provide preclinical and clinical evidence that supports the contribution of prenatal programming in shaping immune profiles that favor structural and brain circuit disruption leading to aberrant motivated behaviors after birth.We hope this minireview encourages future research on novel insights into the mechanisms underlying maternal programming of motivated behavior by central immune networks.

关键词： addiction autism behavior cytokines diet maternal immune activation prenatal programming sociability trained immunity western-diets

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Increased hepatic peroxisome proliferator-activated receptor coactivator-la expression precedes the development of insulin resistance in offspring of rats from severe hyperglycemic mothers

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Chinese Medical Journal 2012年第7期125卷 1224-1229页

作者： MA Jing-mei ZENG Chan-juan ZHANG Li SHOU Chong YANG Hui-xia Department of Obstetrics and Gynecology Peking University First HospitalBeijing 100034China Department of Obstetrics and Gynecology International Peace Maternity&Child Health HospitalShanghai 200030China

Background prenatal hyperglycaemia may increase metabolic syndrome susceptibility of the offspring. An underlying component of the development of these morbidities is hepatic gluconeogenic molecular dysfunction. We hypothesized that maternal hyperglycaemia will influence her offsprings hepatic peroxisome proliferator-activated receptor coactivator-la （PGC-la） expression, a key regulator of glucose production in hepatocytes. Method We established maternal hyperglycaemia by streptozotocin injection to induce the maternal hyperglycaemic Wistar rat model. Offspring from the severe hyperglycemia group （SDO） and control group （CO） were monitored until 180 days after birth. Blood pressure, lipid metabolism indicators and insulin resistance （IR） were measured. Hepatic PGC-la expression was analyzed by reverse transcription polymerase chain reaction and Western blotting, mRNA expression of two key enzymes in gluconeogenesis, glucose-6-phospha-tase （G-6-Pase） and phosphoenolpyruvate carboxykinase （PEPCK）, were analyzed and compared. Results In the SDO group, PGC-la expression at protein and mRNA levels were increased, so were expression of G-6-Pase and PEPCK （P〈0.05）. The above effects were seen prior to the onset of IR. Conclusion The hepatic gluconeogenic molecular dysfunction may contribute to the metabolic morbidities experienced by this population.

关键词： prenatal programming peroxisome proliferator-activated receptor coactivator-l a phosphoenolpyruvate carboxykinase insulin resistance

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