Animal model for assessment pro‐inflammatory response of fat tissue and liver induced by prenatal stress and diet high in sugar and fat (840.14)

Abstract

Life style diseases (LSD) recognized as one of the non‐inflectional epidemic worldwide and LSD‐related liver pathology is common distributed. Recent data had shown intrauterine (prenatal) programming of adult metabolic phenotype. No study has explored potential interaction between maternal diet high in sugar and fat and stress on adipocytokine secretion and changes of liver functions in adulthood.The aim: To create a animal model of prenatal stress in rats to examine role of maternal stress and diet on activities of adipose tissue and hepatocellular organization in the offspring which can provide basis in treating hepatopathologies in preclinical and clinical settings.We used rat offsprings of mothers which had during all period of pregnancy social stress with (1) ad libitum access to 30% saccharose (Kozar, 2009); (2) high‐fat diet (to 45% kcal, Lintermans, 2009); and (3) binary those factors vs control. Scoring lesion (LI), vascular indexes (VI) by fat, liver histomorphology, IL‐1β, GRO/CINC‐1, leptin, adiponectin by ELISA.Relative to the control the most changes were determined in the 3d group: histologically ‐ both in the visceral fat tissue and liver appeared the cell reorganization with signs of inflammation, rise IL‐1β (217%), GRO/CINC‐1 (99%), leptin (79%) levels and decreased of adiponectin (41% ); rise of ratio Leptin/Adiponectin was in twice.Conclusion: Taken together maternal stress and high sugar‐fat diet reveal both prenatal effect on prenatal programming of offspring adipocyte secretion with liver proinflammatory changes. This animal model can be useful for follow up pharmacology investigation of pro‐inflammatory and metabolic state in adulthood.