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Effects of maternal nutrient restriction, intrauterine growth restriction, and glucocorticoid exposure on phosphoenolpyruvate carboxykinase‐1 expression in fetal baboon hepatocytes in vitro
Author(s) -
Li Cun,
Shu ZhenJu,
Lee Shuko,
Gupta Madhulika B.,
Jansson Thomas,
Nathanielsz Peter W.,
Kamat Amrita
Publication year - 2013
Publication title -
journal of medical primatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.31
H-Index - 42
eISSN - 1600-0684
pISSN - 0047-2565
DOI - 10.1111/jmp.12048
Subject(s) - baboon , phosphoenolpyruvate carboxykinase , biology , fetus , endocrinology , medicine , hepatocyte , glucocorticoid , in vitro , andrology , enzyme , pregnancy , biochemistry , genetics
Background The objective of this study was to develop a cell culture system for fetal baboon hepatocytes and to test the hypotheses that (i) expression of the gluconeogenic enzyme phosphoenolpyruvate carboxykinase‐1 ( PEPCK ‐1) is upregulated in hepatocytes isolated from fetuses of nutrient‐restricted mothers ( MNR ) compared with ad libitum ‐fed controls ( CTR ), and (ii) glucocorticoids stimulate PEPCK ‐1 expression. Methods Hepatocytes from 0.9 G CTR and MNR fetuses were isolated and cultured. PEPCK ‐1 protein and mRNA levels in hepatocytes were determined by W estern blot and quantitative PCR , respectively. Results Fetuses of MNR mothers were intrauterine growth restricted ( IUGR ). Feasibility of culturing 0.9 G fetal baboon hepatocytes was demonstrated. PEPCK ‐1 protein levels were increased in hepatocytes isolated from IUGR fetuses, and PEPCK ‐1 m RNA expression was stimulated by glucocorticoids in fetal hepatocytes. Conclusions Cultured fetal baboon hepatocytes that retain their in vivo phenotype provide powerful in vitro tools to investigate mechanisms that regulate normal and programmed hepatic function.