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Molecular mechanism of RBP4 on the basis of insulin signaling pathway in primary hepatocytes
Author(s) -
Namkung Jun,
Kim Moon Young,
Woo Mi Kyoung,
Sohn Joon Hyung,
An Sung Wan,
Yeh ByungIl
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.889.3
Subject(s) - gluconeogenesis , protein kinase b , metabolic syndrome , glycolysis , insulin receptor , signal transduction , endocrinology , insulin , medicine , insulin resistance , pathogenesis , diabetes mellitus , biology , mechanism (biology) , microbiology and biotechnology , metabolism , philosophy , epistemology
Metabolic syndrome is a cluster of symptoms closely associated with diabetes, obesity, and cardiovascular disease such as hypertension. Thought the prevalence is being increased the mechanism is not known so far. In this study, we tried to confirm the molecular mechanism of RBP4 which is regarded one of the critical factors in the pathogenesis of metabolic syndrome. Recombinant mouse RBP4 was treated to the primary hepatocytes prepared from the ICR mouse and cDNA microarray was performed. We focused insulin signaling pathway and mRNA expressions were measured real‐time PCR. The results are: 1) RBP4 has an undesirable effect for metabolic syndrome by increase of gluconeogenesis and decrease of glycolysis. 2) The increase of gluconeogenesis is due to decreased expression of Akt. 3) The effects of several factors which influences on PIP 3 expression, which plays a role as controller at the upper level than PKCα and Akt in the insulin signaling pathway, are not constant by RBP4. In summary, RBP4 increase gluconeogenesis mediated by Akt and decrease glycolysis in insulin signaling pathway. To get the clue to solve the metabolic syndrome the researches to confirm the phosphoryation of the factors and protein expression analysis are needed.