Open AccessAdipocyte pyruvate dehydrogenase kinase 4 expression is associated with augmented PPARγ upregulation in early‐life programming of later obesity
Author(s) -
Holness Mark J.,
Zariwala Gulrez,
Walker Celia G.,
Sugden Mary C.
Publication year - 2012
Publication title -
febs open bio
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.718
H-Index - 31
ISSN - 2211-5463
DOI - 10.1016/j.fob.2012.02.003
Subject(s) - pdk4 , adipocyte , medicine , endocrinology , peroxisome proliferator activated receptor , chemistry , downregulation and upregulation , pyruvate dehydrogenase complex , biology , adipose tissue , microbiology and biotechnology , receptor , biochemistry , enzyme , gene
We studied adipocytes from 8‐week‐old control rat offspring (CON) or rat offspring subjected to maternal low (8%) protein (MLP) feeding during pregnancy/lactation, a procedure predisposing to obesity. Acute exposure to isoproterenol or adenosine enhanced PDK4 and PPARγ mRNA gene expression in CON and MLP adipocytes. Enhanced adipocyte Pdk4 expression correlated with increased PPARγ expression. Higher levels of PDK4 and PPARγ were observed in MLP adipocytes. SCD1 is a PPARγ target. Isoproterenol enhanced adipocyte PDK4 and SCD1 gene expression in parallel. This could reflect augmented PPARγ expression together with enhanced lipolytic stimulation to supply endogenous PPARγ ligands, allowing enhanced adipocyte PDK4 and SCD1 expression via PPARγ activation. In contrast, the effect of adenosine to increase PDK4 expression is independent of stimulation of lipolysis and, as SCD1 expression was unaffected by adenosine, unlikely to reflect PPARγ activation. Increased adipocyte expression of both PDK4 and SCD1 in the MLP model could participate as components of a “thrifty” phenotype, favouring the development of obesity.