Fiche publication
Date publication
janvier 2017
Journal
Diabetes
Auteurs
Membres identifiés du Cancéropôle Est :
Dr GHYSELINCK Norbert
,
Dr MARK Manuel
Tous les auteurs :
Thompson SJ, Sargsyan A, Lee SA, Yuen JJ, Cai J, Smalling R, Ghyselinck N, Mark M, Blaner WS, Graham TE
Lien Pubmed
Résumé
RBP4 is produced mainly by hepatocytes. In type 2 diabetes and obesity, circulating RBP4 is increased and may act systemically to cause insulin resistance and glucose intolerance. Observations that adipocyte RBP4 mRNA increases in parallel with circulating RBP4 in these conditions, whereas liver RBP4 mRNA does not, led to a widely held hypothesis that elevated circulating RBP4 is a direct result of increased production by adipocytes. To test this, we generated mice with hepatocyte-specific deletion of RBP4 (liver RBP4 knockout or LRKO mice). Adipose tissue RBP4 expression and secretion remained intact in LRKO mice and increased as expected in the setting of diet-induced insulin resistance. However, circulating RBP4 was undetectable in LRKO mice. We conclude that adipocyte RBP4 is not a significant source of circulating RBP4, even in the setting of insulin resistance. Adipocyte RBP4, therefore, may have a more important autocrine or paracrine function that is confined within the adipose tissue compartment.
Mots clés
Adipocytes, metabolism, Animals, Blotting, Western, Female, Genotype, Hepatocytes, metabolism, Insulin Resistance, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, RNA, Messenger, genetics, Retinol-Binding Proteins, Plasma, genetics, Reverse Transcriptase Polymerase Chain Reaction
Référence
Diabetes. 2017 Jan;66(1):58-63
