FABP4 is secreted from adipocytes by adenyl cyclase-PKA- and guanylyl cyclase-PKG-dependent lipolytic mechanisms.

摘要: Objective Fatty acid-binding protein 4 (FABP4) is expressed in adipocytes, and elevated plasma FABP4 level associated with obesity-mediated metabolic phenotype. Postprandial regulation secretory signaling of has been investigated. Methods Time courses levels were examined during an oral glucose tolerance test (OGTT; n = 53) or a high-fat meal eating (n = 35). Effects activators inhibitors adenyl cyclase (AC)-protein kinase A (PKA) guanylyl (GC)-protein G (PKG) on secretion from mouse 3T3-L1 adipocytes investigated. Results FABP4 significantly declined after the OGTT eating, while insulin was increased. Treatment low high concentration palmitate for 2 h did not affect adipocytes. increased by stimulation lipolysis using isoproterenol, β3-adrenoceptor agonist (CL316243), forskolin, dibutyryl-cAMP atrial natriuretic peptide, induced suppressed inhibitor PKA (H-89), PKG (KT5823) hormone sensitive lipase (CAY10499). Conclusions FABP4 secreted association regulated AC-PKA- GC-PKG-mediated signal pathways. Plasma declines postprandially, suppression insulin-induced anti-lipolytic may be involved this decline level.