Journal
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume 282, Issue 5, Pages 1126-1131Publisher
ACADEMIC PRESS INC
DOI: 10.1006/bbrc.2001.4702
Keywords
insulin-like growth factor-binding protein-1; AMP-activated protein kinase; H4-II-E rat hepatoma cells; insulin action; insulin resistance; AICAR; catabolic stress; exercise
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Insulin-like growth factor-binding protein-1 (IGFBP-1) is stimulated during intensive exercise and in catabolic conditions to very high concentrations, which are not completely explained by known regulators such as insulin and glucocorticoids. The role of AMP-activated protein kinase (AMPK), an important signaling system in lipid and carbohydrate metabolism, in regulating IGFBP-1 was studied in H I-II-E rat hepatoma cells. Arsenic(III) oxide and 5-aminoimidazole-4-carbosamide-riboside (AICAR) were used as activators. AICAR (150 muM) stimulated. IGFBP-1 secretion twofold during a 5-h incubation (P = 0.002). Insulin (100 ng/ml) inhibited IGFBP-1 by 80% (P < 0.001), but this was completely abolished in the presence of 150 muM AICAR. The effect of dexamethasone in stimulating IGFBP-1 threefold was additive to the effect of AICAR (P < 0.001) and, in the presence of AICAR, was incompletely inhibited by insulin. In conclusion AMPK is identified as a novel regulatory pathway for IGFBP-1 stimulating secretion and blocking the inhibitory effect of insulin. <(c)> zool Academic Press.
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