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The measured correlate is intracellular ATP, so this is an energy-state mechanism rather than a signalling one.\nexposure: Metformin dose-response in hepatocytes lacking AMPK or LKB1\nevidence_span: {\"source_cache\": \"artifacts/metformin-research/20577053.abstract.txt\", \"locator\": \"Indexed abstract; zero-based, end-exclusive Unicode character offsets\", \"file_sha256\": \"f6019de6b5a35f860f55b39d91656e5fd1077d34e301d244a1ea498b96faac14\", \"start_char\": 0, \"end_char\": 1707, \"text_sha256\": \"f6019de6b5a35f860f55b39d91656e5fd1077d34e301d244a1ea498b96faac14\"}\n[metformin-p20577053] Metformin inhibits hepatic gluconeogenesis in mice independently of the LKB1/AMPK pathway via a decrease in hepatic energy state. 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