Since PI3K-AKT is the canonical pathway of energy metabolism, and SREBP2-PCSK9-LDL-R pathway is reported to play a vital role in hepatic lipids metabolism, and combined with the aforementioned clues from IPA generated molecular networks, we hypothesized that THF improved glucose intolerance and hepatosteatosis in DIO rats by potentially targeting the AKT-SREBP nexus [33]. Here, AKT1 is linked to Glucose intolerance.