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In this paper, based on Hill kinetics and Michaelis-Menten equation, we built a theoretical model to study the physical mechanism of insulin regulating hepatic gluconeogenesis through cAMP-response element binding protein(CREB). The theoretical model considers that insulin regulates Peroxisome Proliferator-activated Receptor γ Coactivator(PGC) cascade signaling through CREB, thereby regulating hepatic gluconeogenesis and affecting the characteristics of glucose metabolism signaling pathway. We found that under the action of abnormal insulin(Ginsulin), the expression of CREB is increased, which further stimulates the expression of Pck1. By the regulation of Recombinant Phosphoenolpyruvate Carboxykinase 1(Pck1), citrate, α-keto glutarate, Malate, and Oxaloacetate show different metabolic levels. The highly expressed CREB upregulates the expression level of Pck1, and regulates the conversion of phosphoenolpyruvate to Pyruvate through regulatory factors such as CREB and Pck1. It in turn results in a significant increase in citrate, α-keto glutarate, Malate, and Oxaloacetate. The cellular glucose metabolism can be ultimately affected. Under the regulation of gluconeogenesis genes, higher Glocose concentration leads to the promotion of phosphoenolpyruvate. Under the regulation of Pck1, the conversion of phosphoenolpyruvate to Pyruvate increases, which will also greatly increase concentrations of citrate, α-keto glutarate, Malate, and Oxaloacetate. The theoretical results further reveal the new regulatory mechanism of insulin, CREB protein, and gluconeogenesis genes on cellular glucose metabolism. The results can provide a theoretical basis for designing therapeutic programs to block the diabetes transition pathway. [ABSTRACT FROM AUTHOR]

In this paper, based on Hill dynamics and Michaelis-Menten equation, we built a theoretical model to study the mechanism of Hepatitis B virus (HBx) promoting the development of hepatocellular carcinoma (HCC) through interaction with CREB (cAMP-response element binding protein).The theoretical model takes the HBx-CPAP (centrosome P4.1 associated protein)-AKT (protein kinase B)-GSK3 (Glycogen Synthase Kinase3)-P53 pathway into consideration. We found that with the increase of CREB concentration (CREB concentration=0.01-0.05), HBx has amplification effect, which leads to the significant decrease of tumor suppressor function of P53. The overexpression of inflammatory factor (NF-κB) creates an inflammatory microenvironment. CREB also regulates the secondary growth of AKT and affects cell glycogen metabolism. These factors contribute to the occurrence and development of HCC. Our theoretical results are consistent with the experimental observations, and provide a fundamental understanding of the HBx promoting the development of HCC through interaction with CREB. The results provide a theoretical basis for designing treatment plans that blocks the transition of hepatitis to HCC. [ABSTRACT FROM AUTHOR]

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