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BBR inhibits mitochondria function and decrease intracellular ATP. This leads to a reduction in gluconeogenic and lipogenic transcription factors (FoxO1, SREBP1, and ChREBP). As a result, expression of gluconeogenic genes (PEPCK and G6Pase) and lipogenic gene (FAS) are decreased. These molecular changes represent a signaling pathway for improvement of fasting glucose and liver steatosis in the BBR-treated diabetic rats.
