Figure 1.

Regulation of adipose tissue aquaporins (AQPs), AQP3/AQP7, and liver AQP9 during fasting and feeding states. Fasting induces lipolysis in adipocytes, and gluconeogenesis in liver (as depicted on the left side of the figure); AQP7 and AQP3 messenger RNA (mRNA) levels are elevated in adipose tissue (AT), facilitating glycerol release into the blood stream. In turn, AQP9 mRNA levels in liver are also increased in order to transport glycerol in the portal vein. In the liver, glycerol is transformed into glycerol 3-phosphate (Gly-3P), and used as a substrate for gluconeogenesis, increasing glucose levels in the blood. In the fed state, the abundance of nutrients triggers a metabolic switch from lipolysis to lipogenesis in adipocytes, suppressing glucose production in the liver. Thus, adipose AQP3 and AQP7 mRNA levels decrease, and free fatty acids (FFA) are stored in the form of triglycerides (TGs). Circulating glycerol levels also decrease in parallel with the reduction in adipose AQP-mediated glycerol shuttling, and liver AQP9 levels. HSL—hormone-sensitive lipase; ATGL—adipose triglyceride lipase; VLDL—very low-density lipoprotein; and CM—chylomicrons. Increased (↑) decreased (↓).