Key Concepts of Section 16.8

• A rise in blood glucose stimulates the release of insulin from pancreatic β cells (see Figure 16-39).

• Subsequent binding of insulin to its receptor on muscle cells and adipocytes leads to the activation of protein kinase B, which activates several signal transduction pathways. Together with PKB-independent pathways, these pathways lead to translocation of the GLUT4 glucose transporter from intracellular vesicles to the plasma membrane and thus to an increase in glucose uptake and (in muscle) glycogen synthesis, resulting in a decrease in blood glucose (see Figure 16-40).

• A lowering of blood glucose stimulates glucagon release from pancreatic α cells. Binding of glucagon to its G protein–coupled receptor on liver cells promotes glycogenolysis by the cAMP-triggered kinase cascade (similar to epinephrine stimulation under stress conditions) and an increase in blood glucose (see Figures 15-28a and 15-35b).

• PPARγ, a member of the nuclear receptor family, is the master transcriptional regulator of adipocyte differentiation.

• Extracellular hormones such as insulin that promote adipocyte differentiation induce signal transduction pathways that lead to enhanced production of PPARγ. Conversely, signaling proteins such as Wnt and TGF-β that prevent preadipocyte differentiation activate signaling pathways that prevent expression of the PPARγ gene (see Figure 16-41).