Figure 1.

Metabolic effects of AT₁ receptors. The schematic shows the influence of angiotensin II on the adipose tissue, liver, skeletal muscle, pancreatic β-cells, and the SNS. Adipocytes are a major source of circulating angiotensinogen, along with the liver. In adipose tissue, AT₁ receptors inhibit differentiation of new adipocytes, thereby reducing the ability of adipose tissue to take up glucose and lipid. In the liver, AT₁ receptors increase glycogenolysis, which favors hyperglycemia, but have an opposing action of gluconeogenesis. AT₁ receptors also promote secretion of triglycerides into the circulation. Hemodynamic effects link AT₁ receptor-mediated vasoconstriction to reduced delivery of glucose and insulin to skeletal muscle. In the pancreas, AT₁ receptors promote insulin secretion in the short-term, but chronic stimulation leads to apoptosis and a loss of function. Activation of the RAS ties into SNS overactivity through actions in the central nervous system and presynaptic effects to promote norepinephrine release. Increased catecholamines promote impairments in glucose and lipid metabolism through multiple mechanisms. Modified with permission from [7]; figure created using Smart-Draw 6 (Smart-Draw, San Diego, CA).