Abstract
Fibroblast growth factor 21 (FGF-21) regulates nutritional status through the control of glucose, lipid, and energy metabolism. Liver is the major source of circulating, hormone-like FGF-21, the expression and secretion of which increase in response to peroxisome proliferator-activated receptor alpha (PPAR-α)/retinoic acid receptor RXR heterodimer activation. In adipose tissue, the action of FGF-21 is largely of a paracrine/autocrine nature and FGF-21 expression is regulated by the PPAR-γ/RXR heterodimer. In rodents, increased circulating FGF-21 during fasting, ketosis, and cold exposure mediates an adaptation process to starvation by increasing hepatic lipid oxidation, ketogenesis, gluconeogenesis, and resistance to somatotropin/growth hormone action. If administered in pharmacological doses to rodents or primates, systemic FGF-21 or FGF-21 analogs produce weight loss without suppressing food intake, decreasing liver fat content, and lowering glucose and triglyceride plasma concentrations. The role of FGF-21 in human physiology is not fully understood. In humans, elevated circulating FGF-21 levels, considered a sign of FGF-21 resistance, are found in metabolic syndrome, type 2 diabetes, and chronic diseases associated with an unhealthy obesity pattern and the accumulation of ectopic fat.
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