As already mentioned, PPARα is activated in liver after transition from the fed to the fasted state. Although PPARα has mostly been connected with fatty acid catabolism, several lines of evidence indicate that PPARα has an important role in the control of glucose homeostasis as well. For a start, fasting PPARα −/− mice display marked hypoglycemia (see Section 3.1) [3, 7, 18–25]. Next, several enzymes of carbohydrate metabolism were shown to be regulated by PPARα (see Sections 2 and 3). Finally, PPARα was proposed to have a role in influencing insulin sensitivity (see Section 4). In this multitude of studies, often, contradictory findings were published. These sometimes depended on the experimental system used, but opposing results were also obtained for comparable paradigms. Therefore, this paper focuses on the links between PPARα and glucose homeostasis in rodent liver and on the potential direct and indirect mechanisms governing this regulation.
