Perilipin 1 ablation in mice enhances lipid oxidation during exercise and does not impair exercise performance

Perilipin 1 is involved in the control of adipose tissue triacylglycerol hydrolysis. Its ablation in mice decreases fat mass and induces a partial resistance to diet-induced and genetic obesity. However, the consequences of perilipin 1 invalidation on energy balance are not fully defined. Moreover, the impact of perilipin 1 ablation on exercise performance and on fatty acids mobilization and utilization during exercise has not been studied. We compared energy balance (food intake, energy expenditure, spontaneous physical activity) and response to exercise of Plin1(-/-) and wild-type mice receiving a chow diet. The Plin1(-/-) mice had less fat, comparable food intake, comparable or slightly decreased energy expenditure, and no change in spontaneous physical activity. Mean 24-hour respiratory quotient was slightly lower, suggesting enhanced fatty acid oxidation. Exercise performance (both acute and endurance) was not impaired. Changes in nonesterified fatty acid levels during exercise were comparable, showing that triacylglycerol mobilization was unimpaired. Oxygen consumption increased faster (both tests) and to higher values (acute exercise) in Plin1(-/-) mice. Respiratory quotient increased during both types of exercise in Plin1(-/-) and control mice, but less in Plin1(-/-) mice. These lower respiratory quotient values show that Plin1(-/-) mice rely more on fatty acid oxidation during exercise. This is probably related to an overexpression in liver and muscle of genes for fatty acids oxidation. Perilipin 1 ablation has limited consequences on energy balance. It does not impair exercise performance; fatty acids mobilization during exercise is not impaired, whereas their oxidation is enhanced.