Surgical stress may lead to a catabolic state. One consequence of this is lipolysis or the hydrolysis of triglycerides into glyceride and free fatty acids. It is thought that lipolysis is largely a result of stimulating beta-2 adrenergic receptors. The beta-2 agonism results in an increase in intracellular cAMP and downstream activation of triglyceride lipase by protein kinase A. Free fatty acids are then liberated and undergo beta-oxidation in the liver.
Of note, a process known as hypermetabolism may occur in the stress response. In this situation, insulin levels are actually normal to high (different from the fasting state) which leads to less ketone production. Therefore, glyceride from triglyceride breakdown enters into the gluconeogenesis cycle. However, due to insulin resistance (mediated by tumor necrosis factor alpha, IL-1, INF-alpha, and INF-gamma) there is concomitant fatty acid oxidation that which essentially results in opposing processes. Importantly, beta-oxidation is the major route of forming ATP in the stressed state. See diagrams from Miller’s Anesthesia (1), which further illustrate the process of lipolysis and the futile metabolic cycles that arise in the stressed state.
An important component in understanding metabolism is the respiratory quotient (RQ), the ratio of CO2 elimination to O2 consumption. By definition, the RQ for carbohydrates is 1. Therefore, more calorically dense molecules such as fat (9 kcal/gram) will have a lower respiratory quotient (~0.7) as carbon dioxide production falls relative to oxygen consumption with the intake of more calorically dense foods.
- Miller RD, Eriksson LI, Fleisher L, Wiener-Kronish JP, Cohen NH. Miller’s Anesthesia, 8th ed. Philadelphia, PA: Elsevier Saunders; 2014: Ch. 106, pp. 3121-3157.
Defined by: Isaac Shields, MD