How does the absence of insulin affect fatty acid oxidation?

The absence of insulin significantly impacts fatty acid oxidation by increasing fatty acid release from adipose tissue, which is due to unregulated lipolysis. Insulin normally plays a crucial role in promoting the storage of fats and carbohydrates; it stimulates the uptake of glucose by cells and facilitates the storage of fatty acids in adipose tissues.

When insulin levels are low or absent, as seen in conditions like uncontrolled diabetes, there is reduced inhibition of lipolysis—the process where triglycerides stored in adipose tissue are broken down into glycerol and free fatty acids. This breakdown leads to an increased release of free fatty acids into the bloodstream. Consequently, the elevated levels of free fatty acids can be utilized by various tissues as an alternative energy source, especially when glucose is not effectively taken up by cells due to the lack of insulin. This leads to an increase in fatty acid oxidation, especially in muscle and liver cells, as the body attempts to compensate for the lack of available glucose.

Understanding this process is essential, especially in managing diabetic emergencies, as an excess of circulating free fatty acids can contribute to further complications, including ketoacidosis.