Your body is always burning fuel. Sometimes it relies more heavily on glucose. Other times, it burns more fat.
What determines which fuel wins?
A major part of the answer is insulin.
In this episode of the Metabolic Classroom, Dr. Ben Bikman explains how insulin helps control the body’s fuel selection—and why chronically elevated insulin can make it harder for the body to access and burn stored fat.
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Sugar and Fat Compete for Fuel
Scientists have known for decades that glucose and fatty acids compete with one another inside the body.
When fat burning increases, glucose burning tends to decrease. But the reverse is also true: when glucose and insulin rise, fat oxidation falls.
Human experiments have shown that this happens even when researchers deliberately keep fatty acids available in the bloodstream. In other words, the decline in fat burning isn’t simply because there is less fat available.
The body is actively changing which fuel it chooses to use.
Insulin Controls Fat Burning in Two Ways
Insulin affects fat metabolism at two important points.
First, it suppresses lipolysis—the release of stored fat from fat cells into the bloodstream.
Second, it can reduce the movement of long-chain fatty acids into the mitochondria, where fat is burned for energy.
This means that after a carbohydrate-containing meal, insulin simultaneously increases glucose use while decreasing both the availability and oxidation of fat.
The body shifts toward burning sugar.
What Happens When Insulin Falls?
When insulin levels remain lower, stored fatty acids can be released more easily and transported into the mitochondria.
This is one reason lower-carbohydrate diets can produce such large changes in fuel use.
Studies of people following ketogenic or very-low-carbohydrate diets consistently show much higher rates of fat oxidation. In endurance athletes adapted to low-carbohydrate diets, peak fat-burning rates have been measured at more than twice those seen in comparable high-carbohydrate athletes.
The body isn’t suddenly learning how to burn fat.
It is gaining greater access to a fuel-burning pathway that was already there.
When the Metabolic Switch Stops Working
A healthy metabolism should be flexible.
During fasting, the body should increase its reliance on fat. After eating carbohydrates, it should shift toward glucose.
But in insulin resistance, that flexibility can begin to disappear.
Muscle may rely too heavily on glucose even during fasting while becoming less responsive to insulin when glucose does need to be used.
This is often referred to as metabolic inflexibility.
And when fatty acids aren’t being oxidized efficiently, they can accumulate inside tissues. Those accumulated lipid products can interfere with insulin signaling, which may cause insulin levels to rise even further.
The result can become a reinforcing cycle of elevated insulin, reduced fat oxidation, and worsening insulin resistance.
The Bigger Picture
Fat burning is not controlled simply by how much fat happens to be circulating in your bloodstream.
It is regulated by metabolic signals.
And insulin is one of the most important.
Because carbohydrate intake is a major driver of insulin secretion, reducing the carbohydrate load can directly affect the signal controlling whether the body relies more heavily on glucose or fat.
The capacity to burn fat is already there.
Sometimes the key is allowing the hormonal environment to make that fuel accessible again.