This article is for educational purposes only. It's not medical advice. Talk to a healthcare provider before making changes to your diet or health routine.

Quick Answer

Carbohydrate digestion starts in the mouth with salivary amylase, continues in the small intestine with pancreatic amylase and brush border enzymes, and ends with glucose absorbed into the bloodstream via GLUT transporters. Your cells use glucose through glycolysis to make ATP. Excess glucose gets stored as glycogen in the liver and muscle, and only converts to fat when those stores are full.

The Science

Your mouth is already digesting carbohydrates before you swallow. That’s not a figure of speech. Salivary amylase, the enzyme in saliva, starts cleaving the bonds in starch the moment food makes contact with your tongue. By the time you swallow, some of that starch is already broken into shorter chains.

This is where carbohydrate digestion begins, though it’s far from where it ends.

From Starch to Sugar: The Digestion Process

Starch is made of long chains of glucose molecules linked together. Salivary amylase cuts those chains into smaller pieces (oligosaccharides and maltose), but the enzyme gets deactivated when it hits the acid environment of your stomach. Digestion pauses there.

The real work happens in your small intestine. Pancreatic amylase, secreted from the pancreas into the small intestine, picks up where saliva left off. It breaks down the remaining starch fragments into disaccharides and short oligosaccharides.

Then comes the final step. The brush border of your small intestine, the dense layer of microvilli that lines the intestinal wall, is packed with enzymes called brush border enzymes. Maltase, sucrase, and lactase each break specific disaccharides down to their component monosaccharides. Maltose becomes two glucose molecules. Sucrose becomes glucose plus fructose. Lactose becomes glucose plus galactose.

These single sugars are what actually get absorbed.

Crossing Into the Bloodstream: GLUT Transporters

Glucose doesn’t just drift through the intestinal wall. It gets actively transported. GLUT transporters, a family of proteins embedded in cell membranes, move glucose into intestinal cells and then into the portal bloodstream (Mueckler and Thorens, 2013, Molecular Aspects of Medicine).

GLUT2 handles glucose absorption from the intestine into the blood. GLUT4 is different. It’s the transporter in muscle and fat cells, and it only moves to the cell surface when insulin is present. This is the mechanism by which insulin “clears” glucose from the blood. Without insulin, muscle and fat cells can’t absorb glucose efficiently. That’s the core problem in type 2 diabetes and insulin resistance.

Think of GLUT4 as a door that only unlocks when insulin shows up with the key.

What Happens to Glucose After Absorption

Once glucose enters the portal bloodstream, it goes to the liver first. The liver acts as the body’s glucose traffic controller. It takes up some glucose directly, storing it as glycogen or using it for energy. The rest passes into systemic circulation, raising blood glucose, which triggers insulin release from the pancreas.

Insulin then directs glucose to three main destinations. Muscle cells take it up and store it as muscle glycogen or burn it immediately for energy. The liver can convert it to liver glycogen or, in times of excess, start down the path of fat synthesis. Fat cells take up some glucose as well.

The destination depends on current energy status. Cells that need fuel burn glucose through glycolysis right away. When cells are fed and glycogen is low, glucose goes into storage. When glycogen stores are full and calories are still coming in, the overflow goes somewhere else.

Glycolysis: Turning Glucose Into Energy

Glycolysis is the 10-step process that breaks one glucose molecule into two molecules of pyruvate, generating a small amount of ATP (the cell’s energy currency) in the process. It happens in the cytoplasm of every cell.

Pyruvate’s fate depends on oxygen availability. When oxygen is plentiful (aerobic conditions), pyruvate enters the mitochondria and gets converted to acetyl-CoA, feeding into the citric acid cycle and the electron transport chain. This generates a much larger yield of ATP, around 30-32 molecules per glucose. When oxygen is limited (intense exercise, for instance), pyruvate converts to lactate instead. This is faster but less efficient.

Carbohydrates are the preferred fuel for high-intensity work. Fat can’t be burned fast enough when you’re sprinting or lifting heavy. Glucose can. That’s why trained athletes with high glycogen stores can sustain power output that fat burning alone can’t support.

Glycogen: The Storage Tank

The body stores carbohydrates as glycogen, a branched polymer of glucose. The liver holds about 100g of glycogen. Skeletal muscle holds roughly 300-400g total, distributed throughout muscle tissue. Together, that’s about 400-500g of stored carbohydrate, representing roughly 1600-2000 calories.

Liver glycogen maintains blood sugar between meals. It’s constantly being drawn down and replenished. Muscle glycogen is reserved almost exclusively for the muscles that hold it. Unlike liver glycogen, muscle glycogen can’t release glucose back into the blood.

After a meal, glycogen synthesis takes priority. Insulin promotes glycogen synthase activity and suppresses glycogen breakdown. After an overnight fast, liver glycogen is partly depleted. After prolonged exercise, muscle glycogen drops significantly. This is why athletes focus on carbohydrate timing around training.

When Carbs Become Fat

The idea that carbohydrates directly cause fat gain is common but oversimplified. The actual process, called de novo lipogenesis, requires specific conditions to become a meaningful contributor to body fat (Hellerstein, 1999, European Journal of Clinical Nutrition).

De novo lipogenesis only ramps up significantly when glycogen stores are full and caloric surplus is substantial and sustained. In controlled studies on humans eating typical diets, de novo lipogenesis accounts for a small fraction of total fat storage. Most dietary fat gain comes from dietary fat being stored directly, not from carbohydrates being converted.

That said, a sustained caloric surplus does lead to fat gain regardless of which macronutrient provides the excess calories. Carbohydrates are no exception. But the mechanism is mostly indirect. Eating more carbs than you burn means less dietary fat gets burned for energy, so more dietary fat gets stored. The carbs didn’t become the fat. They just crowded out fat oxidation.

Context matters enormously here. A sedentary person eating 400g of carbohydrates daily in caloric surplus is in a very different metabolic situation than an endurance athlete eating the same amount.


This article is for educational purposes only. It’s not medical advice. Talk to your doctor or a registered dietitian before making significant changes to your diet.

What This Means for You

Eating carbohydrates with fiber, fat, or protein slows their digestion and smooths out blood sugar response. Your body is good at handling carbohydrates in moderate doses throughout the day. Glycogen stores (about 400-500g total) refill after meals and deplete during exercise, so timing carbohydrate intake around activity can be useful for athletes and active people.

References

  1. Cummings JH, Englyst HN. (1995). Gastrointestinal effects of food carbohydrates. American Journal of Clinical Nutrition. 61(4 Suppl):938S-945S.
  2. Augustin LS, Kendall CW, Jenkins DJ, et al. (2015). Glycemic index, glycemic load and glycemic response: An International Scientific Consensus Summit. Nutrition, Metabolism and Cardiovascular Diseases. 25(9):795-815.
  3. Mueckler M, Thorens B. (2013). The SLC2 (GLUT) family of membrane transporters. Molecular Aspects of Medicine. 34(2-3):121-38.
  4. Hellerstein MK. (1999). De novo lipogenesis in humans: metabolic and regulatory aspects. European Journal of Clinical Nutrition. 53 Suppl 1:S53-65.