What Happens to Sugar in Your Body

Sugar is one of the most talked-about substances in nutrition, but what actually happens to it after you eat a biscuit, drink a juice or chew a piece of bread? Following sugar through the body shows how digestion, hormones and energy storage work together to keep your blood glucose within a narrow range — and what goes wrong when that system is overloaded.

First, what counts as “sugar”?

In chemistry, sugars are the smaller carbohydrates (see carbohydrates explained):

• Monosaccharides (single sugars): glucose, fructose (fruit sugar) and galactose. All three have the formula C₆H₁₂O₆ but different structures — they’re isomers.
• Disaccharides (double sugars): sucrose (table sugar = glucose + fructose), lactose (milk sugar = glucose + galactose) and maltose (glucose + glucose). See disaccharides.

Starch, the main carbohydrate in bread, rice, pasta and potatoes, isn’t sweet, but it’s a long chain of glucose units. After digestion, it ends up as glucose too — so as far as your blood is concerned, a slice of white bread and a spoonful of sugar aren’t that different.

Step 1: digestion — breaking big into small

Only single sugars can be absorbed into the blood. So larger carbohydrates must be broken down by hydrolysis: water is used to split the bonds between sugar units, with enzymes as catalysts (see the chemistry of digestion).

1. Mouth: salivary amylase starts breaking starch into shorter chains and maltose. (Chew a piece of bread for a minute and it starts to taste slightly sweet — that’s maltose appearing.)
2. Stomach: the acid stops amylase working, so little carbohydrate digestion happens here.
3. Small intestine: amylase from the pancreas finishes breaking starch into maltose and short chains. Then enzymes on the surface of the gut wall split disaccharides:
   • maltase: maltose → 2 glucose
   • sucrase: sucrose → glucose + fructose
   • lactase: lactose → glucose + galactose

Many adults produce less lactase after childhood. Undigested lactose passes to the large intestine, where bacteria ferment it, producing gas and discomfort — lactose intolerance.

Step 2: absorption — into the blood

The single sugars cross the cells lining the small intestine:

• Glucose and galactose are pumped in by a transporter that moves them together with sodium ions (SGLT1). This lets the gut absorb glucose even when there’s more glucose inside the cells than in the gut.
• Fructose enters by a different carrier (GLUT5), by facilitated diffusion.

All three then pass into the blood vessels that lead first to the liver through the hepatic portal vein. The liver gets first pick of everything absorbed from the gut.

How fast glucose reaches the blood depends on the food. Sugary drinks and white bread cause a quick rise; foods with fibre, fat and protein slow digestion and cause a gentler rise. This is the idea behind the glycaemic index (GI).

Step 3: keeping blood glucose steady

Healthy blood glucose sits at around 4 to 6 mmol dm⁻³ when fasting, rising to perhaps 7–8 mmol dm⁻³ after a meal. (That’s roughly a teaspoon of glucose in the whole of an adult’s blood — a surprisingly small amount.) Two hormones from the pancreas act like opposite controls on a thermostat.

When glucose rises: insulin

After a meal, beta cells in the pancreas detect rising glucose and release insulin (see insulin). Insulin is a signal of plenty. It:

• Tells muscle and fat cells to move glucose transporters (GLUT4) to their surface, so they take up glucose from the blood.
• Tells the liver to store glucose as glycogen and stop releasing glucose.
• Encourages the body to build — making glycogen, fat and protein.

When glucose falls: glucagon

Between meals and overnight, blood glucose begins to drop. Alpha cells in the pancreas release glucagon, which mainly acts on the liver:

• It triggers glycogenolysis: breaking glycogen back into glucose and releasing it into the blood.
• It stimulates gluconeogenesis: making new glucose from non-carbohydrate sources such as lactate, glycerol and some amino acids.

Adrenaline can do something similar in an emergency, mobilising glucose for “fight or flight” (see adrenaline).

Step 4: what cells do with glucose

Glucose that enters a cell has three main fates:

1. Burned for energy. Through glycolysis, the Krebs cycle and the electron transport chain, glucose is oxidised to carbon dioxide and water, producing ATP (see cellular respiration). The brain is a big glucose user — it consumes roughly 120 g a day, around a fifth of the body’s resting energy.
2. Stored as glycogen. Glucose units are linked into glycogen, a highly branched polymer (see polysaccharides). An adult stores roughly 100 g in the liver and about 400 g in muscles, though this varies with diet, size and training. Liver glycogen is released into the blood for the whole body; muscle glycogen is used only by the muscle itself.
3. Turned into fat. When glycogen stores are full and energy intake stays high, excess glucose can be converted into fatty acids and stored as triglycerides in fat tissue.

The fructose difference

Fructose follows a different route. Almost all of it is processed in the liver (and some in the small intestine), and it doesn’t need insulin to get into liver cells. Fructose bypasses one of the main control points of glycolysis, so the liver processes it rapidly, converting it into glucose, glycogen, lactate or fat.

In the amounts found in whole fruit, this isn’t a problem. But large amounts of added sugar — especially in sugary drinks, where a lot of fructose arrives quickly — can push the liver to make more fat. That’s one reason high sugar intake is linked to fatty liver disease. Whole fruit is a different package: its fibre, water and bulk slow absorption and make it hard to eat very large amounts (see biochemistry myths).

When the system goes wrong: diabetes

In type 1 diabetes, the immune system destroys the beta cells, so little or no insulin is made. Cells can’t take up glucose properly, blood glucose rises, and the body starts breaking down fat rapidly, producing ketones (see ketosis). People with type 1 diabetes need insulin injections or pumps.

In type 2 diabetes, cells become resistant to insulin, and over time the pancreas can’t make enough to compensate. It’s strongly linked to excess body fat and inactivity, although genetics also plays a role. Consistently high blood glucose damages blood vessels and nerves, because glucose slowly reacts with proteins (glycation). One lab test, HbA1c, measures how much haemoglobin has become glycated, giving an average of blood glucose over the previous two to three months.

Common misconceptions

• “Sugar goes straight into your blood.” Disaccharides and starch must first be hydrolysed to single sugars.
• “Starchy foods aren’t sugar.” Chemically, starch is digested to glucose.
• “Brown sugar is healthier than white.” Both are almost entirely sucrose; brown sugar has a little molasses.
• “Eating sugar makes children hyperactive.” Controlled studies haven’t found this effect; the idea persists largely through expectation.
• “The brain can only use glucose.” It normally relies on glucose, but during fasting it can get a large share of its energy from ketones.

Key takeaways

• Carbohydrates are hydrolysed to glucose, fructose and galactose before absorption.
• The liver gets first access to absorbed sugars via the hepatic portal vein.
• Insulin lowers blood glucose (uptake and storage); glucagon raises it (glycogen breakdown and new glucose).
• Glucose is burned for ATP, stored as glycogen or converted to fat.
• Fructose is handled mainly by the liver; diabetes is a failure of insulin production or response.

For the structure of the main molecule in this story, see glucose structure.