Sugar: From Kitchen Chemistry to What Your Body Does With It

Sugar is two different things depending on where you’re looking at it. In your kitchen, it’s a functional ingredient with chemistry that experienced cooks learn to control. In your body, it’s a disassembled pair of simple sugars that take very different routes.

Understanding both sides explains why a cookie made with sugar is different from a cookie made without it, and why a can of soda affects your metabolism differently than an apple does even though both contain sucrose and fructose.

Sugar in the Kitchen

Table sugar is sucrose: a molecule made of one glucose unit and one fructose unit joined by a glycosidic bond. That structure drives everything it does in cooking.

Maillard Browning

The Maillard reaction happens when a reducing sugar meets an amino acid at high heat, around 310°F (154°C) and above. Strictly speaking, sucrose is not a reducing sugar because the glucose-fructose bond blocks the reactive carbonyl group. But sucrose breaks down into glucose and fructose under heat and acid conditions, and those monosaccharides are reducing sugars. So in most baked goods, which contain both sugar and protein (from eggs, dairy, or flour), the Maillard reaction runs.

This is the reaction behind the brown crust of bread, the surface of a cookie, and the color of a roasted marshmallow. It produces hundreds of flavor compounds that don’t exist in the raw ingredients. Controlling it is central to controlling flavor in baked goods.

Caramelization

Caramelization is a different reaction entirely. It’s purely about sugar with no protein required. Sucrose begins caramelizing at around 340°F (170°C). The molecules degrade and reform into complex compounds called caramelans, caramelens, and caramelins, plus volatile compounds that produce that characteristic toasty, bitter, sweet aroma.

Caramel sauce, caramelized onions (yes, their natural sugars caramelize), and the top layer of a crème brûlée are all examples. The reaction strips away the clean sweetness and adds complexity.

Moisture Retention

Sugar is hygroscopic, meaning it attracts and holds water molecules. This property affects texture in multiple ways. Cookies and cakes with more sugar stay moist longer. Sugar competes with starch and gluten for water, reducing the water available for those structures to form. This is why high-sugar doughs are often soft and tender rather than chewy.

Syrup and jam rely on this same hygroscopicity. High sugar concentration pulls water out of spoilage microorganisms through osmosis, slowing or preventing microbial growth.

Gluten Interference and Tenderness

When flour is mixed with water, glutenin and gliadin proteins hydrate and form gluten networks. Sugar competes for water during this process, limiting gluten development. Less gluten means a more tender, crumbly texture rather than a chewy one.

This is why pie crust recipes use powdered sugar rather than granulated sugar. Fine sugar disperses more quickly and suppresses gluten more thoroughly. It’s chemistry, not tradition.

Yeast Fermentation

Yeast produces carbon dioxide and ethanol from fermentable sugars. In bread dough, the CO2 is what makes dough rise. Sucrose works, but yeast also produces invertase, an enzyme that splits sucrose into glucose and fructose before fermenting them. At high concentrations (above about 10% by flour weight), sugar actually inhibits yeast by creating osmotic stress. Very sweet doughs use osmotolerant yeast varieties for this reason.

Sugar in the Body

When you eat sucrose, the first breakdown happens in your mouth. Salivary amylase doesn’t touch sucrose, but the acid environment and small amounts of sucrase begin the process. The real digestion happens in the small intestine.

Sucrase-Isomaltase

Sucrase-isomaltase is an enzyme embedded in the brush border membrane of small intestinal cells. It cleaves the glycosidic bond linking glucose and fructose in sucrose. This is one of the fastest digestion steps in carbohydrate metabolism. Sucrose breaks down to glucose and fructose almost immediately on contact with the intestinal lining.

Absorption: Two Different Transporters

Glucose and fructose don’t use the same transport systems.

Glucose is absorbed primarily through SGLT1 (sodium-glucose transporter 1), an active transport protein that moves glucose into intestinal cells against a concentration gradient, powered by sodium. At high glucose concentrations, GLUT2, a passive transporter, also contributes.

Fructose uses GLUT5, a passive transporter. GLUT5 is present at lower concentrations than SGLT1 and has a lower capacity. This is part of why very large fructose doses from beverages can overwhelm intestinal absorption, with some fructose reaching the colon and being fermented by bacteria, causing bloating.

Different Fates After Absorption

Once absorbed, the two monosaccharides travel together in the portal vein toward the liver. But they diverge at the liver door.

Glucose passes through the liver with only partial extraction. The liver takes up some for glycogen storage or immediate energy use, but most glucose continues into systemic circulation, where it raises blood glucose and triggers insulin secretion. Every cell in your body can use glucose.

Fructose is almost entirely extracted by the liver on first pass. The liver is the primary site of fructose metabolism because it has the enzyme fructokinase, which phosphorylates fructose in the first step of its breakdown. Fructose metabolism is essentially unregulated: fructokinase doesn’t have the negative feedback controls that glucokinase has. The liver processes fructose regardless of its own energy state.

This is why large fructose loads drive hepatic de novo lipogenesis (DNL), the conversion of excess carbohydrate carbon into fatty acids and eventually triglycerides (Tappy and Le, 2010, Physiological Reviews). When glycogen stores are full and energy is ample, fructose has nowhere efficient to go except fat synthesis. The resulting triglycerides leave the liver as VLDL particles.

The Glycogen Buffer

None of this matters much when glycogen storage has room. Your liver can store roughly 100g of glycogen. Muscle can store another 300-500g. After a normal mixed meal, some glucose refills glycogen, some feeds ongoing energy needs, and relatively little goes to fat.

The problem is when you’re eating above energy needs or consuming large sugar loads on top of full glycogen stores. Then both glucose and fructose have fewer places to go, and fat synthesis increases.

The Added vs. Intrinsic Distinction

An apple contains fructose. A can of soda contains fructose. They’re the same molecule. But they’re not the same food.

The apple’s fructose sits inside cells, surrounded by fiber, water, and pectin. Digestion must work through that matrix, slowing the release and absorption of the sugars. Gastric emptying is slower. Fructose arrives at the liver in a lower-dose, more gradual wave. The body handles it without overloading the liver’s processing capacity.

The soda’s fructose is in liquid solution with nothing slowing it down. It leaves the stomach quickly, hits the small intestine in a concentrated bolus, and gets absorbed rapidly. The liver sees a large fructose load in a short window.

Same molecule. Very different metabolic processing. This is the food matrix effect, and it’s why nutrition science on isolated nutrients often fails to translate to real food contexts.

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.