De novo lipogenesis (DNL) is the biological process by which the body converts excess carbohydrates—especially sugars—into fatty acids, which are then stored as fat. The term ""de novo"" means ""from the beginning,"" and in this case refers to the creation of fat from non-fat sources. This process is most active in the liver, though it can also occur in fat tissue and other organs under certain conditions.

DNL is a normal metabolic function, designed to help store energy for later use. But in today's environment of constant caloric surplus—particularly from refined carbohydrates—DNL can become chronically overactive, turning the liver into a fat factory.

Not all carbohydrates are equal when it comes to fat creation. Fructose is uniquely powerful at activating DNL because:
- It is absorbed quickly and shuttled directly to the liver
- It bypasses the normal insulin-regulated steps of glucose metabolism
- It rapidly generates acetyl-CoA, the key building block for fatty acid synthesis

In practical terms, this means a high-fructose meal can flood the liver with substrates that are immediately used to create fat—even when overall fat intake is low. This is why fructose is considered lipogenic: it promotes fat creation from sugar.

When DNL becomes overactive, it leads to:
- Non-alcoholic fatty liver disease (NAFLD) – fat accumulation in liver cells, often silent but potentially progressive
- Insulin resistance – as liver fat disrupts glucose metabolism and hormonal signaling
- Hypertriglyceridemia – elevated triglyceride levels in the blood, a risk factor for heart disease
- Visceral fat gain – fat stored around organs, associated with metabolic syndrome and inflammation

Critically, DNL can continue even without high dietary fat, which is why people following “low-fat” but high-carb diets can still gain visceral and liver fat.

Even if you're avoiding added sugars, your body can **create fructose internally** via the **polyol pathway**—especially during dehydration, stress, alcohol consumption, or high salt and carb intake. This means the trigger for DNL can be **endogenous**, further complicating efforts to reduce fat accumulation through diet alone.

At LIV3, we see DNL not just as a result of overeating—but as a metabolic switch flipped by fructose metabolism, whether that fructose is from diet or created internally. Our goal isn’t simply to cut calories or fats—but to interrupt the fructose-driven pathways that lead to excessive fat creation in the first place.

By supporting the body with fructokinase inhibitors like luteolin, and uric acid reducers like tart cherry extract, we believe we can calm the metabolic storm upstream—before sugar ever becomes fat.