Insulin resistance is a metabolic condition in which the body’s cells—particularly in the liver, muscle, and adipose (fat) tissue—no longer respond effectively to the hormone insulin. Insulin’s primary job is to help shuttle glucose out of the bloodstream and into cells for energy. When cells resist insulin’s signal, blood sugar levels rise, the pancreas compensates by producing more insulin, and over time this leads to a cascade of metabolic dysfunction.

Insulin resistance is a core feature of type 2 diabetes, polycystic ovary syndrome (PCOS), metabolic syndrome, and a wide array of related health issues. Common symptoms include fatigue after meals, stubborn weight gain (especially around the waist), sugar cravings, and hormonal imbalances.

Fructose is metabolized differently than glucose. It bypasses insulin regulation entirely and is processed almost exclusively in the liver. While this may seem harmless, the metabolic consequences are significant. During fructose metabolism, the enzyme fructokinase rapidly converts fructose into fructose-1-phosphate, consuming ATP in the process. This energy depletion triggers a rise in uric acid, mitochondrial dysfunction, and lipogenesis—the creation of fat.

This combination of events promotes non-alcoholic fatty liver disease (NAFLD), which directly impairs insulin signaling in liver cells. Over time, as liver fat increases, the body becomes less responsive to insulin, even if blood sugar levels are still in a “normal” range.

This explains why insulin resistance often begins before blood sugar rises, and why some people with normal fasting glucose levels may still be experiencing significant metabolic dysfunction.

Insulin resistance isn’t just about carbs or calories—it’s about cellular energy. When mitochondria are stressed from ATP depletion (as happens during excessive fructose metabolism), they send signals that reduce the cell’s ability to respond to insulin. This creates a vicious cycle of:
- More fat storage
- More inflammation
- More insulin resistance

Even if someone avoids added sugars, endogenous fructose (made internally from glucose or sorbitol via the polyol pathway) can still activate this pathway under conditions of **stress**, **dehydration**, or **high-carb meals**.

Yes—but it requires addressing the underlying metabolic drivers, not just managing blood sugar. Reducing dietary fructose, improving mitochondrial health, and supporting the body’s ability to regulate uric acid and inflammation are all key.

Strategies often include:
- Lowering total carbohydrate load (especially refined sugars)
- Supporting mitochondrial function with nutrients
- Using supplements like berberine, luteolin, or tart cherry extract
- Getting adequate sleep, exercise, and hydration

At LIV3, we believe insulin resistance is not simply a glucose problem—it’s a fructose metabolism problem. By understanding and supporting the pathways involved—especially those driven by fructokinase and uric acid—we aim to restore the conditions under which cells can regain insulin sensitivity.

Recognizing and addressing insulin resistance early is one of the most powerful moves you can make to reclaim your metabolic health.