- The main cause of prediabetes is insulin resistance: your muscles, liver and fat cells stop responding well to insulin.
- At first the pancreas makes extra insulin to compensate. When it can no longer keep up, blood sugar rises.
- Fat stored around the waist and in the liver, inactivity, poor sleep and genes are the biggest drivers.
- Most of these drivers can be changed, which is why prediabetes is often reversible.
To understand prediabetes, it helps to understand insulin. After a meal, carbohydrates are broken down into glucose, which enters your blood. Your pancreas senses the rise and releases insulin. Insulin acts like a key: it unlocks your muscle, liver and fat cells so glucose can move in and be used for energy or stored for later. Blood sugar then falls back to normal within a couple of hours.
In prediabetes, that lock-and-key system starts to jam. Understanding why is the first step to fixing it.
Insulin resistance: when the key stops working
How insulin resistance develops
Insulin resistance usually begins years before blood sugar changes, and it often goes unnoticed because the pancreas quietly compensates. Two organs matter most:
- Normally absorb most of the glucose from a meal.
- When they are inactive or loaded with fat, they take up less glucose, so more stays in the blood.
- Normally stops releasing glucose when insulin rises after a meal.
- When it becomes fatty and insulin resistant, it keeps releasing sugar, especially overnight, which raises fasting glucose.
Researchers describe a “twin cycle”: extra fat in the liver makes it resistant to insulin, the high insulin levels that follow make the liver store even more fat, and some of that fat spills over into the pancreas, where it slowly weakens the cells that make insulin. The reverse is also true. When people lose weight, fat leaves the liver first and then the pancreas, and blood sugar often improves within weeks.
Years in the making
A long-term British study of more than 6,000 civil servants tracked blood sugar and insulin for years before people were diagnosed with diabetes. It showed that the changes build slowly and then speed up.
Insulin sensitivity starts to fall. Blood sugar still looks normal.
Insulin resistance worsens more quickly. The pancreas is working flat out.
Fasting and after-meal glucose rise into the prediabetes range.
The pancreas can no longer keep up and blood sugar reaches the diabetes range.
Based on Tabák et al., Lancet 2009 (Whitehall II study).
The encouraging part: the earlier you act on this timeline, the easier it is to turn around.
What drives insulin resistance?
Deep belly (visceral) fat and liver fat release fatty acids and inflammatory signals that block insulin. See Visceral Fat.
Inactive muscles take up less glucose. Long periods of sitting are linked with higher diabetes risk even in people who exercise.
Large, fast sugar loads push insulin up and add to liver fat.
Even a few nights of short sleep make the body less sensitive to insulin.
Having a parent or sibling with type 2 diabetes raises your risk, as does South Asian, Black or Hispanic heritage.
Age, smoking, chronic stress, polycystic ovary syndrome and some medicines, such as steroids, also play a part.
How much do everyday habits matter?
Higher risk of type 2 diabetes linked with each habit
Wilmot et al., Diabetologia 2012; Pan et al., Lancet Diabetes Endocrinol 2015; Cappuccio et al., Diabetes Care 2010; Malik et al., Diabetes Care 2010. These are averages from observational studies.
Signs your body may be insulin resistant
- A waist measurement more than half your height.
- High triglycerides and low HDL (“good”) cholesterol on a blood test.
- High blood pressure or a fatty liver on an ultrasound.
- Dark, velvety skin patches on the neck or in the armpits (acanthosis nigricans).
- A history of gestational diabetes or polycystic ovary syndrome.
These often cluster together as metabolic syndrome.
The good news: it works in reverse too
Insulin resistance is not fixed. Muscles become more sensitive to insulin within hours of exercise, and losing even a modest amount of weight can remove fat from the liver and pancreas. In the Diabetes Prevention Program, every kilogram lost lowered diabetes risk by about 16%. The changes that matter most are covered in Treating Prediabetes.
MythPrediabetes is caused by eating too much sugar.
FactSugar plays a part, but the root cause is insulin resistance, driven mainly by excess body fat, inactivity, sleep and genes.
Common questions
Can thin people get prediabetes?
Yes. Fat stored around the organs and in the liver can cause insulin resistance even when weight looks normal, especially in people of Asian heritage and older adults.
Is insulin resistance the same as prediabetes?
Not quite. Insulin resistance comes first and can last for years with normal blood sugar. Prediabetes is diagnosed once blood sugar rises above normal.
Can a blood test measure insulin resistance?
Tests such as fasting insulin or HOMA-IR exist but are not used routinely. Doctors usually rely on blood sugar, triglycerides, HDL, waist size and blood pressure.
Already diagnosed with type 2 diabetes? Read What Is Type 2 Diabetes? How Insulin Resistance Raises Blood Sugar in our 18-part Type 2 Diabetes Basics series.
- Prediabetes is caused mainly by insulin resistance, plus a pancreas that can no longer fully compensate.
- It builds up over years, long before blood sugar rises.
- Belly and liver fat, sitting, sugary drinks, short sleep and genes are the main drivers.
- Movement, modest weight loss and better sleep improve insulin sensitivity quickly.
- Next: Lifestyle risk factors for prediabetes.
Sources
- DeFronzo RA. From the triumvirate to the ominous octet: a new paradigm for the treatment of type 2 diabetes mellitus. Diabetes. 2009;58(4):773–795.
- Tabák AG, Jokela M, Akbaraly TN, et al. Trajectories of glycaemia, insulin sensitivity, and insulin secretion before diagnosis of type 2 diabetes: an analysis from the Whitehall II study. Lancet. 2009;373(9682):2215–2221.
- Taylor R. Pathogenesis of type 2 diabetes: tracing the reverse route from cure to cause. Diabetologia. 2008;51(10):1781–1789.
- Wilmot EG, Edwardson CL, Achana FA, et al. Sedentary time in adults and the association with diabetes, cardiovascular disease and death: systematic review and meta-analysis. Diabetologia. 2012;55(11):2895–2905.
- Pan A, Wang Y, Talaei M, Hu FB, Wu T. Relation of active, passive, and quitting smoking with incident type 2 diabetes: a systematic review and meta-analysis. Lancet Diabetes Endocrinol. 2015;3(12):958–967.
- Cappuccio FP, D’Elia L, Strazzullo P, Miller MA. Quantity and quality of sleep and incidence of type 2 diabetes: a systematic review and meta-analysis. Diabetes Care. 2010;33(2):414–420.
- Malik VS, Popkin BM, Bray GA, Després JP, Willett WC, Hu FB. Sugar-sweetened beverages and risk of metabolic syndrome and type 2 diabetes: a meta-analysis. Diabetes Care. 2010;33(11):2477–2483.
- Hamman RF, Wing RR, Edelstein SL, et al. Effect of weight loss with lifestyle intervention on risk of diabetes. Diabetes Care. 2006;29(9):2102–2107.
This article is for general education and is not a substitute for advice from your own doctor or healthcare team.