Insulin resistance is when the body’s cells respond less effectively to insulin, so the pancreas must produce more of it to keep blood glucose in range. Sustained long enough, this progresses to prediabetes and type 2 diabetes. It is reasonable to ask what the single biggest driver is — but the honest answer is more specific than “an unhealthy lifestyle”.
The central driver: where fat is stored
The strongest mechanistic explanation is not body weight as such, but where fat is stored. Fat accumulating in the abdomen around the organs (visceral fat) and inside tissues that are not designed to store it — liver and skeletal muscle, known as ectopic fat — is what most directly impairs insulin action [1].
Visceral fat behaves differently from fat under the skin. It releases free fatty acids and pro-inflammatory signalling molecules straight into the portal vein and the liver, disrupting normal insulin action in liver, muscle and fat tissue [2]. This is why two people at the same weight can have quite different insulin sensitivity, and why waist measurement carries information that BMI does not.
What contributes
- Excess energy intake over time, leading to visceral and ectopic fat accumulation.
- Physical inactivity and sedentary time. Time spent sedentary is associated with adipose tissue insulin resistance and visceral adiposity, and low cardiorespiratory fitness with central fat accumulation — independently of total body weight [3].
- Short or poor-quality sleep, which increases energy intake and promotes abdominal fat gain [4].
- Genetics, ethnicity and family history, which set how susceptible you are at any given level of adiposity. People of South Asian, African and African-Caribbean backgrounds develop insulin resistance at lower BMIs [5].
A note on carbohydrates
Carbohydrate intake is often named as the cause. The evidence does not support singling it out: it is chronic energy excess and the resulting fat deposition that drive insulin resistance, not carbohydrate as a macronutrient. Reducing refined carbohydrates and sugary drinks often helps, largely because it reduces total energy intake.
What improves it
Insulin resistance responds well to change, often before much weight is lost. Regular activity improves muscle glucose uptake within days. Losing even 5–10% of body weight meaningfully reduces visceral fat. Improving sleep, reducing sedentary time and stopping smoking all contribute. Change made gradually is more likely to hold.
References
- Després JP, Lemieux I, et al. Ectopic Fat in Insulin Resistance, Dyslipidemia, and Cardiometabolic Disease. New England Journal of Medicine.
- The pathophysiology of visceral adipose tissues in cardiometabolic diseases. PMC11407912.
- Associations of objectively measured physical activity, sedentary time and cardiorespiratory fitness with adipose tissue insulin resistance and ectopic fat. International Journal of Obesity, 2023.
- Covassin N, et al. Effects of Experimental Sleep Restriction on Energy Intake, Energy Expenditure, and Visceral Obesity. JACC, 2022.
- NHS. Type 2 diabetes.
This article is general information and is not medical advice. If you are concerned about your blood sugar or diabetes risk, speak to your GP — insulin resistance is diagnosed with blood tests, not from symptoms.