Insulin resistance: what is happening inside the body

Insulin is a delivery instruction. After a meal, glucose enters the blood and the pancreas releases insulin to tell muscle and fat cells to take it in, and to tell the liver to stop producing more glucose of its own. In a system working well, a modest amount of insulin achieves all of this.

Insulin resistance means the instruction is being heard less clearly. The same amount of insulin moves less glucose, so the pancreas compensates by sending more. For years — often more than a decade — that compensation succeeds. Blood glucose stays entirely normal. The person feels well. Every routine report comes back reassuring. What has changed is the effort required, and effort is not something a glucose test measures.

This is the single most useful idea on this page: a normal sugar report tells you the compensation is still working, not that there is nothing to compensate for.

The mechanism has several parts. Muscle is the largest destination for glucose after a meal, taking it up through a transporter that insulin brings to the cell surface. When muscle mass is low, or muscle is rarely emptied of its stored fuel by exercise, there is less room for glucose to go. Fat cells, meanwhile, have a finite capacity to store fat safely under the skin. When that capacity is exceeded — and the threshold differs enormously between individuals — fat is deposited where it does not belong: around the abdominal organs, inside the liver, inside muscle fibres and around the pancreas. Fat in these places interferes directly with insulin signalling. High insulin then instructs the liver to convert surplus carbohydrate into fat, which adds to the deposit, which worsens the signalling. The loop reinforces itself.

Two consequences explain much of what people see on their reports. Triglycerides rise and HDL falls, because the liver is exporting newly made fat. Uric acid rises, because insulin reduces how much the kidney excretes. Both move before glucose does.

The South Asian part of this story is well documented. Indian research going back to the 1990s described the thin-fat pattern — Indian newborns are smaller than European newborns yet carry proportionally more body fat, a pattern that appears to persist into adult life. At the same BMI, South Asian adults tend to have less subcutaneous storage capacity, more fat around the organs and in the liver, and less skeletal muscle. The practical result is that the threshold at which fat spills into the wrong places is reached at a lower body weight and a younger age. This is not a flaw in Indian bodies; it is a mismatch between a metabolic inheritance and an environment of abundant refined carbohydrate, low activity and short sleep that arrived within a single generation.

ⓘThis information is educational and not a diagnosis.

Insulin resistance has no symptom of its own. It has signs — some visible on the body, some on a report — and learning to read them is most of the skill.

The most useful visible sign is acanthosis nigricans: a velvety, darkened thickening of the skin at the back of the neck, in the armpits, in the groin or over the knuckles. It is frequently mistaken for uncleanliness, particularly on Indian skin, and children are sometimes scolded for it. It is a response to high circulating insulin — one of the few places where the mechanism is visible from outside. Small soft skin tags often accompany it.

The shape of the body carries information too. A waist that has grown while the scale has barely moved suggests fat redistributing toward the organs while muscle is lost. In women, irregular cycles, acne and unwanted hair growth point toward PCOS, which is insulin-driven in a large proportion of cases.

Some people notice a heavy, sleepy hour after a large rice or roti-based meal; hunger returning an hour or two after a full plate; a mid-afternoon slump with a pull toward something sweet; or months of careful eating and walking that the scale has not answered. Each is unreliable alone and worth noticing as part of a pattern.

The reports are where the signal is clearest. Triglycerides above roughly 150 mg/dL with an HDL below 40 in men or 50 in women; fatty liver on a scan done for something else; a raised uric acid; blood pressure creeping upward; an HbA1c that has drifted from 5.2% to 5.5% over three years. Any one alone is unremarkable. Two or three together, in someone with a family history of type 2 diabetes, describe insulin resistance quite reliably without any specialised test.

The signs listed below are of a different kind. They suggest that compensation has already failed and glucose has risen substantially, or that a complication needs urgent attention. They warrant being seen today rather than at the next convenient appointment.

There is no single test that establishes insulin resistance, which frustrates people who arrive wanting one. What exists is a set of measures that, read together, give a fair picture.

The gold standard is a research procedure. The hyperinsulinaemic-euglycaemic clamp measures insulin sensitivity directly and takes several hours. Everything used in clinical practice approximates it.

Fasting insulin and HOMA-IR. Fasting insulin, measured in µIU/mL after a genuine 8–12 hour fast, tells you how much insulin the body is using to keep fasting glucose where it is. HOMA-IR combines it with fasting glucose: insulin × glucose ÷ 405 when glucose is in mg/dL, as in most Indian labs. Indian studies suggest thresholds around 2.5, though published cut-offs vary and there is no consensus figure. Three cautions matter: insulin assays are not standardised between laboratories, so two labs are not comparable; the measure loses reliability once insulin production begins to fall, which is when people are most anxious to use it; and it is a single fasting snapshot of a dynamic system.

The cheaper markers that often say as much. A fasting lipid profile read as a triglyceride-to-HDL ratio, waist circumference, blood pressure and liver enzymes with an ultrasound are inexpensive, widely available and, together, informative. In much of India these are more practical than fasting insulin and the reasonable place to start.

Glucose testing tells you the consequence, not the mechanism. HbA1c and fasting glucose describe how far compensation has been pushed. A normal result alongside clear signs is not a contradiction — it is the expected early finding, and the reason this page sits separately from the one on prediabetes.

Cost and access, honestly. Fasting insulin sits outside most standard health-check packages in India and costs meaningfully more than an HbA1c. It adds most where the picture is suggestive and glucose results are normal. Where prediabetes or diabetes is already established, the mechanism is no longer in doubt and the money is better spent elsewhere.

None of these findings decides what happens next on its own.

The encouraging feature of insulin resistance is that it is among the more responsive things in medicine. What follows is general explanation; what applies to your body, and anything involving medicines, belongs with your doctor.

Build the destination. Skeletal muscle is where most post-meal glucose goes, so increasing how much there is, and how often it is emptied, is the most direct lever available. Resistance training two or three times a week improves insulin sensitivity independent of weight change, which matters for lean insulin resistance where there is little weight to lose. A single session improves glucose uptake for a day or two afterwards — a reasonable argument for frequency over intensity.

Reduce the load arriving. The Indian plate is typically carbohydrate-dominant, and the useful change is proportion rather than prohibition — a measured portion of rice or roti, a larger share given to dal, vegetables and protein, and attention to what arrives between meals. Added fructose from sweets, packaged juices and sugary drinks is handled almost entirely by the liver and contributes disproportionately to liver fat. Protein spread across the day supports the muscle being built.

Sleep is a metabolic intervention. A few nights of restricted sleep measurably reduce insulin sensitivity in healthy people. Where everything else is being done well and nothing is improving, sleep and untreated sleep apnoea are the variables most often overlooked.

Shift what is stored in the wrong place. Where excess weight is present, a sustained 5–7% reduction lowers liver and visceral fat disproportionately. Where weight is normal, the same result comes from composition and muscle rather than the scale.

Medicines treat the consequences, and sometimes the mechanism. Metformin improves insulin sensitivity and is used in specific situations, including PCOS and higher-risk prediabetes. Other agents have roles in defined circumstances. These are individual clinical decisions, and the lifestyle work continues alongside rather than being replaced.

Follow-up. Waist, triglycerides, HDL, liver enzymes and HbA1c at three to six months give an honest reading. Repeating fasting insulin is rarely necessary and, given assay variability, often creates confusion rather than clarity. What you want is a picture moving in one direction over a year, not a number changing between two Tuesdays.

Insulin resistance is the mechanism underneath fatty liver, prediabetes, PCOS, raised triglycerides and a great deal of stubborn abdominal weight. Understanding it once explains all of them, and it changes what you look for on your reports — triglycerides and HDL rather than only cholesterol, waist rather than only weight, liver enzymes rather than only glucose.

If your glucose results have already moved into the 5.7–6.4% band, the page on prediabetes covers what that number means and what the coming year looks like.

The Learning Session below works through reading your own blood reports in a small group, including the markers that shift earliest.

If you would like your reports read together — the ones you have, rather than the ones you might buy — that belongs in a consultation.