A person with visceral obesity, arterial hypertension and acanthosis nigricans may still not have diabetes. But they may already have insulin resistance — a state in which a typical insulin concentration produces a smaller biological response than expected. In its definition of T2DM, ADA 2026 places it "in the background": the loss of adequate insulin secretion often occurs against a background of insulin resistance, not instead of it.
The term needs to be unpacked at once, because it will be used freely from here on. Insulin binds to its receptor on the myocyte, hepatocyte and adipocyte. Inside the cell, the insulin receptor substrate is then phosphorylated, the PI3K–Akt pathway is activated, GLUT4 moves to the membrane of muscle and adipose tissue, and the liver reduces glycogenolysis and gluconeogenesis. In resistance this cascade is weakened. There is no hyperglycaemia yet, as long as the β-cell compensates with more insulin. Compensatory hyperinsulinaemia is the laboratory trace of resistance, not "excess insulin as the cause of everything".
Where this is visible at the bedside, even before glucose. The MoH RK 2022 protocol lists the clinical signs of insulin resistance: visceral obesity, arterial hypertension, acanthosis nigricans. Acanthosis nigricans is a velvety hyperpigmentation of skin folds (neck, axillae, groin). It is a clinical marker, not a diagnostic criterion for diabetes. Its presence raises the index of suspicion, and it is included in the list of conditions "associated with insulin resistance" in ADA 2026 Table 2.5.
Why resistance is linked to visceral fat rather than to "excess weight in general". Visceral adipose tissue is more lipolytically active. The flow of free fatty acids into the portal system of the liver sustains steatosis and disrupts insulin signalling in the hepatocyte: the liver continues to produce glucose in the fasting state, even though there is already a lot of insulin in the blood. In skeletal muscle, intramyocellular lipid interferes with GLUT4-mediated glucose uptake — hence postprandial hyperglycaemia when compensation fails. This is the pathophysiological model on which current reviews rest and which ADA uses in describing T2DM as a heterogeneous disease with the common denominator "secretory defect plus resistance". The course does not present a separate RCT of the kind "remove intramyocellular fat — cure diabetes" as a proven therapeutic law.
What resistance does not explain on its own. It is not equal to T2DM. A person with obesity and acanthosis nigricans may have a fasting glucose of 5.2 mmol/L. There is no diagnosis. It is not equal to "the patient is to blame". Physical inactivity, family history, gestational diabetes and some medications (glucocorticoids, some antipsychotics) are all factors that ADA includes in the risk map, and some of them are not chosen through behaviour. It is not the same as "insulin does not work at all": in T2DM insulin works, but more of it is needed for the same effect, for as long as the β-cell can keep up.
The link to complications starts here, even before "duration of diabetes". Insulin resistance belongs to the same cluster as atherogenic dyslipidaemia, hypertension and low-grade inflammation of adipose tissue. It is a cluster of associations, clearly visible in observational cohorts. It explains why a person with newly diagnosed T2DM may already have coronary heart disease. It does not prove that "by fixing resistance with metformin we are thereby treating the coronary arteries". The cardiovascular benefit of specific classes has been proven in separate RCTs in separate populations — that is Module 4. Here one sentence is enough: resistance is the background against which hyperglycaemia and vascular risk live side by side, but they are not the same process.
The practical conclusion of the lesson. When you see visceral obesity and acanthosis nigricans, you do not make a diagnosis from the skin. You understand which physiology is already switched on, and you order glucose and HbA1c, because β-cell compensation may already have run out.