Insulin resistance is a reduced responsiveness of target tissues to insulin: the same concentration of hormone produces a smaller effect than it should. It is not the absence of insulin, and it is not a defect in the receptor alone. The defect sits at multiple points along the signaling chain and differs by tissue.
In skeletal muscle, insulin normally triggers translocation of GLUT4 (glucose transporter type 4) vesicles to the cell surface, and this step is blunted. Muscle takes up less glucose after a meal, so more of the glucose load stays in the blood.
In the liver, insulin normally suppresses gluconeogenesis (new glucose synthesis) and glycogen breakdown. When the liver is resistant, this brake weakens: hepatic glucose output continues even when insulin is high, adding glucose to the circulation instead of removing it.
In adipose tissue, insulin normally restrains lipolysis (fat breakdown). Resistant adipose tissue releases free fatty acids at a higher rate. Those fatty acids reach liver and muscle, where lipid intermediates such as diacylglycerol and ceramides interfere with insulin signaling, worsening resistance in those tissues.
The result is a coordinated failure: less glucose disposal in muscle, more glucose release from liver, and a lipid signal from adipose tissue that reinforces the first two.