Resistance alone does not cause diabetes. As long as beta cells can secrete enough insulin to overcome the weakened response, blood glucose stays normal. This is compensatory hyperinsulinemia: insulin levels rise above the normal range, and glucose remains controlled.
The compensation has a cost. Beta cells must sustain a higher secretory load for years. Over time, the beta-cell mass and function decline. The transition to diabetes occurs when insulin secretion can no longer match the degree of resistance, so glucose rises despite high insulin levels. At that point the deficiency is relative, not absolute: insulin is still produced, but not enough for the prevailing resistance.
The animation shows this balance. Early on, the secretion curve rises to match the resistance curve, and glucose stays flat. As beta-cell function falls, the secretion curve can no longer keep pace, and the glucose curve begins to climb. The crossing point is where hyperglycemia becomes persistent.