First of all:

In nondiabetic, normotensive obese subjects, the prevalence of insulin resistance is relatively low

Secondly, have you read this study? It doesn't say what you think it does.

Three novel aspects, however, emerge from the data. First, the severity of insulin resistance in obesity was overestimated when insulin-mediated glucose uptake was normalized by body weight (as is often done).

[...]

Second, the prevalence of insulin resistance among the obese subjects was surprisingly low: only one in four subjects was as resistant as the bottom decile of the lean group. Even in the presence of definite obesity (BMIs of 28–50 kg·m22), only one in two individuals was insulin-resistant. Regression analysis showed that a rather large difference in body weight (30 kg) was associated with only a modest (25%) decrement in insulin sensitivity. Thus, we conclude that the quantitative impact of obesity on insulin action in otherwise healthy subjects is not as large as previously thought.

[...]

Third, when whole-body glucose uptake was expressed in absolute terms, the impact of BMI was marginal (Fig. 3). This finding reflects the fact that fat-free mass is expanded in the obese (Table I); though relatively resistant to the action of insulin, this excess fat-free tissue is metabolically active and contributes to glucose tolerance. Conversely, to the extent that weight reduction includes loss of fat-free tissue, this compensatory adjustment is lost.

They then go on to ask:

A relevant question is why a high proportion of obese subjects are not insulin resistant.

and continue to debunk the wrong, yet prevalent ideas about insulin in the obese.

Finally, they conclude:

In summary, in simple obesity insulin resistance is not as prevalent as previously thought, and is less frequent than insulin hypersecretion.

As you probably guessed, all emphases are mine.