The majority of overweight and obese people are normoglycaemic . They produce more insulin than their diabetic counterparts of a similar weight. Whilst they continue to be able to produce sufficient insulin then they do not become diabetic. Their pancreas can compensate (at least to a point, which in some cases can be extremely high)
We see this compensatory increase in production during pregnancy and during adolescence when energy needs increase.
It is only when insulin resistance has also increased and reached the point that the beta cells can't compensate that we get hyperglycemia. It's then that beta cells may be killed by gluco and lipo toxicity (or perhaps in some cases just made dysfunctional)
Insulin resistance is by some researchers today thought to be a defence by cells against too much energy. When fat or muscle cells get too full so they can't take any more they become resistant to insulin preventing energy from entering . They are protecting themselves and don't 'think' of the upstream consequences for the rest of the organism. This happens at a different threshold in different individuals; some people might have to became mega obese before it happens and others may be of 'normal' weight .
This is in a way demonstrated by those very rare cases where people have almost no fat cells. They are diabetic and extremely insulin resistant.
http://www.bbc.com/news/health-22903537
It's also demonstrated when we exercise, we use up some of the cells energy stores we become less insulin resistant.
Conversely Giving injected insulin when the cells are more resistant causes weight gain since it's forcibly overcoming that insulin resistance with more insulin and allowing more energy into the cell. (and thus more is able to be stored)
(I've very much simplified the resistance as a defence against obesity hypothesis; leptin also plays a part
http://www.lsi.umich.edu/newsevents/lsinews/2012-06-05)