We hear so often that diabetes can be the end result of obesity, but what exactly is behind this process? What mechanism is at play which creates diabetes in people that are extremely overweight?

The answers to these questions can be a bit complicated because of each individual's background, but essentially what is happening is that when a person becomes more and more overweight, they become resistant to their own insulin. When an obese person starts to lose weight and get healthy again, their bodies will start to slowly regain its insulin sensitivity.

Scientists and researchers have believed for a long time now that there must be a substance which is produced by fat that may be helpful in explaining the connection between obesity and diabetes. In fact, they have recently discovered a certain compound that exists in the fat tissues of mice which might be the answer they are looking for.

A compound known as resistin

The compound known as resistin was first noted in the journal entitled "Nature" (January issue of 2001) when it was isolated in small rodents. Resistin is a hormone which is created by fat cells and causes the body to become resistant to its own insulin. Scientists then discovered that resistin could be suppressed by a drug known as "rosiglitazone" which is designed to improve insulin resistance.

Another good sign of progress in the attempt to control insulin in obese people is the fact that when resistin was injected into mice, it caused the mice to become resistant to their insulin. However, anti-bodies that were opposed to resistin were given to these same mice which then showed a decrease in the resistance to insulin.

This is not an official finding as of yet

Although the above research looks very promising, the connection is not yet 100% founded on concrete evidence with humans because resistin has not yet been detected in human fat cells. However, Researchers are confident that they will find a similar compound to that of resistin within the human body stemming from fat cells, but it is not yet verified in any recent publications.

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