Researchers at the University of Texas Medical Branch at Galveston ( UTMB ) have linked the hormone gastrin to the body’s ability to maintain normal weight and normal insulin levels.

In experiments conducted on mice, the UTMB researchers found that removing gastrin production triggered obesity, insulin resistance and metabolic changes that — in turn — increased the risk of colon cancer in the animals.

The UTMB research results were published in Cancer, the journal of the American Cancer Society.

The scientists unearthed gastrin’s relationship to metabolic factors that control obesity and insulin while they were conducting separate research on the mice to determine whether the removal of gastrin — a growth hormone secreted in the gastrointestinal system — has a connection to colon cancer.

It is well known that many hormonal factors that promote obesity are also risk factors for colon cancer.
In 2003, Singh’s UTMB team demonstrated for the first time that the removal of gastrin has a link to increased risk for colon cancer in mice.

This latest 2005 study connects the dots by showing that obesity and metabolic changes stemming from the removal of gastrin increase the risk of colon cancer.

“ We have for the first time connected three things that weren’t known to be connected: gastrin, obesity and cancer,” Singh said. “We believe that the increase in obesity and the increase in insulin are increasing the risk of colon cancer in mice.”

In the current study, the researchers have uncovered previously unknown functions for gastrin. Until now, nobody had suspected that gastrin had anything to do with obesity or metabolic homeostasis — the physiological process that controls whether people have many or few fat cells, Singh said.

The experiments compared normal mice with mutant mice whose gastrin production capability was removed through genetic engineering. Researchers observed that if gastrin is removed in mice with normal diet, the mice become obese. So, the team set out to find out why removing gastrin made mice fat. Upon further evaluation, they learned that removing gastrin had disturbed the normal metabolic homeostasis.

Removing gastrin not only made the mice obese, but also had the unexpected result of raising the mice’s insulin levels. Since people who are morbidly obese are at high risk for diabetes, the team wanted to know if the fat mice were becoming diabetic. But the fat mice didn’t have diabetes or high glucose.
That’s paradoxical because typically, diabetics have both a high glucose level and a high insulin level.
In diabetics, the body produces extra insulin to try to get rid of excess glucose in the blood, a process known as insulin resistance.
The mice without gastrin appear to display characteristics of insulin resistance, but not signs of diabetes.

Source: University of Texas Medical Branch at Galveston, 2005


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