It has been long contemplated that Gastrin is responsible for controlling the urge to eat and therefore can be effectively used for weight management programmes. Researchers today // have found it to be responsible for much more.
For the first time, researchers at the University of Texas Medical Branch at Galveston 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 discoveries likely will have wide implications for clinical research on obesity, colon cancer and metabolism.
The team leader was Pomila Singh, Ph.D., professor of neurosciences and cell biology at UTMB. The co-authors were Stephanie Cowey Ph.D.; Michael Quast, Ph.D.; Dr. Ligia Maria Belalcazar; Dr. Jingwa Wei; Xiaoling Deng; and Randall Given, Ph.D.
“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
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