This data is published in the Nov. 3 edition of the Proceedings of the National Academy of Sciences ( PNAS ).

UC professor Manoocher Soleimani, MD, and colleagues found that when transporter Slc26a9 - the gene responsible for the production of chloride in the stomach-is eliminated from the mouse model's system, acid secretion in the stomach stops.

Gastric acid, comprised mainly of hydrochloric acid (HCL), is the main secretion in the stomach and helps the body to break down and digest food.

"Investigators were already aware of the gene that caused hydrogen to secrete in the stomach, but the gene that caused chloride to secrete has remained an unknown," Soleimani says. "When we knocked out-or eliminated-this specific transporter in mouse models, acid secretion in the stomach completely halted."

"The hydrogen and chloride genes must work together in order for the stomach to produce acid and function normally."

Soleimani, director of UC's nephrology division and principal investigator of the study, hopes that this data can help researchers create more therapies for people who overproduce stomach acid.

"A very large number of people have acid reflux-caused by regurgitation of stomach acid into the esophagus-or peptic ulcers-caused by the passing of excess stomach acid into the small intestine," Soleimani says. "This occurs because of overproduction of acid in the stomach, and current medications that help control this condition cause undesirable side effects."

He adds that long-term use of these kinds of drugs could cause damage to the lining of the stomach, among other problems.

"With this information, we hope to one day be able to administer gene therapies to patients and avoid this painful and damaging problem altogether," he says.

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"That is a very high effect for a mental illness, because most mental illnesses have many potential causes," Provencio noted. "A mental illness may arise from many mutations, and we have found one that has a clear link."

The melanopsin gene encodes a light-sensitive protein that is found in a class of photoreceptors in the retina that are not involved with vision, but are linked to many non-visual responses, such as the control of circadian rhythms, the control of hormones, the mediation of alertness and the regulation of sleep.

The mutation in this gene may result in aberrant regulation of these responses to light, leading to the depressive symptoms of SAD. About 29 percent of SAD patients come from families with a history of the disorder, suggesting a genetic or hereditary link.

"The finding suggest that melanopsin mutations may predispose some people to SAD, and that if you have two copies of this mutation, there is a very high probability that you will be afflicted," Provencio said. "An eventual understanding of the mechanisms underlying the pathological response to light in SAD may lead to improved treatments."

Provencio adds that the finding, with further study, could also lead to improved testing for SAD.

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