According to foreign media reports, scientists at the University of Virginia and the Medical College of Wisconsin have discovered that a gene involved in the rules of biological rhythms may also be a major control factor involved in regulating metabolism. The study reported that a gene controlled by the biological clock would have an effect on weight gain in mammals through high-fat foods. The study was led by Joseph C. Besharse of the Medical College of Wisconsin and Carla B. Green of the University of Virginia, and their paper was published this week in the Journal of the National Academy of Sciences (PNAS). Pishas and Green discovered the gene, called nocturnal protein, more than a decade ago, and the protein it encodes is found in a variety of mammalian body tissues, including the liver. In their paper, Pishas and Green noted that when the biological clock gene night protein gene was inactivated in rats, they did not gain weight even when they were fed a high-fat diet. “We have evidence that the biological clock itself is functioning normally in the mutant rats,” Pishas said, “but many aspects of fat and glucose metabolism are disrupted.” The biological clock is the body’s internal clock that regulates organs and cycles of activity and rest by controlling energy, alertness, growth, mood and the effects of aging. Research in this area has addressed aging, jet lag, sleep disorders, shift work and dieting. The researchers disrupted the nocturnal protein gene gene in a group of rats and then fed some of them a standard diet while feeding the others a high-fat diet. When the normal rats were fed the standard diet, they were no different in appearance or behavior from the normal rats. They looked small and compact, kept scurrying around on their wheels, and remained active at the same time of day. Rats lacking the nocturnal protein gene in their bodies gained only slightly in weight when fed a high-fat diet. When normal rats were fed a high-fat diet, they gained twice as much weight as rats lacking the nocturnal protein gene. In addition, the wild rats collected a lot of fat around their livers, while the rats lacking the nocturnal protein gene gene did not. “If you’re just focusing on obesity, then not having the gene is pretty good for them,” Pishas said, but “the mutant rats also had altered glucose metabolism when they were fed a normal diet. It’s likely that the nocturnal protein gene, a protein produced in multiple tissues (including liver, mast cells, pancreas, viscera), has effects on lipid and glucose metabolism at multiple levels.” He added that this effect triggers an impediment to insulin secretion by the pancreas, which functions to transport glucose from the blood to individual cells and convert it to energy. People with low insulin secretion or impedance to secretion are prone to type II diabetes. Pishas said his group will continue to study the molecular mechanisms of action of the nocturnal protein gene gene, not just in the liver but also in other body tissues that produce the protein, such as the eyes, brain and kidneys. We certainly hope to find a drug to inhibit the activity of the nocturnal protein gene in order to affect fat storage, he said, but this all awaits further research.