No, they are not designed as a tasty alternative low-calorie cat chow diets. But scientists have created a strain of mice that can not produce cholesterol. The animals are viable, the study shows because another fat molecule can pick up most cholesterol functions.
Despite its bad reputation, cholesterol is an important part of our lives. Cell membranes are full, enzymes to alter sex steroid, and developing embryos rely on it to grow. In cells, two biochemical pathways convert sterols cholesterol, and disruption of one or the other leads to serious diseases of the human endocrine system. Researchers had already eliminated a route in mice and found that scurriers can not live without it. Now, another group of scientists, led by Elena Feinstein Quark Biotech in Cleveland, Ohio, arrested another generation cholesterol pathway, they report in the December issue 19 Science .
team has found the gene encoding a key enzyme, desmosterol reductase, which converts desmosterol to cholesterol, and created mice lacking both copies of the gene. Compared to normal mice, the modified mice had very low levels of cholesterol both in the blood and liver; they also had about 20% to 60% less total sterols. The team found that desmosterol was the predominant sterol, suggesting that this molecule can take over in the absence of cholesterol. They also found that embryos, transgenic mice had almost normal cholesterol concentrations, probably they received from their mother and that allowed them to develop normally until birth. As they grew up, however, they developed health problems, including infertility.
The novelty of the results is that "desmosterol seems to be able to perform for cholesterol," said clinical geneticist Forbes Porter of the National Institute of Child Health and Human Development in Bethesda. The work can help researchers understand why cells bother to cholesterol instead of using its precursors, he said. metabolic clinical geneticist Hans Andersson at Tulane University Medical School says the work might not be relevant to human disease because that humans with mutations in desmosterol reductase are sick and yet have high levels of cholesterol, unlike rodents. "mice can not be the best model for human disorders of sterol biosynthesis," he said.
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