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LGD 4033 was developed with the goal of preventing muscle loss in the elderly and in those who suffer from muscle dystrophy. As a result, the compound seems to help lower the markers of frailty in both individuals and mice. In the study, the researchers divided the mice into two groups—one which received the daily dose for four days with food, and the other which was given the drug for two weeks without food. The researchers tested the mice's heart, muscle and lipid metabolism in the following four months. Mice on the diet treated with the drug showed a significantly lower body weight and triglyceride levels than those on the placebo, while lipid levels actually declined during the fourth month of the test. Researchers believe that the drug, which targets the "on-off" switch in cells that control fat storage and fat production, can have important beneficial effects on the regulation of both body weight and lipid level—and even muscle function. These were observed in two ways. First, this drug treated mice with a genetic defect that caused them to be unable to process the energy-rich glucose needed for energy production. Thus, it prevented the mice from using up their stored fatty acids. Secondly, it prevented their muscle cells from storing fat, thus preventing their muscle mass to become excessive. "Our research suggests that anti-diabetics, who cannot afford medication that increases their daily calorie intake, could take the dietary benefits of LDO-4033 for the first time with the help of a supplement without fear of an increased daily calorie requirement," said Dr. Chia. The team plans to conduct further studies to determine the effects of the drug on the body's energy metabolism and muscle recovery. "We hope to understand how this drug affects the body and how it interacts with other drugs, especially in patients with certain metabolic conditions, such as type 2 diabetes or hypertension," Dr. Chia said. SOURCE: https://www.ncbi.nlm.nih.gov/pubmed/21698409 Citation: The effects of LDO-4033 on mitochondrial activity and the regulation of obesity-associated metabolic disorders by S. Chia, R. A. Fett, F. Wu, J. P. Le, B. R. A. Mokdad, and W. M. S. Lee. CISPN: 2016;1771:1-20. Related Article: