In the experiments reported in the Kobe Journal of Medical Sciences, the investigators looked at the effect of insulin on ß2-stimulated fat loss. Those who are really interested in the science of fat loss can read the study online at http://www.med.kobe-u.ac.jp/journal/contents/53/99.pdf free of charge. ß2-stimulated fat loss occurs in a series of steps, with one reaction causing another until stored fat is broken down and released. Using isoproterenol, a potent stimulator of ß-receptors, the scientists measured fatty acid release from fat cells exposed to the drug. They compared these results to fat cells that had been exposed to insulin before being stimulated by isoproterenol and found that insulin blocked fatty acid release to a remarkable degree. The researchers then worked down the biochemical pathway, finding that the negative effect of insulin on fat loss also blocked the fat-loss effect of caffeine (which represents the second step in ß2-stimulated fat loss). A third step in fat loss involves an enzyme called PKA, which activates or turns on the actual fat breakdown process. Not surprisingly, insulin also blocked this step from being activated. PKA turns on the enzymes that open the perilipin envelope surrounding the stored triglyceride-fat, as well as the enzyme that attacks triglycerides and breaks them down to individual fatty acids and glycerol.

Clearly, insulin interferes with fat loss in several different ways, making it very difficult for anyone to lose fat when insulin levels are high. Not only that, but under the long-term influence of insulin, fat cells burn less fat, because insulin interferes with the creation of mitochondria, which are the tiny parts of the cell that burn fatty acids to make energy. The experiment did not look at other cell types, but it is likely that a similar effect would be noted in other insulin-sensitive tissue, like muscle.

Fascinating as such research is to physio geeks and Biochem nerds (like me), what practical use are the discoveries revealed in the study? First, it gives greater credence to the power of low-carbohydrate and low glycemic-load diets. If insulin is blocking the release of stored fat, it makes little sense to incorporate a diet that periodically stimulates the release of high concentrations of insulin (traditional low-fat diets). When fat loss is the goal, carbohydrate intake should be reduced and the choice of carbohydrates should be limited to slow-releasing, low glycemic carbohydrates to keep insulin levels from becoming elevated. Secondly, it appears that insulin can severely limit, nearly blocking fat loss, even when the sympathetic system is activated. In other words, it does little good to exercise or take a fat burner sooner than 2 hours after eating if the main intent of training is to break down and burn stored fat. All those bottles of ephedrine-caffeine and other stimulants were wasted if they were taken right before or after a meal, even if they gave a “buzz.” Perhaps some of the success noted by people following Atkins-type diets was due to an increased fat-loss effect of Fat Burners. Third, it also shows the folly of drinking a “sports drink” in the gym. The simple ingestion of a 60-gram carbohydrate-laden drink not only replaces the calories that might be expended exercising, but also prohibits the fat cells from contributing to the energy needs by releasing fatty acids, so the body is forced to use up muscle and liver glycogen stores and rob certain Amino Acids to maintain blood sugar levels when glycogen levels drop. Fourth, it introduces a suggestion that long-term eating habits that stimulate elevated insulin concentrations may reduce fat burning or the basal metabolic rate (how many calories are burned at rest) by inhibiting the production of mitochondria, which is the part of a cell that burns fat for calories.