As a result of natural aging, AMPK levels are lowered, which is a major cause of increased amounts of unwanted belly (abdominal) fat. AMPK is an enzyme found in each and every cell in your body. This is because abdominal fat can create compounds that may cause inflammation and oxidative stress. Belly fat can actually escalate various natural aspects of the aging process that takes place in the body. One of the worst kinds of fat is belly fat. One might think that all body fat is the same, but in fact specific types of body fat causes greater health concerns than others. "There are broader questions beyond NAFLD to ask about whether genetic activation of AMPK in muscle mimics exercise and whether activation of AMPK later in an organism's life can promote life span," says Shaw.The active ingredients (Gynostemma pentaphyllum) and citrus flavonoid hesperidin) in AMPK Metabolic Activator activate AMPK enzyme which helps reduce unwanted abdominal fat, by targeting this kind of fat specifically for cellular energy production, thereby reducing belly fat. The researchers next plan to study AMPK activation in a plethora of other tissues, including muscles, where scientists have hypothesized AMPK could have a dramatic effect. "These results indicate that AMPK could potentially be a powerful treatment to a host of diseases in humans," says Shaw, who holds the William R. In addition to the effects on liver fat, AMPK activation - even though it was limited to the liver - also lowered levels of fats elsewhere in the body, suggesting that hormones released by the liver into the rest of the body were affected. "It's further confirmation that AMPK activators should be tested clinically." "This paper confirms that AMPK is a good target for treating NAFLD," says Garcia. Moreover, when AMPK was activated in mice that were fed a high-fat diet, the mice were protected against weight gain and obesity and had fewer signs of liver inflammation. In both mice with and without NAFLD, levels of fats in the liver dropped when AMPK was activated - new fat production was slowed and existing fats were metabolized. This condition is equivalent to nonalcoholic fatty liver disease (NAFLD) in humans, the leading form of chronic liver disease in American adults. Then, they fed a subset of these mice high-fat diets leading to diet-induced obesity and an excess accumulation of fats in the liver. To test the utility of the new model, the researchers developed mice that could have AMPK activated in the liver. Moreover, by double-engineering the inducible AMPK gene in the mice, the researchers can also control where in the body this AMPK activation happens - everywhere, or just in a select tissue or tissues. "The model we've developed is much more similar to what you would see in a clinic if you target AMPK with drugs," says Garcia. So Garcia, Shaw and their colleagues enabled a mouse to have a special version of AMPK that lets the researchers activate the gene by feeding the adult mouse an antibiotic. "When AMPK is overactivated from the very beginning of embryogenesis, we don't know what effects it's having on normal development," says Daniel Garcia, a senior research associate at Salk and first author of the new paper. Until now, the only way to study the specific impact of genetically increasing AMPK activity was to change its activity in an organism for its entire life, starting at embryogenesis. In different tissues throughout the body and at different time points in development, AMPK likely has varying effects. In response, AMPK alters the activity of many other genes and proteins, helping keep cells alive and functioning even when they're running low on fuel. Cells activate AMPK when they are running low on energy, and AMPK is activated in tissues throughout the body following exercise or during calorie restriction. "It really gives us a new way to define the health benefits of this specific enzyme in a wide variety of diseases."ĪMP-activated protein kinase, or AMPK, is known as a master regulator of metabolism. "This model will allow us to answer questions that scientists could not answer before," says Salk Professor and Salk Cancer Center Director Reuben Shaw, who led the new work. In the paper, published Januin the journal Cell Reports, the Salk team uses the new model to activate AMPK in the livers of adult mice with fatty liver disease. Now, Salk researchers have developed a new system that lets them study in more detail than ever exactly how, where and when AMPK carries out its molecular and therapeutic functions.
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