Researchers Identify Strategy to Target Fat Cells’ Sodium-potassium Pump That Might Reduce Obesity

Researchers Identify Strategy to Target Fat Cells’ Sodium-potassium Pump That Might Reduce Obesity

In a recent study published in journal Science Advances, a team of scientists from the Marshall University Institute for Interdisciplinary Research (MIIR) and the Marshall University’s Joan C. Edwards School of Medicine (SOM) were able to identify a method to block the signal by which the cellular sodium-potassium pump augments oxidants, known to lead to the development of metabolic syndrome and obesity.

According to Joseph I. Shapiro, MD, study lead author and dean of the school of medicine, the study is the result of a major collaborative research effort. “I am extremely proud of this work, as the studies were conceived of, performed and analyzed entirely at Marshall University,” Dr. Shapiro said in a press release. “This work was based on two important components. We employed a peptide, pNaKtide, which was derived from the novel hypothesis developed by Marshall’s MIIR director, Dr. Zijian Xie. Specifically, Dr. Xie has shown that, in addition to its well-described role as an ion transporter, the sodium pump also regulates signal transduction and oxidant amplification. We also exploited work from Marshall’s SOM vice-dean for research, Dr. Nader Abraham, who has demonstrated a key role for oxidant stress in adipocytes in the development of obesity. The studies, which address a critical problem in the Appalachian population we serve, were performed entirely by our research staff at Marshall University.”

The study’s first author Komal Sodhi, MD, who is an assistant professor of pharmacology and surgery at Marshall University, said that in the study entitled “pNaKtide inhibits Na/K-ATPase reactive oxygen species amplification and attenuates adipogenesis,” he and his colleagues studied a specific peptide called pNaKtide, which is able to block the sodium potassium Na/K-ATPase signaling cascade. Using a cell culture system, this mechanism resulted in a change in the phenotype of fat cells (adipocytes).

“We found this decreased the development of obesity and metabolic syndrome in mice subjected to a high-fat diet,” Sodhi said. “The studies performed strongly supported this idea and suggest that if this is confirmed in humans, the Na/K-ATPase might ultimately be a therapeutic target for clinical conditions like obesity and metabolic syndrome, which are particularly relevant to West Virginia where more than one-third of the population is currently obese.”

Shapiro noted that many years of research are still necessary to understand the effect of these findings in humans, however, the researchers believe that they have discovered a valid method that can be used to develop treatments for metabolic syndrome and obesity.

“The bottom line is that we’ve identified a novel mechanism by which to address oxidant stress and, through this mechanism, treat obesity,” Shapiro said. “Our work opens up a new target for intervention in this disease as well as possibly other diseases characterized by oxidant stress.”

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