New research from a team at the Marshall University Joan C. Edwards School of Medicine establishes that adipocyte-derived cytokines are major players in the development of obesity and its companion diseases. They also found that targeting Na/K-ATPase signaling in adipocytes may prove to be an effective therapeutic strategy. The findings were published this week in Scientific Reports.
“I am very excited about the work in the current Scientific Reports article and the clinical relevance it presents for the role of adipocytes in obesity and other disease states,” says senior author Komal Sodhi.
The new research examined more closely the role of adipocytes—cells that are specialized for fat storage—in obesity. The researchers also looked into how these cells impact the comorbidities of obesity such as oxidative stress, inflammation, neurodegeneration, and NASH (non-alcoholic steatohepatitis). They activated the Na/K-ATPase signaling by feeding mice a diet representative of the western diet, which increased obesity, various plasma cytokines, and biomarkers of neurodegeneration.
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Using a lentiviral vector, the team selectively expressed NaKtide in adipocytes. NaKtide is a peptide that targets the Na/K-ATPase oxidant amplification loop and has been previously shown to decrease oxidative stress and adiposity. Its expression in the current study reduced the severity of all the effects of the western diet, including the biochemical alterations in the brain.
“Our data clearly suggests that obesity and the Na/K-ATPase oxidant amplification loop plays a role in neurodegeneration,” says first author Rebecca Pratt. “Even targeting NaKtide to adipocytes alone still showed a whole-body effect, which highlights the much larger role that adipocytes play in obesity and whole body homeostasis.”
This work builds on the body of work initiated by the Marshall Institute for Interdisciplinary Research (MIIR) Director Zijian Xie, Ph.D., on the previously unappreciated signaling function of the NaK-ATPase.