News Finding: The results from this study at Marshall University demonstrate that the Na/K-ATPase oxidant amplification loop in adipocytes, or cells specialized for fat storage, when impaired, could cause adipocyte dysfunction, worsening obesity and potentially increasing the severity of related diseases.
Paper Finding: In particular, the increases in plasma levels of leptin and inflammatory cytokines (i.e., IL-6, TNFα, and MCP1) in mice fed a WD were dramatically attenuated by NaKtide expression in adipocytes.
News Context: "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," said Komal Sodhi, M.D., senior author, and associate professor of surgery and biomedical sciences at the Joan C. Edwards School of Medicine. The results from this study at Marshall University demonstrate that the Na/K-ATPase oxidant amplification loop in adipocytes, or cells specialized for fat storage, when impaired, could cause adipocyte dysfunction, worsening obesity and potentially increasing the severity of related diseases. The basis of the research examined more closely the role of the adipocyte in obesity, including how it impacts oxidative stress, inflammation, neurodegeneration and NASH.
Paper Context: Attenuation of the NKAL in the adipocytes during exposure to the WD ameliorated oxidant stress within these cells as well as the WD-induced hypertension, dyslipidemia, and insulin resistance. In particular, the increases in plasma levels of leptin and inflammatory cytokines (i.e., IL-6, TNFα, and MCP1) in mice fed a WD were dramatically attenuated by NaKtide expression in adipocytes. This suggests a central role of the Na/K-ATPase signaling loop within adipocytes in the development of obesity and systemic oxidative stress in response to a WD.