Researcher(s)
- Arielle Mahugu, Biological Sciences, University of Delaware
Faculty Mentor(s)
- Ibra Fancher, Kinesiology & Applied Physiology, University of Delaware
Abstract
Obesity is linked to problems with blood vessel function, partly due to high levels of saturated fatty acids such as palmitic acid. These fatty acids can affect endothelial cells, which line blood vessels and help regulate vascular health. Our lab has previously shown that visceral adipose tissue (VAT) reduces the function of an important potassium channel in these cells, called Kir2.1, without changing how much of the protein is present. This suggests that the channel is being affected in ways other than expression. One possible factor involved is CD36, which is a protein that aids in bringing fatty acids into cells.
In this study, we investigated how palmitic acid affects the expression and function of CD36 and Kir2.1 in human adipose microvascular endothelial cells (HAMECs). We treated HAMECs with palmitic acid and analyzed the cells using Western blotting, immunocytochemistry, and whole-cell patch clamp recordings.
We found that Western blotting showed that CD36 protein levels decreased after treatment. Analysis of Kir2.1 expression is ongoing. However, imaging with fluorescently labeled palmitic acid, which tracks its movement and uptake into cells, showed that fatty acid uptake increased. This suggests that the cells may be using other transporters or that the remaining CD36 is more efficient or active. Patch clamp studies showed that palmitic acid reduced Kir2.1 channel activity. When CD36 was knocked down using siRNA, Kir2.1 function was partially restored even in the presence of palmitic acid. This suggests that CD36 still plays a role in how palmitic acid impairs Kir2.1 function, possibly through signaling pathways rather than by changing channel levels.
These results help explain how fatty acids like palmitic acid contribute to endothelial dysfunction in obesity. Even though Kir2.1 protein is still present, its function can be disrupted by changes in cell signaling and fatty acid transport.