A team of UC Davis Biomedical Engineers, led by Assistant Professor Anthony G. Passerini, has established a link between inflammation of the arterial lining, waist size, and triglyceride levels in the blood after eating a high-fat, fast food meal. The study reinforces the link between belly fat and inflammation of the arterial linings, which is the main cause of atherosclerosis.

The study is published online by the American Journal of Physiology Heart and Circulatory Physiology.

Triglycerides are types of fat molecules, commonly associated with “bad cholesterol.” Scientists know that high levels of triglycerides in the blood can increase risk of inflammation of the lining of arteries, known as the endothelium. This can lead to atherosclerosis and, eventually heart attacks and strokes. Measuring these early changes in the endothelium is not straightforward. Passerini collaborates with another department faculty member, Professor Scott Simon, on the development of special cell culture-based models that mimic certain properties of blood vessels for use in measuring outcomes that address an individual’s risk.

Passerini’s team wanted to learn the mechanisms by which triglyceride levels cause endothelial inflammation, and to find a way to assess an individual’s inflammatory potential. They recruited 61 volunteers with high and normal fasting triglyceride levels and a range of waist sizes, then measured triglyceride levels after they ate two breakfast sandwiches, hash browns, and orange juice purchased from a major fast food franchise. They selected this meal because it contains foods typically eaten together for breakfast in America, and is a popular fast food breakfast.

Passerini found that after eating the high-fat meal, the size of a type of a particle called Triglyceride-Rich Lipoprotein (TGRL) varied directly with the individual’s waist size and preexisting blood triglyceride level. Lipoproteins are particles that transport cholesterol and triglycerides in the blood. These particles can bind to the endothelium, which triggers inflammation and an immune response, sending white blood cells to repair the damage. Over time, this leads to atherosclerosis.

To measure the inflammatory potential of the triglycerides in the laboratory, the scientists inoculated endothelial cells with the TGRLs they had isolated from the volunteers’ blood. Surprisingly, they found that in response to the TGRLs, the expression of certain markers of inflammation went up in some individuals and in others, it went down.

The “tipping point” was pre-existing triglyceride levels and waist size. Passerini’s team found that individuals with both waist size > 32 inches (not terribly large by most standards) and high triglyceride levels had large lipoprotein particles that bound easily to the endothelial cells and caused inflammation in response to an immune chemical “trigger.” The TGRLs only caused inflammation when exposed to this immune molecule, which suggests that people with existing low-grade inflammation may be more susceptible to endothelial dysfunction related to triglyceride “spikes” that occur after eating high-fat meals. The TGRLs caused the inflammation even though they had not been oxidized.

Passerini thinks that these findings suggest that metabolic stress can sensitize the endothelium to pathological change. In metabolically predisposed people, atherosclerosis can develop gradually in response to repeated episodes of inflammation. Abdominal obesity is associated with metabolic abnormalities, which may predispose people to high triglyceride levels and heightened inflammatory response. Passerini’s ongoing studies investigate the mechanisms by which dyslipidemia leads to endothelial inflammation and atherosclerosis.

Endothelial inflammation correlates with subject triglycerides and waist size after a high-fat meal. Ying I. Wang, John Schulze, Nadine Raymond, Tyler Tomita, Kayan Tam, Scott I. Simon, and Anthony G. Passerini Am J Physiol Heart Circ Physiol 300: H000–H000, 2011.  First published December 17, 2010; doi:10.1152/ajpheart.01036.2010.