Belly fat, high-fat meals lead to heart disease
A new UC Davis study has suggested that the effect of a high-fat meal on blood vessel walls varies among individuals depending on factors such as their waist size and triglyceride levels. The new research reinforces the link between belly fat, inflammation and thickening of the arterial linings that can lead to heart disease and strokes.
"The new study shows that eating a common fast food meal can affect inflammatory responses in the blood vessels," said lead author Anthony Passerini of the UC Davis.
"Our techniques allowed us to measure the inflammatory potential of an individual`s lipids outside of the body and to correlate that with easily measured characteristics that could be used to help better understand a person`s risk for vascular disease," he said.
Passerini collaborated with Scott Simon, of the UC Davis, to develop cell culture models to mimic the properties of blood vessels. They wanted to learn how triglyceride levels can cause endothelial inflammation, and 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 levels of triglyceride particles in their blood after they ate a typical fast food breakfast from a major fast food franchise: two breakfast sandwiches, hash browns and orange juice.
The team 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.
The researchers tested whether TGRL particles from the volunteers` blood could cause cultured endothelial cells in the laboratory to express markers for inflammation.
There was a mixed response: individuals with both a waist size over 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 suggested 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, he said.
In people who are predisposed, repeated episodes of inflammation could lead to atherosclerosis.
The findings have been published online in the journal American Journal of Physiology—Heart and Circulatory Physiology.