Tomato therapy: Engineered veggies target intestinal lipids, improve cholesterol

UCLA researchers report that tiny amounts of a specific type of lipid in the small intestine may play a greater role than previously thought in generating the high cholesterol levels and inflammation that lead to clogged arteries.

The study, in the December issue of the Journal of Lipid Research with an accompanying editorial, focused on a group of lipids found in the small intestine called unsaturated lysophosphatidic acids (LPAs).

"These lipids may be a new culprit that we can target in the small intestine in fighting atherosclerosis," said senior author Dr Alan Fogelman, executive chair of the department of medicine and director of the atherosclerosis research unit at the David Geffen School of Medicine at UCLA.

Big effect of small amount of LPA

Previously, it was thought that the role of the small intestine in response to a high-fat, high-cholesterol diet was simply to package the fat and cholesterol for transport to the liver. Once delivered to the liver, the large load of fat was thought to cause increased blood levels of LDL ("bad") cholesterol, decreased levels of "good" cholesterol and the rise of systemic inflammation.

But that may not be the complete story. The UCLA researchers revealed that LPAs, previously considered very minor because they are found in far smaller amounts in the small intestine than other lipids, like cholesterol, may play a more direct role in contributing to the factors that cause atherosclerosis.
Scientists found that mice fed a high-fat, high-cholesterol diet (21 per cent fat) showed a two-fold increase in the amount of LPAs in the small intestine over mice fed normal low-fat mouse chow (4 per cent fat).

When researchers added LPAs at only one part per million (by weight) to the normal low-fat, low-cholesterol mouse chow, they observed the same increase in LPAs in the small intestine as when the mice were fed the high-cholesterol, high-fat diet.

Surprisingly, with the addition of LPAs to the low-fat diet, the UCLA team also found alterations in the patterns of gene expression in the small intestine, changes in cholesterol levels (increases in LDL and decreases in HDL) and increases in blood markers of inflammation typically seen when the mice consumed a high-fat, high-cholesterol diet.

The findings suggest that some of the factors leading to atherosclerosis occur in the small intestine and not just the liver. Targeting LPAs in the small intestine may be a way to help stop changes in blood cholesterol and inflammation before the load of packaged fat even reaches the liver, the researchers said.

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