A study conducted by researchers at Washington University School of Medicine in St. Louis has led to the identification of a protein that absorbs lipids in the upper part of the intestine, raising hopes that it may provide a novel approach for obesity treatment in the future.
Principal investigator Dr. Nada A. Abumrad, the Dr. Robert C. Atkins Professor of Medicine and Obesity Research at Washington University School of Medicine, first identified CD36 protein that facilitates the uptake of fatty acids. The protein is located on the surface of cells and distributed in many tissues, including fat cells, the digestive tract, heart tissue and skeletal muscle tissue.
Dr. Abumrad says that the intestine makes large amounts of CD36, and that it is important to the absorption of fatty acids.
During her initial experiments, wherein she compared normal mice that made the protein to genetically altered mice lacking the protein, she could not find any net difference in their fat absorption. In the present study, the researcher has found the reason why it was not possible to identify a difference.
She says that CD36 normally absorbs fatty acids in the upper, or proximal part of the intestine, but in its absence, lower, more distal, sections of the intestine compensate and absorb the fat.
"We think of the intestine as a single organ, but it's really made up of distinct areas that are so specialized it's almost like several organs. The fat that is not absorbed in the proximal areas ends up being bumped into the distal intestine where different systems absorb it," Abumrad says.
The researchers believe that targeting the upper part of the intestine and interfering with normal CD36 function may be a useful tool in weight loss. They say that animals that cannot make CD36 absorb fat less efficiently, due to which they tend to eat less of it.
"And the most exciting part for us right now is the fact that these things may apply to humans. Humans with mutations in the gene that makes CD36 don't seem to process fat normally either," Abumrad says.
The researcher further said that her goal was to determine the same the findings of mice studies into humans, where variations in the CD36 gene are common. She, however, admitted that before so doing, she wanted to learn more from animal studies.
"There is evidence that people have different amounts of CD36 and that mutations in the gene are quite common," she said.
"Those variations are associated with abnormalities of blood lipids, with high levels of fatty acids in the blood, abnormal blood triglycerides and increased risk of diabetes-associated heart disease. It's clear that some of us have different amounts of this protein in different tissues, and some individuals don't have any of it," she added.
The study has been published in the Journal of Biological Chemistry.