A key protein that regulates fat metabolism
Many foods contain a lot of fat, and the fatty acids in them are one of the essential nutrients that people depend on to survive. When more fatty acids are consumed than the body can convert into energy immediately, the excess fat is stored in tissues and served as a reserve supply.
The amount of fatty acids that the blood transports to the tissue and deposits in the tissue is determined by many factors. In a recent study, researchers from the Max Delbruck Center for Molecular Medicine at the Helmholtz Institute revealed the importance of the protein EHD2 in fat storage.
If this protein is completely absent, the lipid-storing cells will absorb more fatty acids from the cellular environment. Dr Claudia Matthaeus first observed this phenomenon in the brown adipose tissue of mice while working at MDC. She is particularly excited that EHD2 also obviously plays a key role in human fat metabolism. "We found that overweight people produce less EHD2 than normal-weight people," Matthaeus said. It is not clear why this is the case. Based on these new insights, Matthaeus and her colleagues, including researchers from the MDC research team led by Professor Oliver Daumke, believe that EHD2 controls a metabolic pathway that regulates fatty acid uptake in fat cells. And that pathway has been altered in the context of obesity. The results were published recently in the journal PNAS.
EHD2 is a membrane protein found in muscle and fat cells. During the cell envelope folding inward, a small flask membrane structure called a pore is formed. These traps either remain on the surface of the cell membrane, or they trap and carry foreign matter, such as fatty acids, into the cell. Daumke explained that this process is called endocytosis. The researchers hypothesized that EHD2 protein assembles into a ring structure around the membrane structure, thus hindering the endocytosis process. Daumke thinks that if EHD2 is missing, the cells will absorb more fat. Matthaeus observed with an electron microscope that there was more endocytosis in the cells of EHD2-deficient mice compared to normal mice. She also found that cells lacking EHD2 had a higher intake of fatty acids.
To understand the effect of EHD2 on human fat metabolism, the authors studied tissue samples of men and women of different weights. The authors found that in people who were overweight (with a body mass index of 25 or higher), the cells produced fewer EHD2 levels than those who were slim. Researchers believed there is a correlation between frequent endocytosis and the formation of fat deposits.
The amount of fatty acids that the blood transports to the tissue and deposits in the tissue is determined by many factors. In a recent study, researchers from the Max Delbruck Center for Molecular Medicine at the Helmholtz Institute revealed the importance of the protein EHD2 in fat storage.
If this protein is completely absent, the lipid-storing cells will absorb more fatty acids from the cellular environment. Dr Claudia Matthaeus first observed this phenomenon in the brown adipose tissue of mice while working at MDC. She is particularly excited that EHD2 also obviously plays a key role in human fat metabolism. "We found that overweight people produce less EHD2 than normal-weight people," Matthaeus said. It is not clear why this is the case. Based on these new insights, Matthaeus and her colleagues, including researchers from the MDC research team led by Professor Oliver Daumke, believe that EHD2 controls a metabolic pathway that regulates fatty acid uptake in fat cells. And that pathway has been altered in the context of obesity. The results were published recently in the journal PNAS.
EHD2 is a membrane protein found in muscle and fat cells. During the cell envelope folding inward, a small flask membrane structure called a pore is formed. These traps either remain on the surface of the cell membrane, or they trap and carry foreign matter, such as fatty acids, into the cell. Daumke explained that this process is called endocytosis. The researchers hypothesized that EHD2 protein assembles into a ring structure around the membrane structure, thus hindering the endocytosis process. Daumke thinks that if EHD2 is missing, the cells will absorb more fat. Matthaeus observed with an electron microscope that there was more endocytosis in the cells of EHD2-deficient mice compared to normal mice. She also found that cells lacking EHD2 had a higher intake of fatty acids.
To understand the effect of EHD2 on human fat metabolism, the authors studied tissue samples of men and women of different weights. The authors found that in people who were overweight (with a body mass index of 25 or higher), the cells produced fewer EHD2 levels than those who were slim. Researchers believed there is a correlation between frequent endocytosis and the formation of fat deposits.
