Hypertriglyceridemia is a common condition in the U.S. caused by obesity and diabetes. If left untreated, it can lead to more serious health problems such as coronary heart disease, cardiovascular heart disease, and pancreatitis. Hypertriglyceridemia is a condition in which the triglyceride levels in the blood are elevated to an abnormal level.
Aside from obesity and diabetes, hypertriglyceridemia can be caused by a high-fat diet, excessive alcohol intake, and certain medications. More specifically, there are primary and secondary causes of hypertriglyceridemia: Primary hypertriglyceridemia is caused by genetic defects leading to abnormal amounts of triglycerides in the blood and the secondary causes are a high-fat diet, obesity, diabetes, hypothyroidism, and certain medications.
A new study published in April 2017, conducted by researchers at UCLA in collaboration with researchers from Gunma University in Japan, discovered a new subset of people with hypertriglyceridemia, but not as a result of the primary or secondary causes mentioned above. In this subset of people, the patients’ own bodies produced auto-antibodies, molecules that attack their own proteins, that then caused high levels of triglycerides in the blood. This recently discovered cause has been named the GPIHBP1 auto-antibody syndrome. The researchers who discovered this have said that this condition is potentially life threatening but also potentially treatable.
Let’s take a closer look at what the study has found about this potential third cause of hypertriglyceridemia. Triglycerides in the bloodstream are broken down by a specific enzyme called lipoprotein lipase (LPL) in the capillaries of the blood vessels. This is an important process because triglycerides cannot be absorbed by the body in this form, they need to be broken down so that the body can use them as an energy source later when needed. There is another protein called GPIHBP1 that binds to LPL and then moves it into capillaries.
Now imagine not only having an excess of triglycerides (hypertriglyceridemia) but also not being able to break them down efficiently. Some people have mutations in this protein, GPIHBP1 that doesn’t allow it to bind to the LPL. On the other hand, some people have mutations in the LPL. Both of these mutations prevent LPL from reaching the capillaries as it should.
The new research has discovered a new issue that prevents the binding of LPL and GPIHBP1 but it’s not that the LPL can not bind to the GPIHBP1 due to a genetic mutation or vice versa, it’s that there an auto-antibody that acts against GPIHBP1 and prevents it from binding to LPL. More research will be done on this new discovery and on how to treat this cause of hypertriglyceridemia but currently, drugs to reduce the level of antibodies are being considered.
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