Insulin Signaling Could Modify Blood Triglyceride Levels


Patients with diabetes may have a higher risk of heart disease due to hyperactive mTORC1.

Patients with diabetes are known to be at a higher risk of cardiovascular disease than the general population. The American Heart Association reports that adults with diabetes are 2 to 4 times more likely to die from heart disease than those without the condition.

A new study published by the Journal of Clinical Investigation suggests a potential reason that patients with diabetes may have a higher risk of heart disease. The authors found that insulin may change the movement and storage of fat in the liver and how these alterations can lead to non-alcoholic liver disease and heart disease.

“The production of triglyceride in the liver and its secretion into blood are closely linked to nutrient availability and insulin levels,” said senior author Paul Titchenell, PhD. “After a meal, insulin tells the liver to package and secrete excess nutrients into triglyceride-rich lipid particles into the blood for use by the rest of the body.”

Glucose levels increase after eating, which results in the release of insulin to increase glucose uptake and reduce its production in the liver. Insulin also plays a role in lipid levels by increasing its synthesis, uptake, and storage in fat cells, according to the study.

In the study, the authors discovered that the mTOR complex 1 (mTORC1) is critical for very low-density lipoprotein (VLDL)-triglyceride production. The VLDL-triglyceride molecules carry lipids from the liver to various tissues.

“This is important because in metabolic diseases associated with insulin resistance the liver makes more triglycerides, which leads to increased levels in the blood and eventually cardiovascular disease,” Dr Titchenell said.

In mice without mTORC1 in liver cells, the authors observed an increase of triglycerides in the liver and a reduction in circulating molecules, while activating mTORC1 had the opposite effect, according to the study.

These findings highlight a critical cellular process that is controlled by mTORC1.

The authors also discovered that mTORC1 regulates the production of phospholipids, which are essential for triglycerides to move from the liver, as it helps form a barrier around triglycerides, according to the study.

“In insulin-resistant disorders such as diabetes and obesity, hyperactive mTORC1 in liver leads to excess fat production and export,” Dr Titchenell said. “mTORC1 is what we want to target pharmacologically to decrease the risk of cardiovascular disease that is associated with obesity and diabetes. If we could affect mTORC1 in a balanced way, then maybe could help prevent non-alcoholic fatty liver disease and heart disease.”

The authors said they plan to further investigate the mechanisms that mediate mTORC1’s command of phospholipid synthesis to develop new drug targets for patients with metabolic diseases, including diabetes.

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