According to Dr Suneil Koliwad, Gladstone Institute of Cardiovascular Disease, when individuals become obese from overeating, cells called adipocytes located in the fat tissue
fill up with dietary fats and begin to die. Immune cells called macrophages move out of the blood stream and into this tissue, where they accumulate around dying adipocytes.
As the macrophages work to clear away the dead cells, they are exposed to large amounts of dietary fat that can result in unwanted consequences.
Exposure to saturated fats, in particular, causes the macrophages to enter an inflammatory state. In this state, the macrophages secrete cytokines, such as tumour necrosis factor (TNF) alpha, that encourage the development of insulin resistance, diabetes, and heart disease.
They hope that enhancing the capacity of macrophages to store dietary fats might alter this. The researchers focused their study on an enzyme called DGAT1, which makes triglycerides from dietary fats for storage as cellular energy reserves.
They examined a transgenic strain of mice (aP2-Dgat1) that make large amounts of DGAT1 in both adipocytes and macrophages.
On a high-fat diet, these mice became obese, but the macrophages in their fat tissue did not undergo inflammatory activation, and the mice were protected from developing systemic inflammation, insulin resistance, and fatty livers, all problems that were profound in the control mice.
“We found in experimental mice that a single enzyme, DGAT1, in macrophages is involved in many of the problems associated with obesity,” said Koliwad.
“This is exciting because humans have this enzyme as well, providing the potential for a therapeutic target to examine,” he added.
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