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Brown or White? Which fat cells help treat obesity?

Brown fat cells which help in energy generation seem to be the clue to eradicate white fat cells which store fat but turn foe in increasing the incidence of fat in our bodies. White fat cells also increase risk for diabetes and heart disease since it is linked to visceral fat, which is the build-up of fat around the organs in the belly.

Making a headway in this research, a team of researchers led by Jorge Plutzky, MD, director of the Vascular Disease Prevention Program at Brigham and Women’s Hospital (BWH) and Harvard Medical School has discovered a way to turn white fat into brown fat or a foe to a friend.

In the absence of Aldh1a1, visceral fat (far left) begins producing proteins that characterize brown fat (far right), including UCP1, which releases heat and appears brown in these cells (see arrow). The changes in visceral fat are more pronounced that subcutaneous fat (middle panel).

By manipulating the metabolic pathways in the body responsible for converting vitamin A—or retinol—into retinoic acid, Plutzky’s team has essentially made white fat take on characteristics of brown fat. Their findings put medical science an inch closer in the race to develop novel anti-obesity therapies.

The study was published in May 6, 2012 issue of the journal Nature Medicine.

Retinoids, which are molecules derived from vitamin A metabolism, are responsible for many biological functions. One such function is the control of fat cell development and actions. A key step in retinoid metabolism occurs with help from an enzyme called retinaldehyde dehydrogenase 1, or Aldh1a1. The researchers saw that in humans and mice, Aldh1a1 is abundant in white fat cells, especially in the more dangerous visceral fat (sometimes referred to as abdominal fat or belly fat).

When Aldh1a1 was inhibited in white fat cells, those cells began acting like brown fat cells. One of the defining characteristics of brown fat is its ability to release energy as heat. Mice with either deficiency or inhibition of Aldh1a1 become protected against exposure to cold. The researchers saw this classic indicator of brown fat and its ability to generate heat by oxidizing fat (a chemical reaction involving oxygen) in their research.

Especially exciting for the prospects of targeting Aldh1a1 for therapeutic benefit, the researchers found that knocking down expression of the Aldh1a1 gene by injecting antisense molecules into mice made fat by diet resulted in less visceral fat, less weight gain, lower glucose levels, and protection against cold exposure as compared to control mice.

“Brown fat, and mechanisms that might allow white fat to take on brown fat characteristics, has been receiving increasing attention as a possible way to treat obesity and its complications,” said Plutzky. “Although more work is needed, we can add specific aspects of retinoid metabolism to those factors that appear involved in determining white versus brown fat.”

According to the Centers for Disease Control and Prevention, more than one-third of adults in the United States are obese. Current methods to reduce obesity include exercise, dietary therapy, medications and surgery.

This research was supported by the National Institutes of Health grants HL048743, AR054604-03S1, 5P30DK057521-12; Mary K. Iacocca Professorship; National Institute of Diabetes and Digestive and Kidney Diseases; and Austrian Science Fund.

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