Researchers have found that copper plays a key role in metabolising fat so that it can be used for energy, an advance that may provide new target to treat obesity.
Long prized as a malleable, conductive metal used in cookware, electronics, jewellery and plumbing, copper has been gaining increasing attention over the past decade for its role in certain biological functions, researchers said.
It has been known that copper is needed to form red blood cells, absorb iron, develop connective tissue and support the immune system. "We find that copper is essential for breaking down fat cells so that they can be used for energy. It acts as a regulator," said Chris Chang from University of California, Berkeley. "The more copper there is, the more the fat is broken down. We think it would be worthwhile to study whether a deficiency in this nutrient could be linked to obesity and obesity-related diseases," said Chang.
According to him, copper could potentially play a role in restoring a natural way to burn fat. The nutrient is plentiful in foods such as oysters and other shellfish, leafy greens, mushrooms, seeds, nuts and beans. "Copper is not something the body can make, so we need to get it through our diet. The typical American diet, however, does not include many green leafy vegetables. Asian diets, for example, have more foods rich in copper," said Chang.
Researchers including Lakshmi Krishnamoorthy from University of California made the copper-fat link using mice with a genetic mutation that causes the accumulation of copper in the liver. Notably, these mice have larger than average deposits of fat compared with normal mice. The inherited condition, known as Wilson's disease, also occurs in humans and is potentially fatal if left untreated.
Analysis of the mice with Wilson's disease showed that the abnormal buildup of copper was accompanied by lower than normal lipid levels in the liver compared with control groups of mice, researchers said. They also found that the white adipose tissue, or white fat, of the mice with Wilson's disease had lower levels of copper compared with the control mice and correspondingly higher levels of fat deposits.
Researchers then treated the Wilson's disease mice with isoproterenol, a beta against known to induce lipolysis, the breakdown of fat into fatty acids, through the cyclic adenosine monophosphate (cAMP) signalling pathway.
They noted that the mice with Wilson's disease exhibited less fat-breakdown activity compared with control mice. Researchers used inductively coupled plasma mass spectroscopy (ICP-MS) equipment to measure levels of copper in fat tissue. They found that copper binds to phosphodiesterase 3, or PDE3, an enzyme that binds to cAMP, halting cAMP's ability to facilitate the breakdown of fat.
The findings were published in the journal, Nature Chemical Biology.
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