New York: Excess belly fat in older adults could be linked to inflammation, a finding that can help develop drugs that could enable elderly people burn fat, and decrease their odds of developing chronic diseases such as heart disease, diabetes and strokes, researchers led by one of Indian-origin have found.
Older adults, regardless of body weight, have increased belly fat. However, when they need to expend energy, older people do not burn the energy stored in fat cells as efficiently as younger adults, leading to the accumulation of harmful belly fat, said lead author Vishwa Deep Dixit, Professor at Yale University in Connecticut, US.
The underlying cause for this unresponsiveness in fat cells was unknown yet.
In the study, published in the journal Nature, the researchers discovered a new type of specialised immune cells known as macrophages, that resides on the nerves in belly fat.
These nerve-associated macrophages, which are typically involved in controlling infections, become inflamed with age and do not allow the neurotransmitters, which are chemical messengers, to properly function.
New York, Sep 28 (IANS) Excess belly fat in older adults could be linked to inflammation, a finding that can help develop drugs that could enable elderly people burn fat, and decrease their odds of developing chronic diseases such as heart disease, diabetes and strokes, researchers led by one of Indian-origin have found.
Older adults, regardless of body weight, have increased belly fat. However, when they need to expend energy, older people do not burn the energy stored in fat cells as efficiently as younger adults, leading to the accumulation of harmful belly fat, said lead author Vishwa Deep Dixit, Professor at Yale University in Connecticut, US.
The underlying cause for this unresponsiveness in fat cells was unknown yet.
In the study, published in the journal Nature, the researchers discovered a new type of specialised immune cells known as macrophages, that resides on the nerves in belly fat.
These nerve-associated macrophages, which are typically involved in controlling infections, become inflamed with age and do not allow the neurotransmitters, which are chemical messengers, to properly function.
The researchers also isolated the immune cells from fat tissue of young and old mice, and then sequenced the genome to understand the problem.
"We discovered that the aged macrophages can break down the neurotransmitters called catecholamines, and thus do not allow fat cells to supply the fuel when demand arises," Dixit said.
Further, when a specific receptor that controls inflammation -- the NLRP3 inflammasome -- was lowered in aged macrophages, the catecholamines could act to induce fat breakdown, similar to that of young mice.
"The key finding is that the immune cells talk to the nervous system to control metabolism," Dixit noted.
In further experiments, the researchers blocked an enzyme that is increased in aged macrophages, restoring normal fat metabolism in older mice.
The researchers also isolated the immune cells from fat tissue of young and old mice, and then sequenced the genome to understand the problem.
"We discovered that the aged macrophages can break down the neurotransmitters called catecholamines, and thus do not allow fat cells to supply the fuel when demand arises," Dixit said.
Further, when a specific receptor that controls inflammation -- the NLRP3 inflammasome -- was lowered in aged macrophages, the catecholamines could act to induce fat breakdown, similar to that of young mice.
"The key finding is that the immune cells talk to the nervous system to control metabolism," Dixit noted.
In further experiments, the researchers blocked an enzyme that is increased in aged macrophages, restoring normal fat metabolism in older mice.