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Sight or smell of food causes inflamation in the brain


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The first article reports on how the sight or smell of food can trigger an inflammatory response affecting insulin secretion.  The second article explores how the negative effect of the smell of food is produced in the body.

The mere sight of a meal triggers an inflammatory response in the brain

[The] sight and smell of a meal trigger the release of insulin.  [Researchers] have shown that this insulin release depends on a short-term inflammatory response that takes place in these circumstances.

In the past, however, it was unclear how the sensory perception of a meal generated a signal to the pancreas to ramp up insulin production. Now, researchers from the University of Basel and University Hospital Basel have identified an important piece of the puzzle: an inflammatory factor known as interleukin 1 beta (IL1B), which is also involved in the immune response to pathogens or in tissue damage.

The fact that this inflammatory factor is responsible for a considerable proportion of normal insulin secretion in healthy individuals is surprising, because it's also involved in the development of type 2 diabetes

"The smell and sight of a meal stimulate specific immune cells in the brain known as the microglia," says study author Dr. Sophia Wiedemann, resident physician for internal medicine. "These cells briefly secrete IL1B, which in turn affects the autonomic nervous system via the vagus nerve."

 

 

Serotonin and dopamine modulate aging in response to food odor and availability

A previous study from Leiser's colleague Scott Pletcher, Ph.D., also of the Department of Molecular & Integrative Physiology, found that in fruit flies, attractive food smells are enough to blunt the life-extending effect of a restricted diet.

In the roundworm C. elegans, lifespan extension in response to environmental stressors such as dietary restriction involves the activation of a gene called fmo-2.

When worms were limited in the amount of food they could eat, the FMO protein, which was highlighted using a fluorescent marker, lit up "like a Christmas tree…it was bright red," noted Leiser. However, when the worms were exposed to food smells, there was considerably less activation of FMO, leading to a loss of life extension.

They found three compounds that could prevent the reversal of fmo-2 induction in the presence of food: an antidepressant that blocks the neurotransmitter serotonin, and two antipsychotic drugs used to treat schizophrenia, both of which block the neurotransmitter dopamine.

Ultimately, the drugs enabled the life extension effect of FMO, even in the presence of the smell of food.

These specific drugs are unlikely to be prescribed for this effect however, given their many potentially dangerous side effects.

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