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Smell perception influences food intake

Researchers have succeeded in elucidating how the endocannabinoid system controls food intake through its effects on the perception of smells.

In animals, as in humans, hunger mechanisms are known to stimulate food intake. Hunger triggers a set of mechanisms that encourage feeding, for example by increasing sensory perceptions such as the sense of smell. What links hunger and increased smell perception in the brain, and the resulting urge to eat.was revealed.
The researchers have discovered how this mechanism is initiated in the endocannabinoid system in mice. This system interconnects receptors located in the brain, involved in different sensations such as euphoria, anxiety, or pain that are also sensitive to cannabinoid substances, such as cannabis.

It was discovered that the CB1 cannabinoid receptors control a circuit that connects the olfactory bulb (the region in the nervous system that initially handles olfactory information) to the olfactory cortex (higher structures of the brain). When the sensation of hunger is felt, it triggers the activity of the cannabinoid receptors, which in turn activate the olfactory circuit, which then becomes more responsive. It is therefore this biological mechanism that brings about the increased sensitivity to smell during hunger, explaining one of the reasons for food intake.

‘Chauffeur protein’ may help regulate fat production

Researchers have discovered a biological switch that regulates a protein that causes fatty liver disease in mice. Peter Espenshade, Ph D, professor of cell biology at the Johns Hopkins University School of Medicine, explains that fats are essential for organisms

Crucial to the right balance of fats is a family of proteins called sterol regulatory element-binding proteins (SREBPs). SREBPs are embedded in the membrane of the cellular compartment called the endoplasmic reticulum, or ER. To get to the cell’s nucleus to turn on genes, the business end of SREBPs has to be clipped away from the membrane. Two proteins, S1P and S2P, make those clips in sequence. But S1P and S2P live in a different cellular compartment, known as the Golgi.

To safely make the trip to the Golgi, cells give each SREBP a chauffeur — the protein SCAP — which binds to SREBP before they make their way to the Golgi. Once there, S1P and S2P free SREBP from the membrane. While testing a chemical inhibitor of S1P activity, Espenshade and his team added the chemical to hamster cells and found that SCAP disappeared from the cells. That meant that it was either no longer being made or was being broken down.

When they added both the S1P inhibitor and a chemical that prevents SCAP from leaving the ER, SCAP reappeared. This suggested that SCAP was still being made but that the S1P inhibitor was somehow encouraging the destruction of SCAP  Further testing revealed that SCAP was indeed being broken down in another part called the lysosome. Tweaking the components of the cycle again, they engineered cells to keep SREBP in the ER while allowing SCAP to move to the Golgi on its own. This time, even though S1P was blocked, SCAP was no longer broken down.

Female smokers at higher risk of breast cancer

A new study has revealed that young women, who have been smoking a pack of cigarettes a day for a decade, are at higher risk of most common type of breast cancer.

According to the researchers, young women who are current or recent smokers and had been smoking a pack a day for at least ten years, had a 60 percent increased risk of estrogen receptor positive breast cancer. But, it was found that smoking had no link to a woman’s risk of triple-negative breast cancer. Christopher Li of the Fred Hutchinson Cancer Research Center, Seattle, and his colleagues conducted a population-based study consisting of 778 patients with estrogen receptor positive breast cancer, 182 patients with triple-negative breast cancer and 938 cancer-free controls.

Li said that the health hazards associated with smoking are numerous and his study suggests that smoking might increase the risk of the most common molecular subtype of breast cancer but not influence risk of the aggressive subtypes.

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