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Why We Are Eating Even More: Now Scientists Have a New Explanation For What’s Going on

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Why We Eat Too Much: The New Science of Hunger – and What It Tells Us About Losing Weight

Scientists from the Garvan Institute of Medical Research have identified a cluster of brain cells that amplifies hunger signals in conditions where the body possesses an extended energy excess, like excessive fat buildup in obesity.

The team found that these specific cells not only generate the hunger-inducing compound NPY but also heighten the brain’s receptivity to this molecule, thereby intensifying hunger sensations. These findings were detailed in an article published in Cell Metabolism.

“These cells kickstart changes in the brain,” explains senior author Professor Herbert Herzog, “that make it more sensitive to even low levels of NPY when there is a surplus of energy in the body in the form of excess fat—driving appetite during obesity.”

The author says that their “study addresses a long-standing question about how appetite is controlled in obesity and has the potential to take the development of therapy into a new direction.”

Obesity represents a significant public health concern and a prevalent disease, impacting over 10% of adults and elevating the likelihood of developing other chronic illnesses, including diabetes and heart disease. Although numerous factors can contribute to the onset of obesity, such as excessive fat tissue accumulation, dietary habits and levels of physical activity emerge as pivotal influencers.

The human brain possesses sophisticated mechanisms that detect the amount of energy stored in our body and regulate our appetite accordingly. One of these mechanisms involves the production of a naturally occurring molecule called NPY by the brain in response to various stressors, including hunger, to stimulate the desire for food consumption.

When the amount of energy we consume is lower than what we expend, our brain releases increased levels of NPY, a hormone that stimulates hunger. Conversely, when our energy intake surpasses our expenditure, NPY levels decrease, resulting in reduced feelings of hunger. Nevertheless, in cases of prolonged energy surplus, such as in individuals with excess body fat or obesity, NPY remains active in driving appetite, even at lower levels.

“We wanted to understand why,” adds the author.

In animal models of obesity, scientists examined a specific type of brain cells known as neurons responsible for producing NPY (neuropeptide Y). Surprisingly, their investigation revealed that approximately 15% of these neurons displayed a unique characteristic—they did not suppress NPY production even in the presence of obesity.

According to Professor Herzog, their research revealed that in the presence of obesity, appetite is primarily influenced by NPY generated by a specific group of neurons. These neurons not only produce NPY but also enhance the sensitivity of other brain regions to generate more receptors or “docking stations” for this molecule. This heightened response significantly intensifies the feeling of hunger.

“What we have uncovered is a vicious cycle that disrupts the body’s ability to balance its energy input with energy storage and enhances obesity development.”

Our brain is naturally programmed to resist energy deficiency or weight loss because it perceives them as potential threats to our survival. In response, it activates mechanisms that enhance our appetite, compelling us to actively seek out food.

“As we found now, this even occurs when we have excess energy stored in the body,” Professor Herzog adds.

The researchers assert that their findings present an opportunity to explore a novel avenue for the development of anti-obesity medication by targeting and inhibiting the supplementary, highly receptive receptors for NPY.

“Our discovery helps us better understand the mechanisms in the brain that interfere with a balanced energy metabolism and how they may be targeted to improve health,” says Professor Herzog.

Image Credit: Getty

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