Brain cells that remember food can affect obesity

a A trip to the grocery store is a sensory adventure, and the aisles are filled with eye-catching packaging designed to seduce shoppers. Each display promises a delicious, memorable food adventure. “We all experienced this moment when we weren't physically hungry, but we were craving certain foods,” he said. Guillaume de Lartiguea neuroscientist at the Monell Chemical Senses Center, studying how the brain controls food intake.

Even one whimsical thing of fresh bread from a nearby bakery can evoke appetizing memories and instantly induce hunger. This connection between memory and appetite led de Lartig to wonder how the brain's memory center influenced feeding behavior and contributed to the risk of obesity.

With a new study published in Natural metabolismde Lartig and his team identified two distinct populations of hippocampal neurons that responded to either sugar or fat content in diets that were recently consumed.¹ Activating these neurons enhanced the contextual memory and motivation of mice, which helped them to find and consume these nutrients. Conversely, silencing any population impaired food-related memory recalls, reduced intake of high-calorie foods and prevented excessive weight gain. Understanding how the brain's food-specific memory system affects feeding habits can pave the way for developing new obesity treatments.

These findings revealed previously unknown neurons that promote eating behavior, and shed light on neural mechanisms that may contribute to impaired eating behaviors such as overeating. If you want to understand eating disorders, [first] Understand how food works.” parentneuroscientists from Georgia State University were not involved in the research. “[This study addresses] This huge knowledge gap. ”

Eating causes the intestines, sends information about dietary nutritional content and bloating to the brain, and helps regulate appetite. Previous research shows that Mixed nutritional diethowever, it was unclear whether certain neurons respond to individual nutrients.²

Given De Lartig's interest in the role of neurons in obesity, the team focused on how the hippocampus responded to macronutrients associated with diet-induced obesity. They predicted that a single group of neurons would respond widely to both fat and sugar consumption. Researchers gave mice an intragastric injection of saline, sugar, or fat solutions. Then, 90 minutes later, they removed the brain and measured the FOS protein, a marker of neural activity.

Instead of neurons that responded to both sugar and fat, de Lartig was surprised to see increased FOS levels in two separate neuronal populations in the dorsal hippocampus (DHPC) of mice receiving sugar or fat. Even when mice received sugar and fat injections two weeks apart, the patterns were consistent, suggesting that DHPCs have two spatially distinct groups of nutrition-specific neurons.

As these neurons were activated after meals, De Lartigue investigated whether the important gut brain pathway, Vagus nerve, played a role in activation. The vagus nerve detects nutritional signals and hormonal changes in the intestine, and can convey this information to the brain, affecting hippocampal activity. Indeed, when they surgically impaired the vagus nerve and administered saline, sugar, or fat, FOS expression was significantly reduced compared to control mice.

“[This] He suggests that our brains are actually tracking what we are eating. He assumed that the brain tracks only calories, and explained that what the source of food is not important.

Second, De Lartigue wanted to understand how these DHPC neurons were linked to feeding behaviors and whether they promoted sugar and fat preferences. When the brain forms positive memories of food, it can drive a constant desire for foods that are densely calorie-dense. First, the researchers compared control mice with silent sugar or fat-responsive neurons. They provided two equal bottles to all three groups. One is a sugar solution and the other is a fat. Over the 3-day testing period, control mice preferred fat solutions, whereas mice that removed sugar or fat-responsive neurons consumed 40-50% of their respective nutrients and had no effect on the intake of the other.

After determining these neurons to be specific, De Lartigue sought to understand how these neurons influenced memory and motivation, particularly in recalling the location of sugar and fats and promoting the consumption of these nutrients. “To our even bigger surprise, these two groups do different things,” he said.

In the Food Cup Location Memory Task, mice learned to find dishes that contain nutrition. Control mice recalled both sugar and fat locations, whereas those with silent sugar and fat response neurons showed memory impairment for each nutrient.

Researchers found that stimulating sugar neurons helped mice to remember the sugar placement but had no effect on fat memory, suggesting that sugar-responding neurons are involved in the formation of sugar-related memories.

What about fat-responsive neurons? These neurons do not remember the location of nutrients, but instead play a role in motivation and reward. To test this, researchers measured how much effort the mice were making to lick from a dried sipper bottle and get a little sugar or fat. Mice with silent sugar neurons showed no change in this behavior of sugar compared to control mice, whereas mice with silent fat-responsive neurons were less licked due to fat, suggesting that these neurons promoted fat-specific motivation.

The researchers then investigated how these neurons regulate food intake on a high-fat, high-sugar diet. Silencing of either neuron type reduced the intake of macronutrients in each, but sugar neurons affected memory through different mechanisms, and fat neurons influenced motivation. This reduction ultimately prevented weight gain and provided protection against diet-induced obesity.

“I was very impressed with their findings that different neurons sense different macronutrients. I underestimated the level of hippocampal involvement,” the parent said.

De Lartigue said there is some evidence of similar results humanthe hippocampus is activated in food cues, especially in obese individuals.³ Given these similarities in the food memory circuit, he highlighted the importance of identifying molecular profiles of hippocampal neurons and determining the receptors that are expressed. These findings provide new insights into the development of new strategies to combat overeating and obesity by disrupting memory-driven cravings for unhealthy, calorie-dense foods.