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Key points
- A recent study sheds light on the connection between the gut, brain, and obesity.
- Individuals with obesity have reduced nutrient sensing compared to their lean counterparts.
- <ost people who lose weight eventually regain it. These new findings may help explain why this is the case.
In recent years, there has been a shift in how we perceive obesity. In the past, it had commonly been attributed to an individual's personal failure to eat less food and live a less sedentary lifestyle. There is now a growing understanding that obesity has complex and persistent biological mechanisms.
A recent study, led by researchers from Yale University and published in Nature Metabolism, sheds light on the connection between the gut, brain, and obesity. After a person consumes a meal, the gut sends signals to the brain to inform it about the presence of nutrients. These signals are believed to play a role in regulating eating behavior.
The study used brain imaging to demonstrate that when people without obesity received nutrients, they experienced reduced activity in areas of the brain involved in food intake, suggesting the brain is signaling to these people that they’ve received food and no longer need more. In people with obesity, those changes were not detected. Furthermore, when participants with obesity lost weight, these changes were still not detected. This may explain why it is difficult for many to maintain weight loss over time.
The researchers conducted experiments by infusing glucose or fat directly into the stomachs of lean individuals (those with a BMI of 25 or less) and individuals with obesity (those with a BMI of 30 or higher). They used functional magnetic resonance imaging (fMRI) to analyze brain activity.
The results revealed that in lean participants, both glucose and fat infusion led to reduced brain activity in various regions. However, participants with obesity showed no changes in brain activity. The researchers focused on the striatum, a brain region responsible for the rewarding and motivational aspects of food intake, and found glucose-induced decreased activity in this area for lean individuals but no similar response in participants with obesity. Moreover, dopamine release, which is associated with the striatum's function, was observed in response to glucose in both groups but only lean participants showed a response to fat.
These findings suggest that individuals with obesity have reduced nutrient sensing compared to their lean counterparts. Participants with obesity underwent a 12-week dietary weight-loss program, and those who achieved at least a 10 percent weight loss were re-evaluated through imaging.
Previous studies have shown that most people who lose weight eventually regain it, and these new findings may help explain why this is the case. The impaired nutrient sensing experienced by individuals with obesity may contribute to overeating and difficulty in maintaining weight loss.
The researchers also investigated whether there was a correlation between brain responses and hormones released when nutrients are present in the gut. While they did not observe any association with insulin or glucose, they did find a connection between increased levels of the hormone glucagon-like peptide 1 (GLP-1) and reduced brain activity in certain regions related to food intake after fat infusion in non-obese individuals.
GLP-1 has recently become a hot topic in weight loss interventions. Popular drugs like Wegovy and Ozempic replicate the effects of GLP-1. Although this study did not explore the relationship between the GLP-1 hormone and brain responses, nor did it examine how GLP-1-based medications impact responses in individuals with obesity, these areas could be potential avenues for future investigation.
By unraveling the complexities of nutrient sensing and its connection to obesity, healthcare professionals could develop targeted treatments and preventive strategies to combat overeating and weight regain. The findings from this study further highlight how there are no “one-size-fits-all” solutions to the obesity epidemic, as individual responses to the same weight loss interventions, such as diet, exercise, and medication, vary widely. We need both collective and individual solutions that address the genetic, biological, and environmental factors that account for obesity development, from the development of new medications and addressing the over-use of high fructose corn syrup in our food to creating public spaces that encourage recreation.
