Obesity disrupts the brain's sensing of glucose and lipid signals; MRIs reveal dysregulation and altered dopamine release, which persists even after w
Signals from the foods we consume help regulate eating behaviors, such as whether we should stop or continue eating. A new study has found that obesity diminishes the brain’s responses to these signals, and weight loss doesn’t correct the problem.
The study involved 60 participants: 30 with a healthy body weight and 30 with obesity. To avoid the influence of taste or preference cues on brain activity, they infused glucose, lipids (fats), and water (as a control) directly into the participants' stomachs. Then they measured the participants' brain activities and dopamine release in the striatum, an area involved in reward and motivation. To determine whether weight loss influenced this brain activity, they repeated the experiment 12 weeks later, after the participants achieved a 10 percent weight loss through dieting.
They found that the brain responded to glucose and lipids in participants with healthy body weight. However, obesity impaired the brain’s response to these nutrients. Interestingly, the impaired brain responses did not improve, even after successful weight loss.
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These findings suggest that impaired brain responses to the signals sent after eating may contribute to overeating and obesity. They also provide insights into why many people struggle to maintain weight loss, as their brains continue to resist these signals even after significant weight reduction.
Notably, this was a relatively small study, and the amount of weight loss – just 10 percent – might have been insufficient to induce global changes in the brain regarding nutrient sensing. Future studies that include more participants and induce greater weight loss may provide different results.