Your brain on food: Brain signals differ between lean vs. obese people

The brains of people who are obese have an impaired response to nutrients which, it turns out, doesn’t improve after losing weight. This likely makes it tougher to keep the pounds off. The brain’s response to signals from the gut is what’s known as the gut-brain axis. And the brain’s response to ingesting food is important because it affects everything from satiation to behaviors around eating, to insulin and ghrelin (known as “the hunger hormone”) release. In recent years, rodent studies suggested that long-term exposure to a high-fat diet can result in an impaired release of dopamine from the striatum—a part of the brain involved in the reward and motivational aspects of food intake, according to researchers writing in Nature Metabolism. Generally, post-ingestive nutrient signals that go the brain contribute to the regulation of eating behavior. But long-term exposure to high-calorie diets impairs or reduces striatal dopamine signaling and may be what promotes overeating and obesity, the paper said. Building on this, the researchers conducted a randomized crossover study to examine whether intragastric infusions of glucose and lipids would modulate cerebral neuronal activity and striatal dopamine release, and how this might differ in lean versus obese individuals. The study also examined whether impaired response to post-ingestive nutrient signals would be reversible in the people who were obese if they later lost 10% of their body fat. Previous studies by the same researchers found that obesity-associated changes in the striatal dopamine system could be partially reversed via bariatric surgery-induced weight loss in women. Direct intragastric infusions of glucose (125 g in 250 ml of water; 500 kcal), lipids (250 ml of 20% Intralipid; 500 kcal) or water (250 ml of tap water; noncaloric isovolumetric control) were used to evaluate the metabolic and cerebral effects of post-ingestive nutrient signals, the study said. It was done this way to bypass the mouth and avoid noise from oral and sensory processing that happens there when eating. A total of 30 lean participants (BMI of 25 kg/m2 or less (12 females, 18 males) and 30 obese subjects (BMI of at least 30 kg/m2; 18 female, 12 males) were recruited for this two-part study. Brain responses to the intragastric infusions were examined using fMRI. Striatal dopamine release was evaluated with single-photon emission computed tomography (SPECT). Three sets of brain studies were conducted at baseline (one each for glucose, lipid and water as a control). The scans for evaluating striatal dopamine response were conducted immediately, and then 20 minutes after subjects consumed a milkshake-like solution. Here, it was found that there were differences in how the brain responded to the different nutrients in the intragastric infusions in lean versus the obese subjects with the obese subjects showing impaired responses—increased fasting glucose and insulin concentrations, which was indicative of insulin resistance This was expected. Obese subjects also had lower levels of fasting ghrelin than the lean cohort. As for dopamine release it was found that the intragastric infusions of glucose lead to dopamine release in both cohorts. However, when it came to the lipid infusions, only the lean participants had the dopamine release. After the baseline studies, the obese participants then underwent a supervised personalized dietary weight loss programme aimed at reducing body weight by 10% over a 12-week period. A total of 26 of the obese subjects completed the intervention and lost the 10%. After the weight was lost, the brain scans were repeated for all the study participants. Here, unexpectedly, it was found that losing weight didn’t make much of a difference when it came to the pattern of dopamine release in response to lipids. It stayed the same as when subjects were heavier. “Our observations that this physiological response is absent in participants with obesity and is not restored following diet-induced weight loss suggest that impaired post-ingestive nutrient sensing may play a role in obesity and may also contribute to the high rate of weight regain after diet-induced weight loss—specifically parts that play a role in the regulation of eating behaviour, primarily located in the striatum,” the study said. The good news was, as expected, insulin resistance improved once the obese participants lost weight. The study “provides robust evidence” that “nutrient sensing is blunted in people with obesity and that it cannot be rescued by a clinically relevant 10% reduction in body weight,” said a commentary accompanying the study in the same journal. The commentators noted that “the failure of weight loss to restore brain response reported here is probably representative of the broader clinical population of individuals with obesity who undergo weight loss.” Generally, the study adds more evidence to the value of bariatric surgery. There is “a growing body of evidence that indicates bariatric surgery could restore brain response to nutrients in a manner that weight loss via dietary and behavioral interventions does not,” it said. However, the study was not able to clarify whether the patterns in post-ingestive signals are a cause or consequence of obesity. In addition, the effects of proteins on brain activity would be worth studying too.

Your brain on food: Brain signals differ between lean vs. obese people

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