New Delhi: Obesity likely creates a communication gap between your brain and your gut that then traps you in a vicious cycle of overeating. So suggests a team of American and Dutch researchers in a study published in the journal Nature Metabolism Monday.
The study, involving 58 Amsterdam-based participants aged 50-70, involved an analysis of signals exchanged between the brain and the gut that are responsible for the sensation of hunger and satiety, and are triggered by the presence of various nutrients
Eating behaviour is not just determined by sensory exposure such as smell and taste, but also by these metabolic signals that kick in after the ingestion of food.
According to the researchers, these signals are blunted in those who are obese. The findings suggest that this impaired gut-brain-axis nutrient-signalling may worsen overeating and obesity.
The study also suggests the effects may be long-lasting, and irreversible even in the event of weight loss.
“Impaired neuronal responses to nutritional signals may contribute to overeating and obesity, and ongoing resistance to post-ingestive nutrient signals after significant weight loss may in part explain the high rate of weight regain after successful weight loss,” wrote the researchers, who bear affiliation to the Amsterdam University Medical Centers, Yale University and the Albert Einstein College of Medicine.
According to the researchers, “human obesity is associated with both global and nutrient-specific defects in post-ingestive nutrient sensing”.
“These impairments may contribute to overeating and subsequent weight gain and provide future targets for the development of therapies against obesity,” they wrote.
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How the study was conducted
Of the 58 study participants, 28 had a healthy body weight, with a Body Mass Index (BMI) of 25 or less, while the rest were obese, with insulin resistance and a BMI of 30 or more.
For the study, the team infused specific nutrients such as lipids and glucose directly into the stomachs of the participants using nasogastric tubes, a medical catheter inserted through the nose into the stomach.
Their brain activity was measured using functional magnetic resonance imaging (fMRI) and single-photon emission computed tomography (SPECT), a nuclear imaging modality used in diagnostic medicine.
For three days, the effect of glucose and lipids — as well as tap water — was assessed in each participant to monitor any signals triggered by these nutrients.
Since the neurotransmitter dopamine is involved in the motivational and rewarding aspects of food intake, the researchers also assessed the post-ingestive nutrient effects of glucose and lipids on each participant’s dopamine system, for two more days.
In those with obesity, the ingestion of these substances was found to create no significant changes in the signals traveling on the gut-brain axis.
In lean participants, glucose and lipids both induced multiple effects on brain activity.
A decrease in the blood-oxygen-level-dependent (BOLD) signal — which essentially reflects the net increase in blood oxygenation following neural activity — was observed in various parts of the brain. In some other parts, a more prolonged neuronal activity was observed.
The researchers observed that glucose caused the most pronounced effects in the striatum, a neuronal circuit, and the frontal pole of the brain. These regions are involved in determining eating behaviour, control and decisionmaking.
Lipid infusions mostly affected the insula in the cerebral cortex and the frontal cortex, regions involved in regulating feelings of reward-related appetite behaviour.
Those with obesity also underwent a 12-week diet, which led to a 10 percent weight loss, and were subject to a functional MRI for three more days.
The researchers said they observed “no significant nutrient-induced changes in BOLD signal in any region” of their brains, and there were also no marked differences between the pre-diet and post-diet conditions.
Among the participants with a healthy body weight, the researchers observed dopamine release in response to glucose and lipids, indicating positive feelings after nutrient infusion. The obese participants showed dopamine release in response to glucose, but not in response to lipids.
Even after weight loss, no differences in dopamine release were observed. This points to an “impaired lipid sensing in nutrient-specific pathways” involved in dopamine release.
Reduced dopaminergic responses to nutrients have been suggested to contribute to energy consumption beyond what is required for the body to be stable — or overeating.
(Edited by Sunanda Ranjan)
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