A new study provides further evidence that metabolic factors have a part to play in obesity, after finding that people who are obese release significantly fewer “satiety hormones” after eating, compared with lean individuals.
In the United States, it is estimated that
Since obesity is a key risk factor for a variety of health conditions – including heart disease, type 2 diabetes, and some forms of cancer – its prevalence has become a major public health concern.
A primary cause of obesity is an
According to co-lead study author Dr. Bettina Wölnerhanssen, of the Department of Biomedicine at University Hospital Basel in Switzerland, there is a widespread belief that “a lack of self-control and discipline” is the key player in obesity.
The new study from Dr. Wölnerhanssen and colleagues adds to the evidence. The team has uncovered a molecular mechanism in individuals with obesity that may prevent them from feeling full after a meal, which may cause them to eat more.
To reach their findings, the researchers collected and examined samples of gastrointestinal tissue from 27 adults with morbid obesity, both before and 3 months after they underwent laparoscopic sleeve gastrectomy (LSG) – a type of weight loss surgery.
For comparison, the team also collected and analyzed gastrointestinal tissue samples from 24 lean adults.
The analysis revealed that the gastrointestinal tissue taken from participants with obesity prior to LSG had significantly fewer enteroendocrine cells than the tissue samples of lean subjects.
In response to food intake, enteroendocrine cells release hormones into the bloodstream that send signals to the brain, telling us when we are full. A reduction in enteroendocrine cells leads to a decrease in the release of these so-called satiety hormones, which may fuel an increase in food intake.
Additionally, the researchers found that, prior to LSG, individuals with obesity demonstrated changes in the expression of transcription factors that regulate enteroendocrine cell formation. “Deregulation of this regulatory network may lead to defective epithelial differentiation resulting in altered functions of the intestinal epithelium,” note the authors.
Interestingly, the analysis of tissue samples from participants with obesity taken after LSG showed that the number of enteroendocrine cells and the expression of transcription factors in gastrointestinal tissue was almost the same as that of the lean subjects.
Overall, the researchers believe their study offers further evidence that obesity can develop as a result of metabolic factors.
“[…] there is no doubt that metabolic factors are playing an important part. The study shows that there are structural differences between lean and obese people, which can explain lack of satiation in the obese.”
Dr. Bettina Wölnerhanssen