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Satiety hormones

Bariatric surgery increases release of satiety hormones

The study shows that there are structural differences between lean and obese people, which explains lack of satiation in the obese

It is known that individuals who are severely overweight have an inhibited sense of satiation as they release fewer satiety hormones than people of normal weight. A study, published in the journal Scientific Reports, has concluded that laparoscopic sleeve gastrectomy (LSG) restores the deregulation in intestinal epithelial homeostasis in obese patients, leading to normalisation of epithelial cell lineage differentiation.

The paper, ‘Deregulation of transcription factors controlling intestinal epithelial cell differentiation; a predisposing factor for reduced enteroendocrine cell number in morbidly obese individuals’, by investigators from St Claraspital Basel, Basel, Switzerland and the University of Liverpool, UK, assessed the reasons for this reduced release of satiety hormones. They examined tissue samples of the gastrointestinal tract in 24 lean volunteers and 30 obese patients before and after LSG.

The team of researchers, led by Dr Bettina Wölnerhanssen from Basel, demonstrated that the number of enteroendocrine cells in obese people is significantly lower than in people with normal weight. This leads to a reduced release of satiety hormone which in turn leads to altered appetite. The obese patients also showed alterations in the pattern of the so-called transcription factors which are responsible for the development of enteroendocrine cells from stem cells. After LSG, the number of enteroendocrine cells and the pattern of transcription factors were almost entirely restored.

"Unfortunately, obese people are often stigmatised, and it is a common belief that the reason for obesity lies in a lack of self-control and discipline," said Wölnerhanssern.

However, 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 explains lack of satiation in the obese.

Morbidly obese patients exhibit impaired secretion of gut hormones that may contribute to the development of obesity. After bariatric surgery there is a dramatic increase in gut hormone release. In this study, gastric and duodenal tissues were endoscopically collected from lean and morbidly obese subjects before and three months after LSG. Tissue morphology, abundance of chromogranin A, gut hormones, α-defensin, mucin 2, Na+/glucose co-transporter 1 (SGLT1) and transcription factors, Hes1, HATH1, NeuroD1, and Ngn3, were determined.

The researchers found that in obese patients, the total number of enteroendocrine cells (EEC) and EECs containing gut hormones were significantly reduced in the stomach and duodenum, compared to lean and returned to normality post-LSG. No changes in villus height/crypt depth were observed.

In addition, a significant increase in mucin 2 and SGLT1 expression was detected in the obese duodenum. Expression levels of transcription factors required for differentiation of absorptive and secretory cell lineages were altered.

“We propose that in obesity, there is deregulation in differentiation of intestinal epithelial cell lineages that may influence the levels of released gut hormones,” the authors write. “Post-LSG cellular differentiation profile is restored. An understanding of molecular mechanisms controlling epithelial cell differentiation in the obese intestine assists in the development of non-invasive therapeutic strategies.”

To access this paper, please click here

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