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The discovery of a molecule that blocks the absorption of ghrelin, the also known as the “hunger hormone” due to its effect in regulating hunger, was reported today in Cell Metabolism. The molecule could pave the way for future medications to control hunger and influence the treatment of conditions as diverse as obesity and anorexia.

A team of scientists from the School of Natural Sciences at UC Merced in California studying the effects of bariatric surgery on metabolism observed that the procedure increased the amount of liver-expressed antimicrobial peptide 2 (LEAP2) in mice by 52 times. LEAP2 acts as a foil to ghrelin by inhibiting its absorption by the Growth Hormone Secretagogue Receptor (GHSR), which effectively stops the effects of ghrelin, including food intake cravings.

Ghrelin is secreted in the stomach and travels through the bloodstream to the hypothalamus where it acts as an appetite stimulatory signal. In humans, the hormone’s levels increase in the bloodstream before meals, causing hunger. In the trial, an injection of ghrelin caused test subjects to become hungry and to begin food intake. Discovered about two decades ago, this hormone was thought at the time to be a sure-fire way to control food intake and weight-related problems in humans. However, experiments in mice discovered that curtailing its quantities in the bloodstream did not stop hunger, food intake or prevent weight gain.

While this research is still in its preliminary stages, it opens up new pathways to study hunger and ways to control it that could eventually lead to new ways to address overweight and obesity, conditions that affect 1.9 billion and 650 million people worldwide, respectively.

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