Research Indicates A Key Link Between Appetite Suppression And Obesity

Nov, 2021 - By WMR

Scientists found protein, XRN1 that is important in the brain regulation of appetite and metabolism is associated with obesity and insatiable appetite.

A new research conducted by scientists from Okinawa Institute of Science and Technology Graduate University (OIST) discovered that loss of protein XRN1 in the forebrain resulted in obese mice with voracious appetite. The study revealed some of the molecular machinery behind its functioning that drives obesity and insatiable appetite in mice.

Obesity is one of the growing health issues across the world with around 650 million people having obesity. Obesity has been related to various diseases such as type 2 diabetes, cardiovascular diseases and cancer. With this new research, the scientist disclosed a key link between a protein and obesity. The team engineered mice that lacked the XRN1 protein found in the forebrain to understand leptin resistance. These mice started gaining weight quickly when they aged six weeks and after 12 weeks they became obese with accumulation of fats in their adipose tissue and liver. When compared to a control group, mice without XRN1 protein ate almost twice the amount every day. In order to find the reason behind this overeating of mice, the team assessed the levels of leptin, which is a hormone that supresses hunger. They noticed that levels of leptin in the blood were unnaturally high in engineered mice. However, engineered mice did not respond to higher presence of leptin, which is a condition known as leptin resistance.

Moreover, the scientists found that these obese mice had high levels of mRNA that builds protein called Agouti-related peptide (AgRP), which is one of the strongest appetite stimulators and these engineered mice developed resistance to insulin, which is a hormone that controls blood sugar levels. The team plants to investigate these mechanisms deeper to get a better understanding of the link between lack of XRN1 and appetite suppression.