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Mice have a gene that controls food cravings and the desire to exercise

Researchers at the National institutes of health have discovered a gene in mice that controls cravings for fatty and sweet foods, and the desire to exercise. 

Editor: Aigerim Akhmetova 

Translator: Tursunova Balkadisha 

Author: Bolysbek Dana 

 

 

The Prkar2a Gene is produced in large quantities in the habenula, a tiny area of the brain involved in the response to pain, stress, anxiety, sleep, and reward. The study was conducted by Edra London, Ph. D., a staff researcher in the endocrinology and genetics section at the National institutes of health (NICHD), and colleagues. 

 

The Prkar2a gene is expressed in the habenula (leash), a tiny area of the brain involved in the response to pain, stress, anxiety, sleep, and reward. 

 

Prkar2a contains the information needed to form two subunits-the molecular components of the protein kinase a enzyme. Enzymes speed up chemical reactions by helping either combine smaller molecules into larger molecules, or break down larger molecules into smaller ones. Protein kinase A is a Central enzyme that accelerates reactions within cells. In a previous study, the NICHD team found that despite a high-fat diet, mice lacking functioning copies of Prkar2a were less likely to be obese than wild-type mice with normally functioning Prkar2a. 

 

The researchers determined that mice without the Prkar2a gene ate less fatty foods than mice with normally functioning Prkar2a, not only with unrestricted access to food, but also after fasting. Similarly, Prkar2a-negative mice also drank less sugar solution than wild-type mice. Prkar2a-negative mice were also more likely to exercise, running 2-3 times longer than wild-type mice on a treadmill. Female Prkar2a-negative mice were less likely to consume high-fat foods than Prkar2-negative males, while Prkar2-negative males showed less preference for sugar solution than Prkar2-negative females. 

 

Source: https://medicalxpress.com/news/2020-11-gene-mice-food-cravings-desire.html 

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