US researchers have discovered a gene that may play an influential role in food cravings and motivation to exercise.
Mice who lack the PrKar2a gene were shown to consume less high-fat or high-sugar food – even after fasting – and would run on a treadmill for two to three times longer than mice with the gene. Even when fed a high-fat diet, mice lacking PrKar2a were less likely to show signs of obesity-linked illness compared to normal mice.
'While being able to experience the rewarding aspects of food is evolutionarily vital, overriding satiety signals in favour of the overconsumption of high-fat and sweet foods can lead to obesity, metabolic dysregulation, and other related comorbidities' wrote the authors in their paper which was published in JCI Insight.
The paper builds on previous work by the same team which showed that mice lacking a functional copy of Prkar2a were less likely to become obese than those with normally functioning Prkar2a.
PrKar2a plays a role in the composition of an enzyme called Protein Kinase A (PKA) which plays a central role in speeding up reactions inside cells. The study concluded that the reduction in PKA signalling in the Prkar2a-knockout mice improved their motivation to exercise and decreased their craving for foods high in sugars and fats.
The researchers found that PrKar2a is highly expressed in a part of the brain called the habenula which is involved in processing rewards, motivation, addiction and pain, which may explain why it is linked to behaviour change.
The researchers suggest that understanding PrKar2a could offer a novel approach to combating obesity-related disease in humans, and recommend 'further study of PKA regulation in the various distinct cell subtypes' as a next step.