Appetite-Controlling Molecule Could Prevent ‘Rebound’ Weight Gain After Dieting
Source: Monash University
Summary: According to a new study, researchers have revealed how mice control their appetite when under stress such as cold temperatures and starvation.
There are 1.9 billion adults overweight or obese worldwide, placing them at increased risk of developing type 2 diabetes, cardiovascular disease, chronic kidney disease and cancer. Most weight-loss strategies focus on creating a negative energy balance, where you burn more calories than you consume, but these strategies frequently fail because of compensatory increases in appetite. The underlying mechanisms that link energy demand to increased appetite are not fully understood. Researchers from the Monash University and St Vincent’s Institute in Melbourne has revealed how mice control their appetite when under stress such as cold temperatures and starvation. The results shed light on the metabolic processes behind why people tend to regain much of their weight after dieting and could lead to treatments to help them keep the weight off for good. The study findings were published in the journal eLife.
The team focused their study on a molecule called AMPK (AMP-activated protein kinase), which is known to control how the body generates and uses energy under different conditions. But the other molecules that AMPK works with to achieve these effects are largely unknown. One theory is that AMPK switches off another molecule called ACC (acetyl-CoA carboxylase)as an essential step in regulating appetite and heat generation. To investigate this further, the team engineered mice with mutated ACC, which made them insensitive to the effects of AMPK, and studied them under various conditions. Finally, they found that under conditions of stress, the lack of ACC control by AMPK increased the animals’ tendency to utilize fat, rather than intake more calories.
First author Dr. Sandra Galic said, “We have identified a distinct signalling pathway that is involved in regulating appetite and fat metabolism distinct from energy expenditure” and further added, “Our results could pave the way for therapies to prevent the regain of weight that so often follows the initial success of diet-induced weight loss, by suppressing hunger signals caused by prolonged calorific deficits.”
More Information: Sandra Galic et al, “AMPK signaling to acetyl-CoA carboxylase is required for fasting- and cold-induced appetite but not thermogenesis”, eLife (2018). DOI: 10.7554/eLife.32656