Researchers are one-step closer to finding the ultimate weight loss treatment – a signal in the human body that stops us from overeating.
The team has identified a molecule sent by fat cells to the fly brain when its energy stores were sufficient and inhibited the insect's feeding.
Because fruit flies replicate many of the feeding-related regulatory mechanisms and genes found in humans, they make a good model for the search for such an inhibitory signal.
The discovery was made by Walton Jones and his colleagues at the Korea Advanced Institute of Science and Technology.
'Our study indicates fat tissue sends a molecular signal to the fly brain to regulate feeding behavior,' said Jones.
'Further studies will be needed to determine if a similar system acts in mammals, and if so, whether it can be safely manipulated to help achieve weight loss, or gain, in people.'
Fat is the primary long-term energy storage molecule in animals, and the control of fat levels is critical for survival.
In mammals, the hormone leptin induces eating in response to fat loss, but so far, no corresponding signal has been identified, either in mammals or any other animal, that inhibits eating in response to fat gain.
During experiments, Jones and his team focused on short non-coding RNAs or microRNAs, which are well-known inhibitors of gene expression.
They first identified MicroRNAs, because this affects the fly's feeding behavior when it is overexpressed in fat tissue.
And team also looked for genes that target those microRNAs.
The team discovered a microRNA called miR-iab-4 increased feeding in fruit flies by more than 27% and a target gene called purple, which was expressed in fat bodies.
The discovery was made by Walton Jones and his colleagues at the Korea Advanced Institute of Science and Technology.
'Our study indicates fat tissue sends a molecular signal to the fly brain to regulate feeding behavior,' said Jones.
'Further studies will be needed to determine if a similar system acts in mammals, and if so, whether it can be safely manipulated to help achieve weight loss, or gain, in people.'
Fat is the primary long-term energy storage molecule in animals, and the control of fat levels is critical for survival.
In mammals, the hormone leptin induces eating in response to fat loss, but so far, no corresponding signal has been identified, either in mammals or any other animal, that inhibits eating in response to fat gain.
During experiments, Jones and his team focused on short non-coding RNAs or microRNAs, which are well-known inhibitors of gene expression.
They first identified MicroRNAs, because this affects the fly's feeding behavior when it is overexpressed in fat tissue.
And team also looked for genes that target those microRNAs.
The team discovered a microRNA called miR-iab-4 increased feeding in fruit flies by more than 27% and a target gene called purple, which was expressed in fat bodies.
Once it reaches the brain, PTP is transformed into an enzyme cofactor called tetrahydrobiopterin (BH4), which neurons use to produce a neuropeptide – a small protein-like molecule that regulates feeding.
What the team discovered was, when purple was removed in the fat body or there was a loss of BH4 in neurons, NPF was released more frequently and feeding increased.
On the other hand, increasing BH4 in neurons reduced NPF release and decreased feeding.
It was also discovered that feeding flies a low-calorie diet reduced expression of the fat body enzymes that control BH4 production and increased feeding.
In the end, the team concluded that BH4 was a key player in suppressing a fly's appetite.
And the PTP released from fat bodies tells its brain that it has stored enough energy and can stop eating.
In the end, the team concluded that BH4 was a key player in suppressing a fly's appetite.
And the PTP released from fat bodies tells its brain that it has stored enough energy and can stop eating.
Although these findings can only be related to flies, the team believes the identification of this appetite-suppression mechanism will surely spur research into related pathways in humans.