Summary: Scientists have uncovered a new nerve form, BNC2, which acts quickly to store hunger-promoting neurons, possibly leading to more efficient taste rules. These BNC2 cells, located in the body’s arcuate atom, respond quickly to starvation cues by inhibiting AGRP cells responsible for driving hunger.
This finding provides new insights into how appetite is controlled by neural pathways and opens the door to novel treatments for obesity and physiological problems. In a matter of minutes, the study suggests that BNC2 neurons was balance hunger urges, making them more efficient than traditional satiety-promoting neurons.
Researchers hope to develop solutions that can better regulate stomach and lower disease risk by targeting BNC2 cells. This discovery was reshape our understanding of brain-driven activities.
Important Information:
- Rapid reply: BNC2 cells act within minutes to suppress appetite, faster than formerly known satiety neurons.
- Medical possible: BNC2 may offer a tale target for obesity and diabetes solutions.
- Broader repercussions: Discovering BNC2 cells ideas at comparable wires for additional instinctive behaviors.
Origin: Rockefeller University
A raised war breaks out in your head as you consider whether to have one more potatoes chip. One type of neuron promotes fullness while another type promotes poverty. How fast one party wins the game determines whether you’ll abandon the bag of chips.
Scientists have now identified a missing link in this neural circuit that controls appetite and satiety, a previously unidentified sort of neuron that acts as an urgent counterbalance to the desire to eat.
The findings,  , published in , Character, develop the typical type of hunger and satiety rules, and may provide novel therapeutic targets for tackling obesity and physiological disorders.
” This new type of neuron changes the conceptual framework for how feeding is regulated” says Han Tan, a research associate in Rockefeller ‘s , Laboratory of Molecular Genetics, headed by , Jeffrey Friedman.
More or less
A plain feedback loop between two different types of brain tissues in the brain was usually thought to drive hunger and neurons expressing a gene called POMC promote hunger.
These two populations were originally thought to be the two major leptin targets, but new studies suggested that this design was insufficient. While activating POMC cells takes time to control appetite, activating AGRP neurons quickly induces hunger. Scientists were curious to find out whether they had missed anything.
” We suspected POMC could n’t counterbalance the hunger neurons quickly enough to curb feeding”, Tan says.
So we began to wonder if there was a missing nerve that may induce fast hunger, on a related time scale to that of AGRP.
The team found a new kind of nerve that expresses a protein called BNC2 along with receptors for the hormone melatonin, which has previously been demonstrated to play a major role in regulating body fat through single-cell RNA scanning of neurons in the body’s arcuate nucleus. This recently discovered BNC2 neuron responds to food signals and effectively stops hunger.
The findings demonstrate that BNC2 neurons, when activated by leptin and possibly other signals, not only suppress appetite but also lessen the negative emotions that come with hunger. Remarkably, these neurons act by inhibiting the AGRP neurons and they can do so rapidly, serving as a complementary signal.
This study expands our understanding of how leptin reduces appetite and adds an important new component to the neural circuit that regulates appetite, according to Friedman.
It also addresses a conundrum regarding how different neurons ‘ feeding is controlled on various time scales.
Redefining hunger
BNC2 neurons have important implications for addressing obesity and metabolic disorders.
We are currently looking into whether utilizing these neurons to treat obesity or diabetes, citing genetic studies that link BNC2 to high body mass index and patient diabetes risk.
The team is also looking into the potential therapeutic effects of modulating these neurons ‘ activity by examining how stimulating or inhibiting these neurons might be.
This finding has broad implications for how we interpret how the brain regulates instinctive behavior. If BNC2 neurons can coordinate hunger regulation, could there be other similar circuits for behaviors like grooming or sleeping?
Similar circuits could help us understand how the brain regulates intricate actions across a range of instinctive behaviors, allowing for further research in behavioral neuroscience.
” We now believe BNC2 and AGRP to be the sort of yin and yang of feeding”, Tan says.
About this news about neuroscience and hunger
Author: Katherine Fenz
Source: Rockefeller University
Contact: Katherine Fenz – Rockefeller University
Image: The image is credited to Neuroscience News
Original Research: Open access.
” Leptin-activated hypothalamic BNC2 neurons acutely suppress food intake” by Han Tan et al. Nature
Abstract
Leptin-activated hypothalamic BNC2 neurons acutely suppress food intake
Leptin is an adipose tissue hormone that regulates the activity of specific neural populations that control appetite and metabolism and maintains homeostatic control over adipose tissue mass.
Leptin regulates food intake by inhibiting orexigenic agouti-related protein ( AGRP ) neurons and activating anorexigenic pro-opiomelanocortin ( POMC) neurons. However, acute activation of POMC neurons has only a minimal effect compared to AGRP neurons, which regulate food intake on a quick time scale.
This has raised the possibility that a previously unknown leptin-regulated neural population is rapidly slowed down by appetite.
We report the discovery of a new subset of leptin-target neurons that express basonuclin 2 ( Bnc2 ) in the arcuate nucleus and directly inhibit AGRP neurons.
BNC2 neuronal activation, which was independent of the effect of AGRP activation, produced a place preference indicative of positive valence in hungry but not fed mice. The activity of BNC2 neurons is modulated by leptin, sensory food cues and nutritional status.
Finally, BNC2 neurons ‘ deletion of leptin receptors resulted in marked obesity and hyperphagia, similar to what AGRP neurons ‘ leptin receptor knockouts showed.
These results provide a crucial link between the neural circuit that maintains energy balance and BNC2-expressing neurons, filling a crucial gap in our understanding of the mechanisms governing food intake and leptin action.
