German scientists have discovered that our brains are actively taking in sugar from the blood stream, overturning the long-held assumption that this was a purely passive process.
Even more surprising, they also found that it’s not our neurons that are responsible for absorbing all that sugar - it’s our glial cells, which make up 90 percent of the brain’s total cells, and until very recently, have been shrouded in mystery.
Not only does the find go against conventional wisdom on how our brains respond to sugar intake, it also shows how cells other than our neurons can actively play a role in controlling our behaviour.
Astrocytes - which are a specialised form of glial cell that outnumber neurons more than fivefold - have long been thought of as little more than ‘support cells’, helping to maintain the blood-brain barrier, carry nutrients to the nervous tissue, and play a role in brain and spinal cord repair.
But we now have evidence that they also play a role in human feeding behaviours, with researchers finding that their ability to sense and actively take in sugar is regulating the kinds of appetite-related signals that our neurons send out to the rest of the body.
And we’re not talking about a little bit of sugar here: the human brain experiences the highest level of sugar consumption out of every organ in the body.
"Our results showed for the first time that essential metabolic and behavioural processes are not regulated via neuronal cells alone, and that other cell types in the brain, such as astrocytes, play a crucial role," explains study leader Matthias Tschöp from the Technical University of Munich.
"This represents a paradigm shift and could help explain why it has been so difficult to find sufficiently efficient and safe medicines for diabetes and obesity until now."
Tschöp and his team decided to investigate how the brain decides to take in sugar from the blood - and how much - because this is directly related to our feelings of hunger.
A better understanding of why we get hungry could quite literally change modern society, with recent estimates putting the number of obese people in the world above those of underweight people.
"We ... suspected that a process as important as providing the brain with sufficient sugar was unlikely to be completely random," says one of the team, neurobiologist Cristina García-Cáceres.
"We were misled by the fact that nerve cells apparently did not control this process, and therefore first thought it to occur passively. Then we had the idea that glia cells such as astrocytes, which had long been misunderstood as less important 'support cells', might have something to do with transporting sugar into the brain."
The team used positron emission tomography (PET) scans to observe how insulin receptors act on the surface of the brain’s astrocytes. Insulin is a hormone produced by the pancreas to allow the body to use or store sugar (in the form of glucose) from carbohydrates in the food we eat.
They found that if these receptors were missing on certain astrocytes, it would result in less activity in the neurons that are responsible for curbing food uptake, called proopiomelanocortin neurons.
Not only that, but they found that astrocytes missing insulin receptors actually became less efficient over time in transporting glucose into the brain - particularly in a region of the hypothalamus that sends out signals that you're full, or satiated.
So it looks like glial cells, not the neurons, are the true 'gate-keepers' for how much sugar our brains absorb, and we now know that sugar has such a powerful influence on them, they're seeking out sugar, rather than just passively absorbing it.
A better understanding of how this works could change everything about how we treat obesity in the future.
The team says that a lot more research is now needed to adjust the old model that assumed the neurons alone were regulating our food intake and metabolism, and suggest that maybe even our immune cells are playing a role in it as well.
"We have a lot of work ahead of us," says García-Cáceres, "but at least now we have a better idea where to look."
The research has been published in Cell.