When gut bacteria break down dietary fibre, they appear to send signals to the body’s brown fat, which acts as an internal radiator. A new study points to a previously unknown link between digestion and heat-producing fat that could both reshape our understanding of metabolism and, in time, pave the way for new treatments for obesity and metabolic disorders.
A bowl of porridge or a hearty salad apparently does more than simply satisfy momentary hunger. When dietary fibre reaches the gut and is broken down by bacteria, it triggers a cascade of chemical signals that travel through the bloodstream and reach the pad of brown fat between the neck and shoulders. This specialised type of fat acts as the body’s own internal heating system, burning calories to generate heat that helps to maintain body temperature in the cold.
Until now, this biochemical pathway had only been observed in laboratory mice, and biologists lacked evidence that a similar connection exists in humans.
But this has now changed. A new study points, for the first time, to a direct biological link between the breakdown of dietary fibre in the gut and the activity of the body’s brown fat – two systems that are normally studied separately. These signalling molecules appear to influence how efficiently brown adipose tissue converts energy into heat.
The study was conducted by researchers from the Turku PET Centre at the University of Turku in Finland, led by Professor and Consultant Kirsi A. Virtanen and Senior Researcher Milena Monfort-Pires.
Their findings suggest that brown fat works closely with the short-chain fatty acids acetate, propionate and butyrate – small molecules produced when gut bacteria break down dietary fibre – have now been published in the Journal of Clinical Endocrinology & Metabolism.
“The study provides new and important insights into the role of dietary fibre in human metabolism. It shows that these short-chain fatty acids can help us understand how brown fat uses these metabolites as fuel,” says Kirsi A. Virtanen.
She and her colleagues think that future studies of the interaction between dietary fibre and brown fat could prove highly valuable.
“In the long term, they could open up new ways of normalising a metabolism that is out of balance – for example, through targeted dietary treatments for obesity and metabolic disorders,” points out Milena Monfort-Pires, who led the data analysis.
The hunt for the signal between the gut and brown fat
The path to the new study began with a simple question in the laboratory, explains Monfort-Pires.
Animal studies have for years shown that eating activates brown fat and internal heat production in mice, and the research team has since observed a similar link in humans. However, exactly what in food triggers this process has remained unclear. This led the researchers to ask whether the short-chain fatty acids produced when dietary fibre is broken down could be part of the explanation.
This suspicion was reinforced by previous cell studies and animal experiments showing that short-chain fatty acids can directly influence adipose tissue and energy balance. In addition, human studies have shown that people with higher levels of these fatty acids often weigh less and have a healthier metabolism. According to the researchers, both observations could be signs that short-chain fatty acids play a role in energy expenditure.
To find out, the researchers recruited 71 healthy adults. They were exposed to cold, which is an effective and natural way to activate brown adipose tissue. Meanwhile, the researchers monitored the body’s responses using advanced PET/CT scanners.
Using four radioactive tracers, the researchers tracked how much blood, oxygen, sugar and fat the brown fat took up during cold exposure. They also analysed tissue samples from both white and brown fat to investigate which genes were active.
The measurements gave the researchers the first clear indication that the connection also exists in humans. Brown fat was clearly associated with molecules released when dietary fibre is broken down – although not as pronounced as in animals.
Propionate and butyrate levels remained stable in individuals with high brown fat activity but fell in those with lower activity – another indication of a link between these signalling molecules and brown fat.
Signalling molecules reveal brown fat activity
Further, the researchers observed that the more acetate there was in the blood during cold exposure, the more fuel in the form of free fatty acids the brown fat drew from the bloodstream. For propionate, however, the link to oxygen consumption appeared only in the group with low brown fat activity.
“This is where human metabolism differs from that of animals, presumably because it is significantly more complex,” says Milena Monfort-Pires.
Nevertheless, genetic analyses confirmed that the genes that help the body metabolise short-chain fatty acids are closely linked to the energy expenditure of brown fat.
“The concentrations of short-chain fatty acids in the blood appear to reflect how active the brown fat is. They could therefore be used as biological markers of how effectively the body’s heat-producing fat tissue is functioning – without the need for advanced scans,” explains Milena Monfort-Pires.
The researchers are cautious about drawing a direct link between diet and brown fat, since the analysis is based on blood samples rather than detailed dietary data.
Extensive analysis of scan images, blood samples and genetic patterns was required to demonstrate a link between the breakdown products of dietary fibre and brown fat.
New leads in the dialogue between the gut and brown fat
The study cannot determine whether a higher-fibre diet itself can boost metabolism or whether the same effect can be achieved through dietary supplements. However, it does reveal a biological connection that researchers had previously observed only in animals. The findings call for new studies that follow diet, gut bacteria and brown fat over longer periods.
If successful, such studies could potentially pave the way for more targeted, diet-based treatments for obesity and metabolic disorders, the researchers say.
But one finding surprised the researchers in particular: the short-chain fatty acid propionate. Although propionate was detected in all participants, the association between propionate levels and brown fat oxygen consumption appeared only in those with low brown fat activity. The researchers think this may mean that the body switches between different fuel sources in the cold, depending on how active the brown fat is.
“Studies of this kind may also help explain why people’s metabolisms respond differently to cold and diet,” says Kirsi A. Virtanen. She adds that she and her colleagues hope to use such studies as a springboard to understanding how adipose tissue and the gut function as parts of the same metabolic system, rather than, as has traditionally been the case, viewing them as separate organs.
“This could change the way we think about the interaction between diet, the gut and energy expenditure.”
“This is an important step towards clarifying whether a high-fibre diet can actually alter the function of brown adipose tissue in humans – and thereby influence one of the body’s key mechanisms for energy expenditure,” adds Milena Monfort-Pires.
“Only now are we beginning to understand how the gut and brown fat communicate with each other – and what significance that communication may have for metabolism.”
