"Belly fat releases proteins that fuel the growth of malignant [cancerous] cells," the Mail Online reports.
It's long been known that obesity is an independent risk factor for a number of cancers, including breast, bowel and liver cancer. But it's less clear why this is the case.
This question has become more pressing, as it's estimated obesity will soon overtake smoking as the leading preventable cause of cancer in the developed world.
A new study has investigated the possible biological mechanisms behind this link. Researchers focused on visceral adipose tissue, the fat that coats internal organs. Visceral fat leads to a bigger waist size and more belly fat.
The researchers found excess visceral fat stimulated the growth of normal, healthy cells and may promote cancerous change by releasing a protein called fibroblast growth factor-2 (FGF2).
But visceral fat wasn't able to stimulate growth when cells lacked FGF2 receptors. Receptors are specialised parts of cells designed to respond to certain chemical signals.
The researchers suggest the findings could pave the way for important cancer prevention strategies targeting FGF2. But this research is still in its very early stages.
Maintaining a healthy weight is one of the most effective ways of reducing your risk of cancer, as well as a number of other serious health conditions.
Where did the story come from?
The study was carried out by researchers in the US from several institutions, including Michigan State University and the Yale School of Medicine.
Although the study wasn't directly funded by any organisation, individual authors received grants from different funding bodies, including the US National Institutes of Health and the Office of the Assistant Secretary of Defense for Health Affairs' Breast Cancer Research Program.
Generally, the Mail Online's coverage was accurate. Their coverage also referenced a narrative review from July 2017 on the influence of visceral fat on health outcomes, but we're unable to comment on the accuracy of the reporting on that study.
What kind of research was this?
This animal and laboratory study aimed to investigate the relationship between excess body fat, specifically fat around the organs (visceral adipose tissue), and cancer risk.
There's plenty of evidence to confirm the link between having excess visceral fat and the risk of developing cardiovascular disease and type 2 diabetes. Recent evidence suggests excess visceral fat may also be linked to the risk of developing breast and colon cancer.
But the exact biological mechanisms aren't well understood. The researchers hoped to study in more detail how visceral fat causes a normal, healthy cell to progress into a cancerous one.
Early-stage research is very useful for improving our understanding of mechanisms that occur at a cellular level. But even though mice are genetically similar to humans in many ways, we aren't identical.
That being said, regardless of whether human or animal cell lines are being studied, there could be external factors playing a role in the association that can't be explored, such as whether or not someone smokes.
What did the research involve?
The study involved both research in mice and tests on human fat cells in the laboratory.
The mice were either fed a low-fat diet, high-fat diet or normal diet, and were induced to grow cancerous cells using ultraviolet-B rays. Their visceral fat was then collected and any tumours analysed.
The researchers also obtained samples of visceral fat tissue from mice and cancer-free obese human subjects. They studied whether incubating this tissue with the epithelial cells that line organs caused cancer.
What were the basic results?
The researchers found visceral fat tissue stimulated the growth of a protein called fibroblast growth factor-2 (FGF2) in some cases if the FGF2 receptors were present.
This in turn stimulated the growth of epithelial cells, which may have the possibility of turning malignant (cancerous).
In the live mice, the researchers also discovered that circulating levels of FGF2 were associated with the formation of non-melanoma tumours.
How did the researchers interpret the results?
The researchers suggest that the release of FGF2 could be a pathway by which visceral adipose tissue leads to tumour generation.
They concluded that, "These data therefore suggest FGF2 stimulation of [FGF2 receptors] as a previously unappreciated link between [visceral adipose tissue] and cell transformation.
"This key finding begins to inform how [high-fat diets] and/or visceral adiposity elevate cancer risk, previously suggested only via epidemiological studies."
This animal and laboratory study investigated the possible cellular relationship between excess body fat – specifically fat around the body organs – and cancer risk.
It seems one key mechanism by which excess visceral fat could stimulate healthy cells to develop into cancerous ones could be through FGF2 levels.
The researchers hope their study could pave the way for possible cancer prevention strategies by stopping FGF2 production in obese people with excess belly fat.
They even go as far as suggesting that blocking FGF2 receptors could be one part of a treatment approach after a diagnosis of breast or skin cancer.
But it's too early to speculate about the implications of this research. Early-stage animal and laboratory studies like this one are useful for better understanding mechanisms that occur at a cellular level.
We don't know that this is the whole answer. Various genetic, health and lifestyle factors are likely to be play a combined role in the association between body fat and cancer development.
Find out more about losing weight.
Analysis by Bazian
Edited by NHS Website
Links to the headlines
Mail Online, 31 August 2017
Links to the science
Oncogene. Published online August 7 2017