A harmful molecule produced by gut bacteria could be fuelling Britain's liver disease epidemic, scientists have warned.
The research reveals that D-lactate, generated by intestinal microbes, prompts the liver to manufacture excessive amounts of sugar and fat.
The team at McMaster University found that obese individuals harbour elevated concentrations of this bacterial byproduct, which proves more potent than conventional L-lactate in raising blood glucose and hepatic fat levels.
Professor Jonathan Schertzer, who led the investigation, stated: "This is a completely new way to think about treating metabolic diseases like fatty liver disease.
Non-alcoholic fatty liver disease results from fat accumulation, triggering hepatic inflammation
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"Instead of targeting hormones or the liver directly, we're intercepting a microbial fuel source before it can do harm."
The research, published in Cell Metabolism, builds upon the Nobel Prize-winning Cori cycle discovered in 1974.
Whilst Carl and Gerty Cori demonstrated how muscles generate L-lactate to stimulate glucose production in the liver, this new study revealed that gut bacteria contribute an additional element to this metabolic process.
The scientists discovered that D-lactate functions differently from its better-known counterpart. When absorbed from the intestines, it triggers the liver to overproduce both glucose and lipids, creating a metabolic imbalance.
Professor Schertzer explained: "We've known for nearly a century that muscles and the liver exchange lactate and glucose. What we've discovered is a new branch of that cycle, where gut bacteria are also part of the conversation."
Researchers developed an innovative intervention they termed a "gut substrate trap" to intercept D-lactate before absorption.
This biodegradable compound binds to the harmful molecule within the intestinal tract, preventing it from entering the bloodstream.
Laboratory trials with mice yielded promising outcomes. Animals receiving the trap demonstrated reduced blood glucose, improved insulin sensitivity, and diminished hepatic inflammation compared to untreated subjects.
Remarkably, the treatment also decreased liver fibrosis - the formation of scar tissue that precedes cirrhosis. These benefits emerged without alterations to the animals' diet or weight.
The findings suggest this novel approach could offer therapeutic potential for metabolic dysfunction-associated steatotic liver disease (MASLD), which affects approximately one in five UK residents.
The condition, previously termed non-alcoholic fatty liver disease, results from fat accumulation triggering hepatic inflammation.
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Britain faces an escalating liver disease crisis, with mortality rates quadrupling over five decades, according to the British Liver Trust.
The organisation reported 11,000 deaths from hepatic conditions last year, many of which were preventable through early detection and lifestyle modifications.
The epidemic coincides with soaring obesity rates. Government data indicates nearly two-thirds of English adults are overweight, with 260,000 joining this category last year alone. Approximately 14 million people - 26.5 per cent of adults - are classified as obese.
Professor Philip Newsome from King's College London warned: "People who develop MASLD are often overweight or have diabetes. We're seeing an increase in liver disease in the UK, and the challenge is that symptoms are often unnoticeable until it's too late."