A molecule produced by gut bacteria, called D-lactate, has been identified as a significant contributor to elevated blood sugar, insulin resistance, fatty liver inflammation and fibrosis in obesity, according to new research. Scientists in Canada report that trapping D-lactate in the gut reduces these metabolic dysfunctions in mice.
Researchers from McMaster University, Université Laval and the University of Ottawa found that obese mice and humans with obesity have higher circulating levels of D-lactate compared with healthier controls. D-lactate, unlike its well-known counterpart L-lactate, originates mainly from gut microbiota. When introduced in equivalent amounts, D-lactate provoked greater increases in hepatic glycogen, triglycerides and blood glucose than L-lactate.
The team engineered a safe, biodegradable polymer known as a “gut substrate trap” that binds D-lactate in the gut, preventing its absorption. Obese mice fed this polymer showed lowered blood glucose, improved insulin sensitivity, reduced liver inflammation and diminished fibrosis, even though their body weight and diet remained unchanged.
Stable isotope tracing in mice and experiments in isolated liver cells revealed that D-lactate is metabolised into pyruvate, TCA cycle intermediates, lipids and glucose. Colonisation of mice with bacterial strains engineered to produce D-lactate led to higher blood sugar than colonisation with strains producing L-lactate.
The polymer’s effects were dose- and length-dependent: more extensive trapping produced more substantial metabolic improvements. Liver inflammation markers and fibrosis typical of metabolic dysfunction-associated fatty liver disease and metabolic dysfunction-associated steatohepatitis were significantly lowered.
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