Acetate mediates a microbiome–brain–β-cell axis to promote metabolic syndrome

Changes to gut microbiota, and altered faecal short-chain fatty acid concentrations, have been associated with obesity, insulin resistance and the metabolic syndrome, but no causal links have been established. Gerald Shulman and colleagues show that a gut microbiotanutrient interaction increases acetate production in rodents on a high-fat diet. This leads to activation of the parasympathetic nervous system the part of the nervous system that controls 'subconscious' operations such as heart rate and digestion which in turn promotes increased glucose-stimulated insulin secretion, ghrelin secretion, hyperphagia and obesity.