Background: Exocrine pancreatic insufficiency (EPI) results in maldigestion and intestinal dysbiosis. Lactate and short-chain fatty acids (SCFAs) are produced by intestinal microbiota and provide energy to colonocytes. Lactate accumulation relates to SCFAs changes, metabolic acidosis, and D-lactate-associated neurotoxicity.
Objective: Assess fecal D- and L- lactate, SCFAs, and lactic-acid bacteria (LAB) in dogs and cats with EPI. Animals: Feces from 27 dogs and 23 cats with untreated EPI, and 29 healthy dogs and 35 cats.
Methods: Retrospective cross-sectional study. D- and L- lactate were measured with an enzymatic assay. SCFAs were measured using an analytically validated GC-MS assay, and LAB were quantified by qPCR. Group comparisons were performed by Mann–Whitney U test (p = 0.05).
Results: D-lactate was increased in dogs and cats with EPI (mean difference vs healthy, 95% CI: dogs 49mM, 30 - 72mM; cats 15mM, 4 - 27mM; p < 0.0001) as was L-lactate (dogs 96mM, 60 - 139mM; cats 18mM, 3 - 40mM; p < 0.0001), with increased LAB abundance (p < 0.01). Dogs with EPI had reduced propionic acid (p < 0.0001). Conversely, cats with EPI had increased total SCFAs, driven by higher butyric (p < 0.0001) and acetic acids (p < 0.05). Conclusions and clinical importance: EPI is associated with dysbiosis characterized by increased lactate production, with potential for metabolic disorders and neurotoxicity. In cats with EPI, increased butyric acid suggests fecal SCFAs alone may not reliably reflect intestinal health. These findings emphasize functional changes caused by dysbiosis in dogs and cats with EPI.
