Fecal Microbiota, Bile Acids, Sterols, and Fatty Acids in Dogs with Chronic Enteropathy Fed a Home-Cooked Diet Supplemented with Coconut Oil

SIMPLE SUMMARY: Medium-chain triglycerides (MCT), which are lipid molecules made up of medium-chain fatty acids (MCFAs), can be rapidly absorbed through enterocytes, bypassing the lymphatics, and appear as interesting energy sources used to manage common canine gastrointestinal disorders such as chronic enteropathies (CE). Virgin coconut oil (VCO) is a vegetal fat source rich in MCT that has been shown to have antimicrobial properties when supplemented in piglet diets. This study aimed to evaluate the effects of a home-cooked diet (HCD) supplemented with VCO (HCD + VCO) on the clinical scores, fecal microbiota, and metabolomes of 18 CE dogs. All dogs responded well to the diet change, demonstrating improvements in their clinical signs. Compared to their habitual diets, HCD reduced fecal fat excretion, increased fecal moisture, and induced changes in the microbiota. HCD + VCO induced changes in their sterol and fecal fatty acid profiles but failed to exert significant effects on fecal microbiota. However, HCD + VCO increased the fecal proportions of certain MCFAs (C10:0 and C12:0), which are theoretically not expected to be found in feces. These results should be considered preliminary and should be confirmed in further studies with healthy dogs. ABSTRACT: Medium-chain fatty acids (MCFAs) are considered to be interesting energy sources for dogs affected by chronic enteropathies (CE). This study analyzed the clinical scores, fecal microbiota, and metabolomes of 18 CE dogs fed a home-cooked diet (HCD) supplemented with virgin coconut oil (VCO), a source of MCFA, at 10% of metabolizable energy (HCD + VCO). The dogs were clinically evaluated with the Canine Chronic Enteropathy Activity Index (CCECAI) before and at the end of study. Fecal samples were collected at baseline, after 7 days of HCD, and after 30 days of HCD + VCO, for fecal score (FS) assessment, microbial analysis, and determination of bile acids (BA), sterols, and fatty acids (FA). The dogs responded positively to diet change, as shown by the CCECAI improvement (p = 0.001); HCD reduced fecal fat excretion and HCD + VCO improved FS (p < 0.001), even though an increase in fecal moisture occurred due to HCD (p = 0.001). HCD modified fecal FA (C6:0: +79%, C14:0: +74%, C20:0: +43%, C22:0: +58%, C24:0: +47%, C18:3n−3: +106%, C20:4n−6: +56%, and monounsaturated FA (MUFA): −23%, p < 0.05) and sterol profile (coprostanol: −27%, sitostanol: −86%, p < 0.01). VCO increased (p < 0.05) fecal total saturated FA (SFA: +28%, C14:0: +142%, C16:0 +21%, C22:0 +33%) and selected MCFAs (+162%; C10:0 +183%, C12:0 +600%), while reducing (p < 0.05) total MUFA (−29%), polyunsaturated FA (−26%), campesterol (−56%) and phyto-/zoosterols ratio (0.93:1 vs. 0.36:1). The median dysbiosis index was <0 and, together with fecal BA, was not significantly affected by HCD nor by VCO. The HCD diet increased total fecal bacteria (p = 0.005) and the abundance of Fusobacterium spp. (p = 0.028). This study confirmed that clinical signs, and to a lesser extent fecal microbiota and metabolome, are positively influenced by HCD in CE dogs. Moreover, it has been shown that fecal proportions of MCFA increased when MCFAs were supplemented in those dogs. The present results emphasize the need for future studies to better understand the intestinal absorptive mechanism of MCFA in dogs.