In dogs, the use of probiotics for preventive or therapeutic purposes has become increasingly common, however the evidence for beneficial effects are often limited. The aim of this study was to investigate the effects of feeding a diet containing Enterococcus faecium NCIMB 10415 on faecal quality, faecal short-chain fatty acid concentrations, serum concentrations of cholesterol, triglycerides, cobalamin and folate as well as faecal microbiome in adult dogs. Eleven healthy client owned dogs were enrolled in a randomized, double-blinded crossover study. All dogs were fed the same balanced diet with or without incorporation of Enterococcus faecium NCIMB 10415 for 16 days each. Blood and faecal samples were collected at baseline and during the feeding trial and owners recorded daily faecal scores. An Enterococcus spp. ASV, likely representing E. faecium NCIMB 10415 was detected in the faecal microbiome of some dogs 18–19 days after withdrawal of oral supplementation. Inclusion of E. faecium decreased circulating cholesterol (p = 0.008) compared to baseline. There were no differences in cholesterol concentrations between diets. Owners reported 0.6 ± 0.3) days less of loose stools compared to the control diet. Comparing to baseline, both diets significantly increased faecal concentration of acetate and butyrate, decreased serum cobalamin and increased faecal microbial diversity. Decreased serum cobalamin, and increased faecal acetate correlated with decreases in the Fusobacterium, Streptococcus, Blautia, and Peptoclostridium. Except for effects on circulating cholesterol and faecal score, effects were observed regardless of the addition of E. faecium. It is therefore likely that these effects can be contributed to dietary prebiotic effects on the faecal microbiome.

Acquired canine proximal renal tubulopathy (Fanconi syndrome) related to excessive ingestion of jerky treats has been recognized since 2007. This study aimed to improve knowledge about the syndrome’s characteristics, especially long-term outcome. By reaching out to veterinarians and dog owners, dogs suspected of jerky induced Fanconi syndrome were identified. The dog’s medical records were reviewed, and owners interviewed. Data was analyzed using linear mixed models (p < 0.05 was considered statistically significant) and descriptive statistics are reported. Thirty dogs, median body weight 6.8 (range 1.2–59) kg and age 6.5 (0.5–14) years, were enrolled as suspected cases based on history of jerkey ingestion and confirmed normoglycemic/hypoglycemic glycosuria. Clinical signs included polydipsia (23/30), polyuria (21/30), lethargy (19/30), weight loss (15/30), hyporexia (11/30), vomiting (7/30), diarrhea (7/30) and no clinical signs (2/30). Para-clinical findings included azotemia (6/28), hypophosphatemia (9/25), metabolic acidosis (3/8), hypokalemia (6/20), proteinuria (13/26), aminoaciduria (4/4), hematuria (22/29) and ketonuria (7/27). Clinical signs resolved in 22/28 within 11 (0.3–52) weeks and glycosuria resolved in 28/30 within 6.5 (1–31) weeks. There were no associations between serum creatinine and urea and the amount/duration of jerky ingestion. Serum symmetric dimethylarginine concentrations were only available for a few dogs, therefore no conclusion was achieved on a possible association with duration of jerky ingestion. Apart from a larger percentage of dogs achieving complete recovery, the current findings are in agreement with previous reports.

Background: Obesity is associated with insulin resistance and affects glycemic control in diabetic patients. Hypothesis/Objectives: Assess the impact of 12-week caloric restriction on remission and glycemic control in overweight diabetic cats using a prospective, randomized controlled trial. Animals: Seventy-two overweight (body condition score ≥ 6/9) client-owned insulin-treated diabetic cats, randomized either to caloric restriction (intervention, 32; target approximately 2% weekly weight loss) or body weight maintenance (control, 40). Methods: All cats received a novel therapeutic diabetic diet, suitable for weight reduction, for 12 weeks (%metabolizable energy [protein/fat/nitrogen-free extract]: dry [49.4/24/26.6]; wet [63.2/25.3/11.5]). Physical examination, serum biochemistry, home blood glucose curves (BGC), diabetic clinical score, and quality of life questionnaires were performed on weeks: −1, 4, 8, and 12. Insulin dose was recorded and glycemic variability (SD of BGC) was calculated. Induction of diabetic remission was the primary outcome measure. Data were analyzed using regression and linear mixed models. Results: By week 12, intervention had 2.1 times higher probability of remission (16/32) compared with controls (12/40, P = .04). Weight loss was 7.2% (95% confidence interval [CI], 5.7-8.7) for the intervention versus 2.7% (95% CI, 1.3-4.1, P < .001) for controls. For cats not achieving remission, glycemic variability decreased 45% (95% CI, 26-65) and 7% (95% CI, 16-21) for intervention and control cats, respectively (P = .01), insulin-dose decreased by 36% (95% CI, 2-70) for intervention and increased 28% (95% CI, 3-53, P = .004) for controls. Conclusions and clinical importance: Caloric restriction, using a therapeutic diabetic diet suitable for weight reduction increased the probability of remission and improved glycemic control in overweight diabetic cats.