Ida Nordang Kieler

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.

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.

Obesity and inactivity are major risk factors of feline diabetes mellitus (FDM) and human type II diabetes mellitus (T2DM). In recent years, changes in the gut microbiota have been suggested as a contributing factor to T2DM. Whether the gut microbiota (GM) composition plays a role in FDM remains unknown. The aim of the current study was firstly a cross-sectional comparison of the GM of diabetic cats, to that of lean, and of obese/overweight non-diabetic cats of a similar age. Specifically, fecal samples from 82 privately-owned cats from Denmark and Switzerland were sequenced using 16S rRNA gene amplicon metabarcoding. Secondly dietary intervention data was generated, by obtaining additional samples from a subset of cats after placing them on a high-protein diet for four weeks. The GM diversity of diabetic cats was lower than that of lean cats in the cross-sectional study, and lower compared to lean and to overweight/obese cats after diet intervention. Diabetic cats also exhibited fewer Anaerotruncus, Dialister, and unknown Ruminococcaceae than lean cats. Serum fructosamine levels correlated negatively with Prevotellaceae abundance and positively with Enterobacteriaceae abundance. In summary the intestinal microbiota of diabetic cats was characterized by decreased GM diversity and loss of butyrate producing bacterial genera.

Obese dogs seem to have a different gut microbiome (GM) composition compared to lean dogs, and in humans, GM composition may negatively impact the ability to lose weight in some individuals. The purpose of this study was to investigate the interaction between exercise, weight‐loss and the composition of GM in dogs. Eighteen obese pet dogs were recruited for a 12‐week weight‐loss intervention. All dogs were fed restrictively with a commercial high‐protein/high‐fibre dry diet, and eight of these dogs were enrolled in an exercise program in addition to the diet intervention. Faecal samples were collected and the dogs were weighed at week 0, week 6 and week 12. GM composition was determined using MiSeq‐based tag‐encoded 16S rRNA gene high‐throughput amplicon sequencing, and concentrations of short chain fatty acids (SCFA) by gas‐liquid chromatography. Total weight loss, food allowance and GM were not changed by exercise inclusion. However, Megamonas abundance negatively correlated with weight loss rate and Ruminococcaceae relative abundance was lower at 12 weeks in dogs with a faster weight loss rate (≥1% per week) compared with slower weight loss rate (Megamonas and Ruminococcaceae produce acetic and propionic acids and we therefore interpret that having a GM that favour SCFA production may negatively affect weight loss rate in dogs. Weight loss rate in dogs may be related to the composition of the GM and its production of metabolites.

Summary: Compared with lean humans, the gut microbiota is altered in the obese. Whether these changes are due to an obesogenic diet, and whether the microbiota contributes to adiposity is currently discussed. In the cat population, where obesity is also prevalent, gut microbiome changes associated with obesity have not been studied. Consequently, the aim of this study was to compare the gut microbiota of lean cats, with that of overweight and obese cats. Seventy‐seven rescue‐shelter cats housed for ≥3 consecutive days were included in the study. Faecal samples were obtained by rectal swab and, when available, by a paired litter box sample. Body condition was assessed using a 9‐point scoring system. DNA was extracted, and the 16S rRNA gene was amplified with a high‐throughput quantitative real‐time PCR chip. Overweight and obese cats had a significantly different gut microbiota compared to lean cats (p < 0.05), but this finding could not be linked to differences in specific bacterial groups. The rectal samples obtained higher DNA concentration than litter box samples (p < 0.0001). In conclusion, overweight and obese cats seem to have an altered gut microbiome as compared to lean cats.