Increased consumption of energy-rich foods is a key factor in overweight, obesity, and associated metabolic disorders. This would be, at least in part, related to microbiota disturbance. In rodent models of obesity, microbiota disruption has been associated with alteration of the intestinal barrier, endotoxemia, inflammation grade, and insulin sensitivity. The aim of the present study was to assess the effects of a high-fat diet (HFD), fed at two energetic levels, on microbiota, intestinal barrier, and inflammatory and metabolic parameters in dogs. A HFD (33% fat as fed, 4,830 kcal/kg) was given to 24 healthy Beagle dogs at 100% (HF-100; n = 8) and at 150% (HF-150; n = 16) of their maintenance energy requirements for 8 weeks. Analysis of similarity revealed a significant difference in gut microbiota β-diversity following the diet compared to week 0 in both groups while α-diversity was lower only in the HF-150 group. Firmicutes/Bacteroidetes ratio was higher in the HF-150 group compared to the HF-100 group at weeks 2 and 8. A reduction in insulin sensitivity was observed over time in the HF150 group. Neither endotoxemia nor inflammation was observed in either group, did not find supporting data for the hypothesis that the microbiota is involved in the decline of insulin sensitivity through metabolic endotoxemia and low-grade inflammation. Colonic permeability was increased at week 4 in both groups and returned to initial levels at week 8, and was associated with modifications to the expression of genes involved in colonic barrier function. The increase in intestinal permeability may have been caused by the altered intestinal microbiota and increased expression of genes encoding tight junction proteins might indicate a compensatory mechanism to restore normal permeability. Although simultaneous changes to the microbiota, barrier permeability, inflammatory, and metabolic status have not been observed, such a causal link cannot be excluded in dogs overfed on a HFD. Further studies are necessary to better understand the link between HFD, intestinal microbiota and the host.

Individuals are more or less prone to excessive fat deposits and body weight. This could result from differences in the expression of gene involved in adipose tissue metabolism in early life. This study aimed to identify such possible differences in puppy dogs. Twenty-four 4-wk old females Beagle puppies were raised in the same environment, and fed with the same diet, ad libitum but for 3.5 h. Dogs were allotted in 3 groups according to their fat-free mass, fat mass, and pelvic circumference at 24 months of age: IW (n = 9; ideal body condition, OW1 (n = 6; moderately overfat) and OW2 (n = 9; overfat/obese). Subcutaneous and visceral adipose tissue (VAT) samples were collected at the time when animals were neutered (8 months). The mRNA level of genes involved in the regulation of lipolysis (perilipin, HSL), lipogenesis (ACC, ADRP, CPT1, FAS, FABP), adipogenesis (PPARg, SREBP-1c), thermogenesis (UCP1, UCP2), glucose uptake (GLUT4), insulin signaling (IRS2), and adiponectin production was assessed by real time RT-PCR. Gene expression levels in the three groups were compared by a Wilcoxon test. Ethics approval was granted by the French Ministry of Research and Royal Canin’s Ethical Committee. Compared to IW, OW2 dogs had a lower expression of UCP1 in the VAT (P = 0.049). This could result in reduced heat production by non-shivering thermogenesis. Moreover, a low UCP1 expression has been linked to obesity. Compared to IW, OW1 dogs had a higher transcription level of ACC and ADRP genes (P < 0.05). ACC is a point of regulation of the FA synthesis whereas ADRP is involved in the differentiation of the pre-adipocytes, and fat storage. These results suggest that the overweight/obesity phenotype could be associated with a lower heat loss, and the moderately overweight phenotype with a higher ability to fat synthesis compared to the lean phenotype.

Obesity and nutritional factors like high-fat diets (HFD) are associated with metabolic alterations, which result from the diet, bodyweight change or both. The objective was to determine the effects of HFD consumed either at maintenance or excess energy levels on BW, metabolic parameters, and colonic permeability markers. A HFD (35% fat as fed, 4923 kcal/kg) was given for 8wks to 24 healthy Beagle dogs, 8 at 100% (G1.0) and 16 at 150% (G1.5) maintenance energy levels for each individual dog. At baseline and after 8wks, basal leptinemia, ghrelinemia, glycemia and insulinemia were measured, while postprandial glycemia and insulinemia were determined for 6h following a challenge test meal. Colonic mucosa biopsies were performed and the expression of proteins involved in permeability was analyzed using RT-rtPCR. Results were analyzed using linear mixed model (nlme package; R) with dog as a random term (data rank-transformed where residuals not normally distributed). Ethics approval was granted by the French Ministry of Research and Royal Canin’s Ethical Committee. In the G1.5 group, increases in bodyweight (15%; P < 0.001), leptinemia (5±2 vs 2±1 ng/ml; P < 0.01), and postprandial insulin AUC (10405±2316 vs 6232±1368 μU.min.ml-1; P = 0.03) were observed at 8wks compared to baseline, whereas ghrelinemia decreased (552±361 vs 633±413 pg/ml; P = 0.04). No such change were observed in the G1.0 group. In both groups at 8wks, mRNA levels of claudin 2 (G1.0: P < 0.05; G1.5: P < 0.01) and syndecan (G1.0: P < 0.01; G1.5: P < 0.01) were higher compared to baseline, while mRNA levels of TJP1 (P < 0.01) increased in the G1.5 group. The changes observed in the G1.5 group but not in the G1.0 group suggest that the metabolic and hormonal parameters are related to weight gain but not to HFD alone. Furthermore, the mechanisms behind the modifications to colonic permeability markers observed in both groups remains to be elucidated.

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