Dietary supplementation with probiotics promotes weight loss by reshaping the gut microbiome and energy metabolism in obese dogs.

Obesity and overweight among companion animals are significant concerns, paralleling the issues observed in human populations. Recent research has highlighted the potential benefits of various probiotics in addressing weight-related changes, obesity, and associated pathologies. In this study, we delved into the beneficial probiotic mechanisms in high-fat-induced obese canines, revealing that Enterococcus faecium IDCC 2102 (IDCC 2102) and Bifidobacterium lactis IDCC 4301 (IDCC 4301) have the capacity to mitigate the increase in body weight and lipid accumulation in obese canines subjected to a high-fat diet and hyperlipidemic Caenorhabditis elegans (C. elegans) strain VS29. Both IDCC 2102 and IDCC 4301 demonstrated the ability to reduce systemic inflammation and hormonal disruptions induced by obesity. Notably, these probiotics induced modifications in the microbiota by promoting lactic acid bacteria, including Lactobacillaceae, Ruminococcaceae, and S24-7, with concomitant activation of pyruvate metabolism. IDCC 4301, through the generation of bacterial short-chain fatty acids and carboxylic acids, facilitated glycolysis and contributed to ATP synthesis. Meanwhile, IDCC 2102 produced bacterial metabolites such as acetic acid and butyric acid, exhibiting a particular ability to stimulate dopamine synthesis in a canine model. This stimulation led to the restoration of eating behavior and improvements in glucose and insulin tolerance. In summary, we propose novel probiotics for the treatment of obese animals based on the modifications induced by IDCC 2102 and IDCC 4301. These probiotics enhanced systemic energy utilization in response to high caloric intake, thereby preventing lipid accumulation and restoring stability to the fecal microbiota. Consequently, this intervention resulted in a reduction in systemic inflammation caused by the high-fat diet.IMPORTANCEProbiotic supplementation affected commensal bacterial proliferation, and administering probiotics increased glycolysis and activated pyruvate metabolism in the body, which is related to propanate metabolism as a result of pyruvate metabolism activation boosting bacterial fatty acid production via dopamine and carboxylic acid specialized pathways, hence contributing to increased ATP synthesis and energy metabolism activity.

Gut microbiota modulation by both Lactobacillus fermentum MSK 408 and ketogenic diet in a murine model of pentylenetetrazole-induced acute seizure.

PURPOSE: Seizures are a threat to the host brain and body and can even cause death in epileptic children. Ketogenic diet (KD) is suggested for children suffering from epileptic seizures and has been investigated for its anti-seizure effect. However, the relationships between KD and gut microbiota (GM) is not yet been deeply understood. Herein, we investigated the anti-seizure effect by administering KD and a lactic acid bacteria (LAB) in murine model of chemically induced seizures. We hypothesized that a single Lactobacillus fermentum MSK 408 (MSK 408) strain with or without KD may exert a neuroprotection by modulating host gut microbiota. METHOD: We performed animal study using pentylenetetrazole (PTZ) to induce seizure. Thirty 3-week-old male Institute of Cancer research (ICR) mice were divided in six groups, Normal diet (ND), ND + PTZ, ND + PTZ + LAB, KD, KD + PTZ, and KD + PTZ. Based on our previous study, 4:1 KD and selected MSK 408 strain was orally gavaged (4 × 109 CFU/mL) with both diets for 4 weeks. PTZ (40 mg/kg) was injected intraperitoneally 30 min before euthanization. RESULTS: Compared to ND, KD significantly reduced the seizure frequency. Administration of MSK 408 with both ND and KD for 4 weeks restored serum lipid profile and tight junction protein mRNA expression of the gut and brain. Additionally, PCoA revealed that MSK 408 independently affected fecal short chain fatty acid (SCFA) content via gut microbiota (GM) modulation. PICRUSt suggested that the modulation of microbiota by KD and MSK 408 led to increased GABA (gamma-aminobutyric acid) metabolism. SIGNIFICANCE: Our findings suggest that MSK 408 strain can be consumed with KD as supplement without interfering the anti-seizure action of KD, and may improve the serum lipid profile, and brain barrier function via gut microbiota and SCFA modulation.