Bifidobacterium(Nitto Pharmaceutical Industries Ltd.)

The disorder of the “gut-kidney axis” exacerbates renal function decline in chronic kidney disease (CKD), and current CKD therapy is insufficient to address this issue. Hirudin has a palliative effect on the decline of renal function. However, whether hirudin can delay CKD by regulating the “intestinal renal axis” disorder remains unclear. Unilateral ureteral ligation (UUO) induced CKD rat model, and the rats were treated with bifidobacterium and hirudin for 36 days. After 14 and 36 days of modeling, kidney and colon tissues were collected for pathology, western blot (WB) assay, and quantitative real-time PCR (qPCR) detection. Serum samples were collected for renal function testing. Fecal samples were used for 16S rRNA sequencing and research on fecal bacterial transplantation. Lipopolysaccharide combine with adenosine 5’-triphosphate (LPS + ATP)-induced intestinal epithelial cell injury was treated with a nod-like receptor pyrin domain-associated protein 3 (NLRP3) inhibitor and hirudin. Protein expression was detected using WB and qPCR. The kidneys and colons of the CKD rats exhibited varying degrees of lesions. Creatinine (CRE), blood urea nitrogen (BUN), N-acetyl-β-D-glucosidase (NAG) enzyme, and serum uremic toxins were elevated. The expression of claudin-1 and occludin was decreased, NLRP3 inflammatory-related proteins were increased, and the gut microbiota was disrupted. These pathological changes were more pronounced after 36 days of modeling. Meanwhile, high-dose hirudin treatment significantly improved these lesions and restored the intestinal flora to homeostasis in CKD rats. In vitro, hirudin demonstrated comparable effects to NLRP3 inhibitors by upregulating claudin-1 and occludin expression, and downregulating NLRP3 inflammatory-related proteins expression. The dysbiosis of the gut microbiota and impaired intestinal epithelial barrier function in CKD are associated with renal dysfunction in CKD. Hirudin delays the progression of CKD by regulating the disorder of the “gut-kidney axis” and inhibiting the activation of the NLRP3-ASC-caspase-1 pathway.

This systematic review aimed to assess the impact of Bifidobacterium genus probiotics on body weight and body composition parameters in overweight and obese individuals.A systematic search for randomized controlled trials was conducted in MEDLINE, EMBASE, LILACS, and Google Scholar databases until April 17, 2023. The inclusion criteria required the trials to involve Bifidobacterium genus probiotics interventions and the evaluation of obesity-related anthropometric and body composition outcomes in overweight or obese subjects. Studies were excluded when involving obese individuals with genetic syndromes or pregnant women, as well as probiotic mixture interventions. The revised Cochrane risk-of-bias tool for randomized trials was utilized to assess the quality of the included studies. A random-effects meta-analysis was performed using the mean difference between endpoint measurements and change from baseline for body mass index, body weight, body fat mass, body fat percentage, waist circumference, waist-to-hip ratio, and visceral fat area.From 1,527 retrieved reports, 11 studies (911 subjects) were included in this review. Bifidobacterium probiotics administration resulted in significant reductions in body fat mass (MD = -0.64 kg, 95% CI: -1.09, -0.18, p = 0.006), body fat percentage (MD = -0.64%, 95% CI: -1.18, -0.11, p = 0.02), waist circumference (MD = -1.39 cm, 95% CI: -1.99, -0.79, p < 0.00001), and visceral fat area (MD = -4.38 cm², 95% CI: -7.24, -1.52, p = 0.003). No significant differences were observed for body mass index, body weight, or waist-to-hip ratio.This systematic review suggests that Bifidobacterium genus probiotics may contribute to managing overweight and obesity by reducing body fat mass, body fat percentage, waist circumference, and visceral fat area. Further research is required to understand strain and species interactions, optimal dosages, and effective delivery methods for probiotics in obesity management. This review was pre-registered under the PROSPERO record CRD42022370057.