Collagen peptides (CP) have been reported to stimulate dermal collagen synthesis through modulation of the gut microbiota in animal studies, but human evidence remains limited. This study aimed to comprehensively evaluate the clinical efficacy and multi-omics effects of oral CP in humans, integrating skin, gut, and metabolomic analyses. In this 8-week randomized, double-blind, placebo-controlled trial, 70 healthy women (39.2 ± 8.8 years) received CP, a collagen–elastin peptide mixture (MP), or placebo. Significant improvements from baseline were observed in facial wrinkle, texture, hydration, and elasticity in the CP and MP groups (wrinkle: 12.00% and 14.83%; texture: 15.21% and 16.87%; hydration: 4.36 and 4.48 units; elasticity: both 0.10 units), whereas no significant improvements were detected in the PL group (P < 0.05). No significant differences were observed between the CP and MP groups, while more pronounced improvements were detected in women older than 40 years. CP supplementation increased the abundance of Cutibacterium and Lactobacillus in the skin microbiota, and altered skin metabolite profiles, characterized by elevated N-undecanoylglycine and Pro-Pro. CP also increased the abundance of gut Roseburia and Faecalibacterium, enhanced the Gut Microbiome Wellness Index, and enriched amino acid metabolism. Skin improvements correlated with the abundance of Roseburia intestinalis, indicating a gut–skin link. These findings indicate that oral collagen peptides represent a promising strategy for improving skin aging by modulating gut–skin microbiota and metabolomic profiles.

This study aims to investigate whether Bacillus coagulans BC2000 can improve the ameliorative effect of ellagic acid (EA) on insulin resistance caused by a high-fat diet in mice and the relationship between BC2000 and gut microbiota remodeling. Fifty C57BL/6J mice were randomly divided into five groups: a low-fat diet group (LFD), a high-fat diet group (HFD), a high-fat diet with EA group (HFD + EA), a high-fat diet with EA and Bacillus coagulans BC30 group (HFD + EA + BC30), and a high-fat diet with EA and Bacillus coagulans BC2000 group (HFD + EA + BC2000). After intervention for 10 weeks, physiological and biochemical indexes and inflammatory cytokine levels were measured. In addition, histological examination of the liver and epididymal adipose tissues was performed, and the microbial community structure in cecal contents was analyzed. The results showed that the combination of BC2000 and EA improved obesity and reduced fat cell hypertrophy and liver steatosis in high-fat diet-fed mice, and significantly reduced the plasma levels of insulin, total cholesterol and low-density lipoprotein cholesterol (LDL-C) and insulin resistance index as well as the plasma levels of lipopolysaccharide (LPS), Zonulin, tumor necrosis factor (TNF)α, hypersensitive C-reactive protein (CRP) and interleukin 6 (IL-6) (P < 0.05). Moreover, the combination of BC2000 and EA improved the gut microbiota by increasing the relative abundance of Actinobacteria and Lactobacillus and decreasing the relative abundance of Desulfovibrio. Taken together, Bacillus coagulans BC2000 enhances the role of EA in regulating glucolipid metabolism and insulin resistance by modulating the gut microbiota. This study provides a theoretical basis for the application of Bacillus coagulans BC2000 as a probiotic in foods.

Limosilactobacillus reuteri QS01 is potential probiotic isolated from the intestinal microbiota of healthy women in early pregnancy. In the current study, we examined whether QS01 can prevent gestational diabetes mellitus (GDM) in an enhanced mouse model of the condition. Female C57BL/6J mouse offspring (F1 generation) born to dams fed a control (CON) or low-protein diet (GDM group) during gestation and lactation were used. Pregnant F1 mice fed a standard diet were randomly assigned to 5 groups: CON, GDM, and GDM mice treated with metformin, QS01 or Lacticaseibacillus rhamnosus HN001. An oral glucose tolerance test was performed before sacrifice at gestational day 17. Glucose tolerance was significantly ameliorated by all 3 treatments. QS01 supplementation fortified the intestinal mucosal barrier and inhibited the escalation of plasma inflammatory cytokines. QS01 treatment altered the cecal microbiota composition and function. Plasma and cecal metabolite profiles were modulated by QS01, prominently demonstrating significant upregulation of indole lactate and L-tryptophan in plasma and 5-hydroxy-tryptophan in the cecum, positively correlated with gut Lactobacillus abundance. In summary, QS01 plays a role in preventing GDM by remodeling the intestinal microbiota, reinforcing the intestinal mucosal barrier and alleviating chronic inflammation.