Nutrients, Vol. 18, Pages 578: The Diet–Microbiota–Polyamine Axis in Intestinal Aging: Microbial Pathways, Functional Foods, and Physiological Implications
Nutrients doi: 10.3390/nu18040578
Authors:
Alice N. Mafe
Dietrich Büsselberg
Intestinal aging is characterized by a gradual decline in epithelial renewal capacity, barrier function, immune balance, and metabolic regulation, often accompanied by shifts in gut microbial composition. Polyamines, including putrescine, spermidine, and spermine, are vital microbial–host metabolites that support intestinal cell growth, autophagy, immune modulation, and mucosal repair. With advancing age, both host-derived and microbiota-mediated polyamine production declines, contributing to intestinal dysfunction and heightened vulnerability to inflammation and age-related disorders. This review explores the diet–microbiota–polyamine axis as a key biological framework influencing intestinal aging. It aims to integrate evidence on how dietary components and functional foods shape gut microbial ecology and, in turn, regulate microbial polyamine biosynthetic pathways that impact intestinal health. The review highlights major microbial contributors to polyamine metabolism, particularly lactic acid bacteria, and outlines mechanistic pathways linking polyamines to epithelial regeneration, inflammatory control, and gut barrier maintenance. It further discusses how age-associated dysbiosis disrupts these interactions and evaluates nutritional and microbial-based strategies such as fermented foods, prebiotics, and probiotics that may enhance polyamine availability and restore gut homeostasis. From the standpoint of food microbiology and human physiology, this synthesis underscores the translational potential of targeting microbial polyamine production through diet-based interventions. This article presents a narrative review synthesizing experimental, animal, and emerging human evidence on microbial and dietary polyamines in intestinal aging. In conclusion, modulating the diet–microbiota–polyamine axis represents a promising strategy to promote healthy intestinal aging, meriting deeper mechanistic exploration and validation through clinical studies.
Intestinal aging is characterized by a gradual decline in epithelial renewal capacity, barrier function, immune balance, and metabolic regulation, often accompanied by shifts in gut microbial composition. Polyamines, including putrescine, spermidine, and spermine, are vital microbial–host metabolites that support intestinal cell growth, autophagy, immune modulation, and mucosal repair. With advancing age, both host-derived and microbiota-mediated polyamine production declines, contributing to intestinal dysfunction and heightened vulnerability to inflammation and age-related disorders. This review explores the diet–microbiota–polyamine axis as a key biological framework influencing intestinal aging. It aims to integrate evidence on how dietary components and functional foods shape gut microbial ecology and, in turn, regulate microbial polyamine biosynthetic pathways that impact intestinal health. The review highlights major microbial contributors to polyamine metabolism, particularly lactic acid bacteria, and outlines mechanistic pathways linking polyamines to epithelial regeneration, inflammatory control, and gut barrier maintenance. It further discusses how age-associated dysbiosis disrupts these interactions and evaluates nutritional and microbial-based strategies such as fermented foods, prebiotics, and probiotics that may enhance polyamine availability and restore gut homeostasis. From the standpoint of food microbiology and human physiology, this synthesis underscores the translational potential of targeting microbial polyamine production through diet-based interventions. This article presents a narrative review synthesizing experimental, animal, and emerging human evidence on microbial and dietary polyamines in intestinal aging. In conclusion, modulating the diet–microbiota–polyamine axis represents a promising strategy to promote healthy intestinal aging, meriting deeper mechanistic exploration and validation through clinical studies. Read More