作者
Zuzanna Szkamruk,Joanna Cielecka,Maciej Walędziak,Anna Różańska-Walędziak
摘要
Growing evidence highlights the gut microbiota as a critical regulator of host metabolism. In type 2 diabetes (T2D), disturbances in microbial composition are increasingly recognized as contributors to insulin resistance, chronic inflammation, and metabolic dysregulation. This review aims to summarize the current understanding of gut microbiota alterations in T2D, their underlying mechanisms, clinical relevance, and potential therapeutic strategies. A literature review was conducted using MEDLINE and SCOPUS databases, with the focus on keywords including “type 2 diabetes,” “gut microbiota,” “dysbiosis,” “short-chain fatty acids,” “intestinal permeability,” “inflammation,” “metabolic endotoxemia,” “probiotics,” “prebiotics,” “synbiotics,” “postbiotics,” and “fecal microbiota transplantation.” Articles published between 2015 and 2025 were considered, with preference given to peer-reviewed original research and systematic reviews. To ensure completeness, additional studies were identified through manual screening of reference lists in key publications, allowing the inclusion of both mechanistic and clinical perspectives relevant to type 2 diabetes and gut microbiota. Type 2 diabetes is linked to reduced gut microbiota diversity, with lower levels of short-chain fatty acid (SCFA) producers such as Faecalibacterium prausnitzii and Roseburia, and higher abundance of pro-inflammatory species including Ruminococcus gnavus and Bacteroides. These alterations are associated with impaired glucose control, elevated glycated hemoglobin (HbA1c), unfavorable lipid profiles, and increased inflammatory markers like C-reactive protein (CRP) and interleukin-6 (IL-6). Diet, lifestyle, medications, and microbiota-targeted interventions can modulate these microbial changes. While probiotics, prebiotics, synbiotics, postbiotics, and fecal microbiota transplantation hold therapeutic potential, further standardized and large-scale studies are required to establish clinical effectiveness and support personalized treatment strategies.