The human gastrointestinal tract harbors a complex ecosystem of microorganisms collectively known as the gut microbiota, playing a crucial role in maintaining host health. Perturbations in the balance of this microbial community, termed dysbiosis, have been increasingly implicated in the development of obesity and its associated comorbidities, including cardiovascular diseases (CVD) and type 2 diabetes (T2D). This abstract provides a concise overview of the interplay between stomach microbiota dysbiosis, obesity, and its implications for CVD and T2D. Recent research has elucidated a bidirectional relationship between gut microbiota and host metabolism. Dysbiosis in the stomach microbiota composition is characterized by alterations in the abundance and diversity of bacterial species, leading to an imbalance in microbial metabolites and signaling pathways. This dysregulation has been linked to increased adiposity and metabolic dysfunction, serving as a potential driver for obesity.
Obesity, a major risk factor for CVD and T2D, is now recognized as a multifactorial condition influenced not only by genetic and lifestyle factors but also by the intricate crosstalk between the gut microbiota and the host. Dysbiosis-induced inflammation, insulin resistance, and altered energy metabolism contribute to the pathogenesis of obesity-related cardiometabolic disorders. Furthermore, emerging evidence suggests that specific microbial signatures may serve as diagnostic markers for obesityrelated complications. Understanding the role of the gut microbiota in modulating host physiology provides new avenues for therapeutic interventions. Probiotics, prebiotics, and fecal microbiota transplantation are among the strategies being explored to restore a healthy gut microbiota and mitigate the risk of obesity-associated cardiovascular events and T2D.
