ABSTRACTBackground: Diabetes mellitus (DM) is conventionally classified as a noncommunicable disorder (NCD) driven by genetic predisposition and lifestyle. However, emerging evidence regarding the gut microbiota and environmental exposure suggests a common inflammatory pathway that transcends this rigid classification. Hypothesis: This paper proposes a "Unified Framework" for all clinical phenotypes of DM, suggesting they are expressions of a single polymicrobial ecological disease. We hypothesize that DM is an acquired condition triggered by environmental interaction with "Diabetogenic Polymicrobial Signatures" (DPS). Mechanism: The framework describes how interspecies polymicrobial exposure induces intestinal barrier failure, leading to systemic chronic low-grade inflammation, insulin resistance, and β-cell dysfunction. This perspective integrates the etiology of Type 1 diabetes (T1D), Type 2 diabetes (T2D), and Gestational Diabetes (GDM) into a single pathophysiological spectrum mediated by environmental microbial shifts rather than isolated genetic failure. Conclusion: By redefining DM as an environmentally acquired polymicrobial condition, this framework bridges the gap between communicable and noncommunicable diseases. This paradigm shift suggests that future prevention and therapeutic strategies should focus on environmental control and the restoration of gut microbial ecology.

This work proposes a unified conceptual framework suggesting that all clinical types of diabetes mellitus may represent a single environmentally acquired condition associated with exposure to diabetogenic polymicrobial fecal signatures. The manuscript integrates epidemiological, microbiological and clinical evidence to support this hypothesis and discusses potential implications for prevention, diagnosis and treatment.