Intestinal bacteria translocation promotes β-cell dysfunction in DIO mice.

Area of Science:

• Microbiology
• Metabolic Diseases
• Medical Technology

Background:

• Growing evidence links gut microbiota to insulin resistance and type 2 diabetes (T2DM).
• Direct mechanical insights into the role of intestinal microflora in T2DM progression are needed.
• Intestinal bacteria translocation (IBT) is a potential mechanism connecting gut dysbiosis to pancreatic dysfunction.

Purpose of the Study:

• To precisely assess changes in intestinal bacteria translocation (IBT) from the gut to the pancreas.
• To investigate the pathological relationship between IBT and pancreatic dysfunction in type 2 diabetes.
• To evaluate the utility of deep learning-assisted methods for tracking IBT.

Main Methods:

• Utilized fluorescence in situ hybridization (FISH), 16S rRNA amplicon sequencing, and deep learning-assisted methods.
• Employed diet-induced obese (DIO) and antibiotic-induced microbiota disruption (AIMD)-DIO mouse models.
• Quantified bacterial loads in the pancreas and assessed pancreatic function and glucose homeostasis.

Main Results:

• Deep learning enhanced the accuracy and objectivity of bacterial tracking.
• DIO mice showed increased IBT, linked to intestinal lipid accumulation and barrier compromise.
• Elevated pancreatic bacterial loads correlated with worsened glucose metabolism and insulin secretion in DIO mice.
• AIMD-DIO mice exhibited reduced IBT, preserved islet structure, and improved glucose homeostasis.
• A strong correlation was found between the number of translocated bacteria and T2DM severity.

Conclusions:

• Provided objective evidence for bacterial migration from the intestine to the pancreas.
• Established a pathological relationship between IBT, pancreatic impairment, and T2DM.
• Demonstrated the potential of AI techniques for evaluating IBT and its role in metabolic disease.