Obesity can lead to insulin resistance, which precedes and predicts high blood glucose and type 2 diabetes. Obesity increases chronic inflammation leading to insulin resistance in tissues such as fat and liver that help control blood glucose. We need to understand how to balance immune responses that help defend against bacteria without causing chronic inflammation and insulin resistance. Protective immune responses in the gut can be very different from chronic inflammation in obese fat or liver tissue, but microbial factors represent a key link. The Schertzer lab is interested in how gut microbiota, nutrition and certain therapeutic drugs conspire to disrupt the balance between immunity and metabolism. We aim to determine the role of host bacterial sensing as a trigger for different immune responses that contribute to insulin resistance. We test how different microbial factors can engage compartmentalized immune responses that promote or defend against insulin resistance. The goal is to restore the ability of insulin to lower blood glucose without necessarily reducing obesity. The relationship between glucose and bacteria works in both directions. We also want to understand how obesity and diabetes impair how the immune system works during functional gastrointestinal disorders, including enteric infection.

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