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BMOL Seminar Series: Dr. Onesmo Balemba

Wednesday, September 25 @ 3:00 pm - 4:15 pm MDT

Onesmo Balemba Headshot

Seminar Details

Speaker: Dr. Onesmo Balemba, Professor of Biological Sciences at University of Idaho

Host: Dr. Javier Ochoa-Repáraz, Biological Sciences

Title: Instigators of Gastrointestinal Neuropathy and Dysmotility in Type 2 Diabetes

Abstract: It is believed that enteric nervous system (ENS) nerve cell damage or ENS neuropathy underlies gastrointestinal (GI) movement abnormalities (dysmotility) in patients with type 2 diabetes (T2D), causing motility-related disorders such as dysphagia, nausea, stomach bloating, constipation, diarrhea, and pain. GI neuropathy and dysmotility are commonly viewed as complications of T2D. However, emerging studies suggest that ENS neuropathy and GI dysmotility precede T2D and are associated with altered gut microbiota (dysbiosis). Unfortunately, we lack a complete understanding of molecules that trigger ENS neuropathy and GI dysmotility, particularly molecules associated with gut microbiota dysbiosis and how and when they trigger the disease process. We do not fully know the changes in ENS neuroactivities that cause GI dysmotility in T2D patients. Research goal. The overarching goal of my research is to improve knowledge about molecular instigators of ENS neuropathy and GI dysmotility in T2D patients. The research presentation will have three parts: 1) The first will focus on characterizing ENS neuropathy using mice fed a high-fat diet and the similarities between high-fat diet mice and T2D patients. The second part will focus on studies of postbiotic fluids extracted from the stools of humans diagnosed with prediabetes and T2D as well as high-fat diet mice to link toxic/antimotility molecules in postbiotic fluids with instigation of ENS neuropathy and GI dysmotility. I will discuss how transplanting postbiotic stools stool filtrates of humans diagnosed with T2D into mice expressing fluorescent Ca2+ indicator GCaMP6 in the ENS affects the activities of cholinergic and nitrergic neurons in the stomach and colon. In the third part, I will highlight our most recent data obtained by testing bacteria culture supernatants of strains isolated from the human gut, suggesting that molecules produced by specific strains of gut bacteria—particularly Phoecoicola vulgatus trigger ENS neuropathy and GI dysmotility.

Publication Related to Talk: Supernatants of intestinal luminal contents from mice fed highfat diet impair intestinal motility by injuring enteric neurons and smooth muscle cells