Abstract

Managing postprandial glycemic response, or the increase in blood sugar following a meal, is a crucial component to maintaining healthy blood sugar in patients with diabetes. To test whether oral probiotics can impact postprandial glycemic response, E. coli Nissle 1917 (EcN) was evaluated in an oral glucose tolerance test. Oral gavage of EcN concurrent with a glucose bolus reduced the post-gavage glycemic response in mice. However, there was no difference in glycemic response when comparing EcN to a mutant deficient in glucose metabolism. This suggests that while EcN can alter glycemic response to a glucose bolus, this effect is not mediated by direct uptake of glucose. Of the possible indirect effects EcN could have, gastric emptying rate was highlighted as a likely cause, but EcN had no effect on gastric emptying rate in mice. This leaves many more possible indirect explanations for the interaction between EcN and host glucose metabolism to be explored in future work.

Highlights

  • IntroductionThe increase in blood sugar following a meal, is a crucial component to maintaining healthy blood sugar in patients with diabetes

  • Managing postprandial glycemic response, or the increase in blood sugar following a meal, is a crucial component to maintaining healthy blood sugar in patients with diabetes

  • We show that concurrent administration of probiotic E. coli Nissle 1917 with a glucose bolus causes a reduction in the glycemic response

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Summary

Introduction

The increase in blood sugar following a meal, is a crucial component to maintaining healthy blood sugar in patients with diabetes. In patients with diabetes, GSIS is impaired, either by reduced function of the insulin producing pancreatic beta islets (as in type I diabetes and MODY genetic diabetes), or by reduced sensitivity of peripheral tissue to insulin signals (as in type II diabetes)[7,8] This leads to impaired postprandial glycemic response, causing long periods of elevated blood sugar after meals, and often requiring pharmaceutical intervention to m­ anage[9]. We hypothesized that by boosting the local concentration of glucose-degrading bacteria in the stomach and small intestine, the microbiome could compete with the host for glucose uptake, reducing the amount of glucose that makes it to the bloodstream To this end, we chose Escherichia coli Nissle 1917 , a probiotic strain that is used commercially as a probiotic and is closely related to model strains of E. coli that are well characterized for their fast growth rates, high affinity for glucose, and relative ease of e­ ngineering[20]. We tested whether E. coli glucose consumption is necessary to see this change in glycemic response but found that a glucose-null mutant had Scientific Reports | (2021) 11:23230

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