AI Article Synopsis
- Gastric emptying plays a crucial role in managing post-meal blood sugar levels, and the delay in gastric emptying is linked to improved glucose control with GLP-1 analogs.
- Researchers found that increased levels of interleukin (IL)-6 slow down gastric emptying, leading to lower blood sugar levels after meals.
- IL-6 also decreases insulin secretion in a way that depends on GLP-1, and these effects were confirmed after exercise; this finding could lead to new treatments for managing gastric emptying and insulin secretion in individuals with type 2 diabetes.
Article Abstract
Gastric emptying is a critical regulator of postprandial glucose and delayed gastric emptying is an important mechanism of improved glycemic control achieved by short-acting glucagon-like peptide-1 (GLP-1) analogs in clinical practice. Here we report on a novel regulatory mechanism of gastric emptying in humans. We show that increasing interleukin (IL)-6 concentrations delays gastric emptying leading to reduced postprandial glycemia. IL-6 furthermore reduces insulin secretion in a GLP-1-dependent manner while effects on gastric emptying are GLP-1 independent. Inhibitory effects of IL-6 on gastric emptying were confirmed following exercise-induced increases in IL-6. Importantly, gastric- and insulin-reducing effects were maintained in individuals with type 2 diabetes. These data have clinical implications with respect to the use of IL-6 inhibition in autoimmune/inflammatory disease, and identify a novel target that could be exploited pharmacologically to delay gastric emptying and spare insulin, which may be beneficial for the beta cell in type 2 diabetes.
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| http://dx.doi.org/10.1016/j.cmet.2018.04.008 | DOI Listing |
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