What is it about?
The maintenance of plasma glucose homeostasis is dependent on central and peripheral glucose-sensing mechanisms. Deregulation of the peripheral portal glucose sensors is pivotal for the understanding of the pathophysiology of obesity and type 2 diabetes, but data on the portal sensor resulted from indirect experimental evidence only. We supply a direct proof for a defective portal glucose sensing in the insulin resistant obese, characterized by a marked suppression of vagal sensitivity to portal glucose. The dysfunction of the portal sensor is the consequence of a reduction in the density of portal GLP-1r especially intense close to the entrance of the portal vein in the liver. Recovering a correct density of GLP1r might represent a new potential molecular target for the prevention of the early events associated with obesity and type 2 diabetes since the underlying vagal portal afferents were still functional.
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Why is it important?
Recovering a correct density of GLP1r might represent a new potential molecular target for the prevention of the early events associated with obesity and type 2 diabetes since the underlying vagal portal afferents were still functional.
Perspectives
We believe that the suppression of GLP-1r based sensing is critical and open new perspectives for the treatment of insulin resistance in obese. This is also a perfect example of what could be a personalized medicine approach.
Charles Malbert
Read the Original
This page is a summary of: Glucose Sensing Mediated by Portal Glucagon-Like Peptide 1 Receptor Is Markedly Impaired in Insulin-Resistant Obese Animals, Diabetes, October 2020, American Diabetes Association,
DOI: 10.2337/db20-0361.
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