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EJE PRIZE 2018: A gut feeling about glucagon.
Filip K Knop1,2,3
1Clinical Metabolic PhysiologySteno Diabetes Center Copenhagen, Gentofte Hospital, University of Copenhagen, Hellerup, Denmark filip.knop@regionh.dk.
European Journal of Endocrinology
|April 22, 2018
Summary
High glucagon levels (hyperglucagonaemia) are key in diabetes. New research suggests the liver and gut, not just the pancreas, significantly regulate glucagon, challenging current understanding.
Area of Science:
- Endocrinology
- Metabolic Diseases
- Gastroenterology
Background:
- Hyperglucagonaemia is a central factor in diabetes, contributing to hyperglycemia.
- It's traditionally attributed to pancreatic alpha-cell dysfunction.
- This study investigates alternative roles of the gut and liver in glucagon regulation.
Purpose of the Study:
- To explore the role of gut-derived factors in diabetic hyperglucagonaemia.
- To investigate the hypothesis of a liver-alpha cell axis in glucagon regulation.
- To re-evaluate the understanding of glucagon secretion beyond pancreatic and glucose control.
Main Methods:
- Clinical experiments involving oral and intravenous glucose administration.
- Analysis of plasma glucagon levels in patients with type 2 diabetes.
- Correlation analysis of fasting hyperglucagonaemia with obesity, liver fat, and amino acids.
Main Results:
- Gut-derived factors, like glucose-dependent insulinotropic polypeptide, promote hyperglucagonaemia.
- Glucagon secretion may originate from extrapancreatic tissues, including enteroendocrine cells.
- Fasting hyperglucagonaemia correlates with obesity and liver fat, independent of diabetes status.
Conclusions:
- The liver and gut play critical roles in regulating fasting and postabsorptive glucagon levels.
- A novel hypothesis suggests a 'liver-alpha cell axis' involving hepatic glucagon resistance and amino acid-mediated compensation.
- This challenges the traditional pancreacentric view of hyperglucagonaemia in diabetes.
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