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The Liver-α-Cell Axis and Type 2 Diabetes
Nicolai J Wewer Albrechtsen1,2,3,4, Jens Pedersen2,5, Katrine D Galsgaard2,4
1Department of Clinical Biochemistry, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark.
Endocrine Reviews
|March 29, 2019
Summary
Nonalcoholic fatty liver disease (NAFLD) may drive type 2 diabetes (T2D) development. Impaired glucagon action in NAFLD contributes to hyperglycemia and hyperinsulinemia, hallmarks of T2D.
Area of Science:
- Metabolic diseases
- Endocrinology
- Hepatology
Background:
- Type 2 diabetes (T2D) and nonalcoholic fatty liver disease (NAFLD) are prevalent metabolic diseases linked to obesity.
- Hyperglucagonemia contributes to hyperglycemia in T2D.
- Emerging evidence suggests glucagon's role in NAFLD, independent of T2D status.
Purpose of the Study:
- To explore the link between NAFLD, glucagon secretion, and T2D development.
- To investigate how hepatic steatosis affects glucagon and insulin sensitivity.
Main Methods:
- Review of emerging data and experimental findings.
- Analysis of the interplay between amino acid turnover, glucagon, and hepatic function.
Main Results:
- NAFLD may impair amino acid turnover, increasing glucagonotropic amino acids and glucagon secretion.
- Hepatic steatosis can impair glucagon's action on amino acid turnover and ureagenesis.
- Impaired hepatic sensitivity to insulin and glucagon in NAFLD contributes to hyperglycemia, hyperinsulinemia, and hyperglucagonemia.
Conclusions:
- NAFLD-induced hepatic steatosis may contribute to T2D development by disrupting amino acid metabolism and impairing hormonal regulation.
- Understanding this link is crucial for managing both metabolic conditions.
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