The feedback cycles between glucose, amino acids and lipids and alpha cell secretion and their role in metabolic fatty liver disease

Marie Winther-Sørensen, Jens J Holst, Nicolai J Wewer Albrechtsen

4 Citations (Scopus)

Abstract

PURPOSE OF REVIEW: Glucagon increases hepatic glucose production and in patients with metabolic diseases, glucagon secretion is increased contributing to diabetic hyperglycemia. This review explores the role of amino acids and lipids in the regulation of glucagon secretion and how it may be disturbed in metabolic diseases such as obesity and metabolic associated fatty liver disease (MAFLD).

RECENT FINDINGS: Human and animal studies have shown that MAFLD is associated with glucagon resistance towards amino acid catabolism, resulting in elevated plasma levels of amino acids. A recent clinical study showed that MAFLD is also associated with glucagon resistance towards lipid metabolism. In contrast, MAFLD may not decrease hepatic sensitivity to the stimulatory effects of glucagon on glucose production.

SUMMARY: Elevated plasma levels of amino acids and lipids associated with MAFLD may cause diabetogenic hyperglucagonemia. MAFLD and glucagon resistance may therefore be causally linked to hyperglycemia and the development of type 2 diabetes.

Original languageEnglish
JournalCurrent Opinion in Lipidology
Volume34
Issue number1
Pages (from-to)27-31
Number of pages5
ISSN0957-9672
DOIs
Publication statusPublished - 1 Feb 2023

Keywords

  • Amino Acids/metabolism
  • Animals
  • Diabetes Mellitus, Type 2/metabolism
  • Feedback
  • Glucagon/metabolism
  • Glucose/metabolism
  • Humans
  • Hyperglycemia
  • Lipids
  • Non-alcoholic Fatty Liver Disease
  • metabolic associated fatty liver disease
  • liver-alpha cell axis
  • type 2 diabetes
  • glucagon
  • obesity

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