The Vicious Circle of Hepatic Glucagon Resistance in Non-Alcoholic Fatty Liver Disease
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The Vicious Circle of Hepatic Glucagon Resistance in Non-Alcoholic Fatty Liver Disease. / Galsgaard, Katrine D.
In: Journal of Clinical Medicine, Vol. 9, No. 12, 4049, 2020.Research output: Contribution to journal › Review › Research › peer-review
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TY - JOUR
T1 - The Vicious Circle of Hepatic Glucagon Resistance in Non-Alcoholic Fatty Liver Disease
AU - Galsgaard, Katrine D.
PY - 2020
Y1 - 2020
N2 - A key criterion for the most common chronic liver disease-non-alcoholic fatty liver disease (NAFLD)-is an intrahepatic fat content above 5% in individuals who are not using steatogenic agents or having significant alcohol intake. Subjects with NAFLD have increased plasma concentrations of glucagon, and emerging evidence indicates that subjects with NAFLD may show hepatic glucagon resistance. For many years, glucagon has been thought of as the counterregulatory hormone to insulin with a primary function of increasing blood glucose concentrations and protecting against hypoglycemia. However, in recent years, glucagon has re-emerged as an important regulator of other metabolic processes including lipid and amino acid/protein metabolism. This review discusses the evidence that in NAFLD, hepatic glucagon resistance may result in a dysregulated lipid and amino acid/protein metabolism, leading to excess accumulation of fat, hyperglucagonemia, and increased oxidative stress contributing to the worsening/progression of NAFLD.
AB - A key criterion for the most common chronic liver disease-non-alcoholic fatty liver disease (NAFLD)-is an intrahepatic fat content above 5% in individuals who are not using steatogenic agents or having significant alcohol intake. Subjects with NAFLD have increased plasma concentrations of glucagon, and emerging evidence indicates that subjects with NAFLD may show hepatic glucagon resistance. For many years, glucagon has been thought of as the counterregulatory hormone to insulin with a primary function of increasing blood glucose concentrations and protecting against hypoglycemia. However, in recent years, glucagon has re-emerged as an important regulator of other metabolic processes including lipid and amino acid/protein metabolism. This review discusses the evidence that in NAFLD, hepatic glucagon resistance may result in a dysregulated lipid and amino acid/protein metabolism, leading to excess accumulation of fat, hyperglucagonemia, and increased oxidative stress contributing to the worsening/progression of NAFLD.
KW - autophagy
KW - amino acids
KW - glucagon
KW - NAFLD
KW - the liver–
KW - alpha cell axis
KW - CARNITINE PALMITOYLTRANSFERASE-I
KW - PANCREATIC ALPHA-CELLS
KW - AMINO-ACID-METABOLISM
KW - RECEPTOR ANTAGONIST
KW - BLOOD-GLUCOSE
KW - POSTPRANDIAL HYPERGLYCEMIA
KW - MALONYL-COA
KW - RAT-LIVER
KW - AUTOPHAGY
KW - GLP-1
U2 - 10.3390/jcm9124049
DO - 10.3390/jcm9124049
M3 - Review
C2 - 33333850
VL - 9
JO - Journal of Clinical Medicine
JF - Journal of Clinical Medicine
SN - 2077-0383
IS - 12
M1 - 4049
ER -
ID: 255113006