The role of metformin and thiazolidinediones in the regulation of hepatic glucose metabolism and its clinical impact

2011 ◽  
Vol 32 (10) ◽  
pp. 607-616 ◽  
Author(s):  
Esther Phielix ◽  
Julia Szendroedi ◽  
Michael Roden
Keyword(s):  
Glucose Metabolism ◽  
Clinical Impact ◽  
Hepatic Glucose Metabolism ◽  
Hepatic Glucose

The role of glucose 6-phosphate in mediating the effects of glucokinase overexpression on hepatic glucose metabolism

FEBS Journal ◽  
2006 ◽  
Vol 273 (2) ◽  
pp. 336-346 ◽  
Author(s):  
Linda Harndahl ◽  
Dieter Schmoll ◽  
Andreas W. Herling ◽  
Loranne Agius
Keyword(s):  
Glucose Metabolism ◽  
Hepatic Glucose Metabolism ◽  
Hepatic Glucose

scholarly journals Exploring the Physiological Role of Transthyretin in Glucose Metabolism in the Liver

2021 ◽  
Vol 22 (11) ◽  
pp. 6073
Author(s):  
Mobina Alemi ◽  
Ângela Oliveira ◽  
Sofia C. Tavares ◽  
José Ricardo Vieira ◽  
Marco G. Alves ◽  
...  
Keyword(s):  
Glucose Metabolism ◽  
Culture Media ◽  
Physiological Role ◽  
Glucose Transporters ◽  
Mitochondrial Oxidative Stress ◽  
Mitochondrial Density ◽  
Hepatic Glucose Metabolism ◽  
Hepatic Glucose ◽  
Evolutionarily Conserved

Transthyretin (TTR), a 55 kDa evolutionarily conserved protein, presents altered levels in several conditions, including malnutrition, inflammation, diabetes, and Alzheimer’s Disease. It has been shown that TTR is involved in several functions, such as insulin release from pancreatic β-cells, recovery of blood glucose and glucagon levels of the islets of Langerhans, food intake, and body weight. Here, the role of TTR in hepatic glucose metabolism was explored by studying the levels of glucose in mice with different TTR genetic backgrounds, namely with two copies of the TTR gene, TTR+/+; with only one copy, TTR+/-; and without TTR, TTR-/-. Results showed that TTR haploinsufficiency (TTR+/-) leads to higher glucose in both plasma and in primary hepatocyte culture media and lower expression of the influx glucose transporters, GLUT1, GLUT3, and GLUT4. Further, we showed that TTR haploinsufficiency decreases pyruvate kinase M type (PKM) levels in mice livers, by qRT-PCR, but it does not affect the hepatic production of the studied metabolites, as determined by 1H NMR. Finally, we demonstrated that TTR increases mitochondrial density in HepG2 cells and that TTR insufficiency triggers a higher degree of oxidative phosphorylation in the liver. Altogether, these results indicate that TTR contributes to the homeostasis of glucose by regulating the levels of glucose transporters and PKM enzyme and by protecting against mitochondrial oxidative stress.

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