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Glucokinase and molecular aspects of liver glycogen metabolism.
  • L. Agius
  • Biology, Chemistry
    The Biochemical journal
  • 15 August 2008
Defects in both the activation of glucokinase and in the dephosphorylation of glycogen phosphorylase are potential contributing factors to the dysregulation of hepatic glucose metabolism in Type 2 diabetes.
New hepatic targets for glycaemic control in diabetes.
  • L. Agius
  • Biology, Medicine
    Best practice & research. Clinical endocrinology…
  • 1 December 2007
The regulatory protein of glucokinase binds to the hepatocyte matrix, but, unlike glucokinase, does not translocate during substrate stimulation.
This study shows that, in hepatocytes incubated with 5 mM glucose as sole carbohydrate substrate, both glucokinase and its regulatory protein bind to the cell matrix by a Mg(2+)-dependent mechanism.
Fructose 2,6-bisphosphate is essential for glucose-regulated gene transcription of glucose-6-phosphatase and other ChREBP target genes in hepatocytes.
An essential role is demonstrated for the bifunctional enzyme PFK2/FBP2 as the phosphometabolite sensor and for its product, fructose 2,6-bisphosphate, as the metabolic signal for substrate-regulated ChREBP-mediated expression of G6pc and other ChRE BP target genes.
Intracellular binding of glucokinase in hepatocytes and translocation by glucose, fructose and insulin.
  • L. Agius, M. Peak
  • Biology, Computer Science
    The Biochemical journal
  • 15 December 1993
The release of glucokinase from digitonin-permeabilized hepatocytes shows different characteristics with respect to ionic strength and [MgCl2] from the release of other cytoplasmic enzymes, suggesting that, in cells maintained in 5 mM glucose, glucokin enzyme is present predominantly in a bound state and this binding is dependent on the presence of Mg2+.
Glucose 6-phosphate regulates hepatic glycogenolysis through inactivation of phosphorylase.
High glucose concentration suppresses hepatic glycogenolysis by allosteric inhibition and dephosphorylation (inactivation) of phosphorylase-a. The latter effect is attributed to a direct effect of
Lipogenesis in interscapular brown adipose tissue of virgin, pregnant and lactating rats. The effects of intragastric feeding.
Brown adipose tissue increased in weight during pregnancy, regressed during lactation and hypertrophied again on weaning; the rate of lipogenesis paralleled these changes, and glucose did not increase brown-adipose-tissue lipogenesis at mid-lactation.
Signalling pathways involved in the stimulation of glycogen synthesis by insulin in rat hepatocytes
It is concluded that PKB, which is activated to a greater extent by insulin than EGF, and peak 2,Which is activated by insulin and counteracted by EGF are possible candidates in mediating the stimulation of glycogen synthesis by insulin.
Stimulation of hepatocyte glucose metabolism by novel small molecule glucokinase activators.
GK activators are potential antihyperglycemic agents for the treatment of type 2 diabetes through the stimulation of hepatic glucose metabolism by a mechanism independent of GKRP.
The rate of production of uric acid by hepatocytes is a sensitive index of compromised cell ATP homeostasis.
Uric acid production by hepatocytes is a very sensitive index of ATP depletion irrespective of whether cell Pi is lowered or raised, which suggests that raised plasma uric acid may be a marker of compromised hepatic ATP homeostasis.