In the present study, we demonstrated that PLD1 phosphorylation is responsible for acute signaling mechanisms in muscle cells and that AMPK is a novel regulator of PLD1 that functions in a glucose dependent manner.
In addition, we can demonstrate a glucose dependent induction of PKCα mRNA and protein in murine and human podocytes.
Activation of the pancreatic GLP-1 receptor on β-cells leads to a glucose-dependent stimulation of insulin secretion and, via indirect pathways, to an also glucose-dependent inhibition of glucagon secretion.
Comparative genomic work [ 30] provided some explanations for a glucose-dependent life style of fission yeasts.
The introduction of a glucose-dependent n would lead to a fully coupled dynamic system for all state variables.
As might be expected of a glucose-dependent therapy, low incidences of hypoglycaemia were observed in clinical trials of exenatide QW, despite continuous exposure to the GLP-1R agonist due to extended release [ 16, 36].
The endogenous ligand of the GLP-1r (i.e. GLP-1), induces the release of insulin in a glucose-dependent manner and promotes beta cell proliferation in adult rodents [ 6].
GLP-1 and GIP are secreted from cells in the intestine in response to food ingestion and act on pancreatic β-cells via distinct receptors to stimulate the release of insulin in a glucose-dependent manner.
The incretin hormone GLP-1, which promotes assimilation of ingested nutrients via a glucose-dependent stimulation of insulin release, apparently improves α-cell glucose sensing.
24 DPP-4 inhibitors enhance the actions ascribed to GLP-1 receptor agonists, including the stimulation of insulin and inhibition of glucagon secretion in a glucose-dependent manner, but are generally not associated with a deceleration of gastric emptying, satiety, or weight loss.
