Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.3.16 (calcineurin)
 17,112 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Stimulation of glycogen synthesis is one of the major physiological responses modulated by insulin. Although, details of the precise mechanism by which insulin action on glycogen synthesis is mediated remains uncertain, significant advances have been made to understand several steps in this process. Most importantly, recent studies have focussed on the possible role of glycogen synthase kinase-3 (GSK-3) and glycogen bound protein phosphatase-1 (PP-1G) in the activation of glycogen synthase (GS) - a key enzyme of glycogen metabolism. Evidence is also accumulating to establish a link between insulin receptor induced signaling pathway(s) and glycogen synthesis. This article summarizes the potential contribution of various elements of insulin signaling pathway such as mitogen activated protein kinase (MAPK), protein kinase B (PKB), and phosphatidyl inositol 3-kinase (PI3-K) in the activation of GS and glycogen synthesis.
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PMID:Potential mechanism(s) involved in the regulation of glycogen synthesis by insulin. 960 22

Insulin rapidly and completely inhibits expression of the hepatic insulin-like growth factor binding protein-1 (IGFBP-1), phosphoenolpyruvate carboxykinase (PEPCK) and glucose-6-phosphatase (G6Pase) genes. This inhibition is mediated through a phosphatidyl inositol 3-kinase-dependent regulation of a DNA element, termed the thymine-rich insulin response element, found within the promoters of each of these genes. This has led to the conclusion that these three promoters are regulated by insulin using the same molecular mechanism. However, we recently found that the regulation of the IGFBP1 but not the PEPCK or G6Pase genes by insulin was sensitive to rapamycin, an inhibitor of mTOR. Here, we present further evidence that different regulatory pathways mediate the insulin regulation of these promoters. Importantly, we identify a protein phosphatase activity in the pathway connecting mTOR to the IGFBP-1 promoter. These data have major implications for the development of molecular therapeutics for the treatment of insulin-resistant states such as diabetes and hypertension.
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PMID:Different mechanisms are used by insulin to repress three genes that contain a homologous thymine-rich insulin response element. 1291 28