File Name: glucose transporters and insulin action .zip
Obesity associated with systemic inflammation induces insulin resistance IR , with consequent chronic hyperglycemia.
- Signaling pathways in insulin action: molecular targets of insulin resistance
- Effects of insulin on glucose transport and glucose transporters in rat heart.
- Insulin Signaling and the Regulation of Glucose Transport
- Glucose transporters and insulin action: Some insights into diabetes management
Although diabetes has been identified as a major risk factor for atrial fibrillation, little is known about glucose metabolism in the healthy and diabetic atria.
Type 2 diabetes mellitus T2DM is one of the most severe public health problems in the world. In recent years, evidences show a commonness of utilization of alternative medicines such as phytomedicine for the treatment of T2DM. Phenolic acids are the most common compounds in non-flavonoid group of phenolic compounds and have been suggested to have a potential to lower the risk of T2DM. Skeletal muscle is the major organ that contributes to the pathophysiology of T2DM.
Signaling pathways in insulin action: molecular targets of insulin resistance
Randhawa, Amira Klip; Insulin action on glucose transporters through molecular switches, tracks and tethers. Biochem J 15 July ; 2 : — Glucose entry into muscle cells is precisely regulated by insulin, through recruitment of GLUT4 glucose transporter-4 to the membrane of muscle and fat cells. Work done over more than two decades has contributed to mapping the insulin signalling and GLUT4 vesicle trafficking events underpinning this response. In spite of this intensive scientific research, there are outstanding questions that continue to challenge us today. Sign In or Create an Account.
Effects of insulin on glucose transport and glucose transporters in rat heart.
Perspective Free access Address correspondence to: Jeffrey E. Phone: ; Fax: ; E-mail: jeffrey-pessin uiowa. Find articles by Pessin, J. Find articles by Saltiel, A.
The ability of insulin to stimulate glucose uptake into muscle and adipose tissue is central to the maintenance of whole-body glucose homeostasis. Deregulation of insulin action manifests itself as insulin resistance, a key component of type II diabetes mellitus T2DM. Both forms of diabetes confer an increased risk of major lifelong complications. In the case of insulin resistance, this includes a fivefold increased risk of coronary vascular disease. The need for an effective treatment for both forms of diabetes as well as for the development of early detection methodologies has, therefore, become increasingly important. Yet for this to be possible, we must first understand the mechanism through which insulin regulates glucose uptake and identify the key molecular players involved.
Insulin Signaling and the Regulation of Glucose Transport
Insulin stimulates glucose uptake in muscle and adipose cells primarily by recruiting GLUT4 from an intracellular storage pool to the plasma membrane. Dysfunction of this process known as insulin resistance causes hyperglycemia, a hallmark of diabetes and obesity. Thus the understanding of the mechanisms underlying this process at the molecular level may give, an insight into the prevention and treatment of these health problems.
GLUT4, the major isoform in insulin-responsive tissue, translocates from an intracellular pool to the cell surface and as such determines insulin-stimulated glucose uptake. However, despite intensive research over 50 years, the insulin-dependent and -independent pathways that mediate GLUT4 translocation are not fully elucidated in any species.
Glucose transporters and insulin action: Some insights into diabetes management
Metrics details. Gaps remain in our understanding of the precise molecular mechanisms by which insulin regulates glucose uptake in fat and muscle cells. Recent evidence suggests that insulin action involves multiple pathways, each compartmentalized in discrete domains. Upon activation, the receptor catalyzes the tyrosine phosphorylation of a number of substrates. One family of these, the insulin receptor substrate IRS proteins, initiates activation of the phosphatidylinositol 3-kinase pathway, resulting in stimulation of protein kinases such as Akt and atypical protein kinase C. The receptor also phosphorylates the adapter protein APS, resulting in the activation of the G protein TC10, which resides in lipid rafts. TC10 can influence a number of cellular processes, including changes in the actin cytoskeleton, recruitment of effectors such as the adapter protein CIP4, and assembly of the exocyst complex.
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