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Monday, July 27, 2020 | History

4 edition of role of protein kinase C in insulin action, resistence and secretion found in the catalog.

role of protein kinase C in insulin action, resistence and secretion

Robert V. Farese

role of protein kinase C in insulin action, resistence and secretion

by Robert V. Farese

  • 125 Want to read
  • 14 Currently reading

Published by R.G. Landes in Austin .
Written in English

    Subjects:
  • Insulin resistance -- Pathophysiology,
  • Protein kinase C -- Physiological effect,
  • Diabetes -- Complications -- Pathophysiology,
  • Insulin -- Secretion,
  • Cellular signal transduction,
  • Phospholipids -- Physiological effect,
  • Insulin -- physiology,
  • Protein Kinase C -- metabolism,
  • Diabetes Mellitus -- metabolism,
  • Signal Transduction -- physiology

  • Edition Notes

    Includes bibliographical references and index.

    StatementRobert V. Farese.
    SeriesMedical intelligence unit, Medical intelligence unit (Unnumbered)
    Classifications
    LC ClassificationsRC662.4 .F37 1994
    The Physical Object
    Paginationp. cm.
    ID Numbers
    Open LibraryOL1111302M
    ISBN 101570592160
    LC Control Number94037107

    Insulin release, peripheral insulin resistance and muscle function in protein malnutrition: a role of tricarboxylic acid cycle anaplerosis - Volume Issue 9 - Claudio C. Zoppi, Leonardo R. Silveira, Camila A. M. Oliveira, Antonio C. Boschero, Rui Curi, Everardo M. Carneiro. In Advances in Drug Research, Basic Characteristics of Transmembrane Signalling through the Insulin Receptor Kinase. The model of the insulin receptor kinase as a signal transducer across the plasma membrane is based on a great number of studies which were initiated by the original finding of Kasuga et al. (a), who showed that insulin stimulation of .

    Insulin resistance is a complex metabolic disorder that defies explanation by a single etiological pathway. Accumulation of ectopic lipid metabolites, activation of the unfolded protein response (UPR) pathway, and innate immune pathways have all been implicated in the pathogenesis of insulin resistance. However, these pathways are also closely linked to changes in fatty acid . OBJECTIVE Insulin resistance is associated with the pathogenesis of metabolic disorders as type 2 diabetes and obesity. Given the emerging role of signal transduction in these syndromes, we set out to explore the possible role that G protein–coupled receptor kinase 2 (GRK2), first identified as a G protein–coupled receptor regulator, could have as a modulator of insulin .

    Insulin action is initiated by an interaction of insulin with its cell surface receptor [].The insulin receptor (IR) is a heterotetramer consisting of two α subunits and two β subunits that are linked by disulphide bonds. Insulin binds to the extracellular α subunit of the insulin receptor and activates the tyrosine kinase in the β subunit {figure 1). [29] Cortright RN et al. Protein kinase C modulates insulin action in human skeletal muscle. American Journal of Physiology. Endocrinology and Metabolism. ; (3):EE


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Role of protein kinase C in insulin action, resistence and secretion by Robert V. Farese Download PDF EPUB FB2

INTRODUCTION. Insulin secretion is subject to precise regulation by nutrient and nonnutrient secretagogues. Despite the well-known depolarization–secretion coupling initiated by metabolism of glucose and other nutrient secretagogues, nutrients also activate intracellular signaling pathways that lead to the activation of protein kinases such as PKC and PKA (Nesher et al., Cited by: Additional Physical Format: Online version: Farese, Robert V., Protein kinase C in insulin action, resistance, and secretion.

Austin: R.G. Lanes Co.,   Insulin action on target tissues is mediated by specific tyrosine kinase receptors. Upon ligand binding insulin receptors autophosphorylate and phosphorylate intracellular substrates on tyrosine residues.

These early events of insulin action are followed by the activation of a number of enzymes, including protein kinase C (PKC). At least 14 PKC Cited by: Atypical protein kinase C in insulin action and insulin resistance Article Literature Review in Biochemical Society Transactions 33(Pt 2) May.

With respect to insulin receptor signaling proteins, insulin receptor substrate-1, phosphatidylinositolkinase, protein kniase B/AK strain transforming, PIP 3-dependent kinase 1, and glycogen synthase kinase 3β are all known to be O-GlcNAcylated.

These modifications have all been observed in adipocytes which are a major target for the. Insulin Secretion. Insulin secretion stimulated by glucose is a complex process of signal transduction in beta role of protein kinase C in insulin action, comprised of proximal events which include glucose internalization through glucose transporters (GLUT) and its catabolism through glycolysis, Krebs cycle, and oxidative phosphorylation, leading to a rise in ATP/ADP ratio, and by distal events, which.

Increased lipid availability is strongly associated with both β-cell dysfunction and insulin resistance, two key facets of type 2 diabetes.

Isoforms of the protein kinase C (PKC) family have been viewed as candidates for mediating the effects of fat oversupply because they are lipid-dependent kinases with wide-ranging roles in signal transduction, including the.

Hepatic insulin resistance in this model was associated with increased hepatic diacylglycerol content and increased translocation of the primary novel PKC isoform in liver, protein kinase-Cε (PKCε) 26,27, to the plasma membrane at which it was found to bind and inhibit the activity of the intracellular kinase domain of the insulin receptor.

Vitamin E also accelerates diacylglycerol kinase activity, thereby decreasing levels of diacylglycerol, which is an allosteric activator of protein kinase C. Increased protein kinase C activity apparently impairs insulin action by phosphorylating serine or threonine residues on insulin receptor and insulin receptor substrate-1 proteins (27).

3. Insulin Resistance. Insulin resistance is a pathological condition characterized by the inability of insulin to elicit a hormone response in insulin-dependent cells to regulate glucose and lipid metabolism [1,2].Insulin resistance is inversely correlated with insulin sensitivity in insulin-dependent tissues [].There are multiple factors responsible for insulin resistance.

Recently, M 3-muscarinic receptor (M3R) has been identified as the bona fide receptor responsible for the cholinergic regulation of glucose-induced insulin molecular mechanisms of such regulation have also begun to be unravelled. These include the conventional G protein-dependent pathways involving calcium mobilization and activation of protein kinase C.

This review provides an overview of insulin, its history, structure, synthesis, secretion, actions and interactions followed by a discussion of insulin resistance and its associated clinical. Griffin, M. et al. Free fatty acid-induced insulin resistance is associated with activation of protein kinase C θ and alterations in the insulin signaling.

The loss of insulin secretory capacity by the beta-cells of the pancreas is an obligatory step in the progression from a state of insulin resistance to a state of overt hyperglycemia. 10 The capacity for insulin secretion is dictated primarily by two factors: the response of existing beta-cells to stimulation of insulin secretion, and the.

protein kinase B (PKB) an d finally, the action of their eff ectors. W e will present regulatory mec hanisms and modula tors o f insulin-mediated gluc ose uptak e. Protein kinase C epsilon (PKC 3) activation in the liver is proposed to inhibit insulin action through phos-phorylation of the insulin receptor.

Here, however, we demonstrated that global, but not liver-specific, deletion of PKC 3 in mice protected against diet-induced glucose intolerance and insulin resistance. We discuss the effects on insulin secretion and action of deleting or over-expressing Slc30a8 highly selectively in the pancreatic β-cell, and the role of zinc in insulin signalling.

While modulated by genetic variability, healthy levels of dietary zinc, and hence normal cellular zinc homeostasis, are likely to play an important role in the. Protein Kinase C-β Inhibition. Decreased insulin secretion and resistance as well as increased glucagon secretion are major players in the pathogenesis of type 2 diabetes.

Insulin resistance plays an important role in type 2 diabetes and this role should be quantified. Agents that decrease insulin resistance should be developed. PK s AS AMPLIFIERS OF THE β-CELL INSULIN RESPONSE. The concept according to which most if not all PKC isoenzymes following their activation are translocated to the site of their action is now widely adopted (8,9).Mochly-Rosen et al.

developed and refined the model by characterizing specific receptors for inactive C kinase (RICK)-anchoring proteins that bind the kinase. Atypical protein kinase C in insulin action and insulin resistance. and insulin secretion. In: Keystone Symposia on Islet and Beta-Cell Development and Transplantation ( Abstract Book Regulation of insulin receptor substrate 1 pleckstrin homology domain by protein kinase C: role of serine 24 phosphorylation.

Mol Endocrinol. Insulin signaling at the target tissue results in a large array of biological outcomes. These events are essential for normal growth and development and for normal homeostasis of glucose, fat, and protein metabolism.

Elucidating the intracellular events after activation of the IR has been the primary focus of a large number of investigators for decades, and for excellent reasons.insulin resistance is a state in which the sensitivity of target cells to respond to ordinary levels of insulin is reduced.

It plays a central role in the development of type 2 diabetes, an emerging epidemic of the 21st century. A variety of agents and conditions that induce insulin resistance, such as TNFα and free fatty acids, activate a number of protein kinases that target elements .Insulin activation of protein kinase C: A reassessment Article (PDF Available) in Journal of Biological Chemistry (17) July with 24 Reads How we measure 'reads'.