By Sudhesh Kumar, Stephen O'Rahilly
Diabetes is now one of many significant factors of morbidity around the world. in lots of situations, the onset of diabetes is innovative, constructing through a of insulin resistance. This publication considers the improvement of this , its results and medical and healing aspects.
The booklet stories the traditional biology of insulin motion on glucose, lipids and proteins. It considers the pathological foundation for insulin resistance in animal versions and people, and discusses the impression of heredity, nutritional elements and workout. scientific results together with dyslipidaemia, high blood pressure and polycystic ovary syndrome, and healing ideas for remedy also are examined.
* presents knowledgeable evaluation of the phenomenon of insulin resistance
* Brings jointly a number of contemporary study for the 1st time
* Written by means of top specialists in organic and scientific researchContent:
Chapter 1 The Insulin Receptor and Downstream Signalling (pages 1–62): Ken Siddle
Chapter 2 Insulin?Mediated rules of Glucose Metabolism (pages 63–85): Daniel Konrad, Assaf Rudich and Amira Klip
Chapter three Insulin motion on Lipid Metabolism (pages 87–103): Keith N. Frayn and Fredrik Karpe
Chapter four The impact of Insulin on Protein Metabolism (pages 105–132): Laura J. S. Greenlund and okay. Sreekumaran Nair
Chapter five Genetically transformed Mouse types of Insulin Resistance (pages 133–153): Gema Medina?Gomez, Christopher Lelliott and Antonio J. Vidal?Puig
Chapter 6 Insulin Resistance in Glucose Disposal and construction in guy with particular connection with Metabolic Syndrome and sort 2 Diabetes (pages 155–178): Henning Beck?Nielsen, Frank Alford and Ole Hother?Nielsen
Chapter 7 imperative legislation of Peripheral Glucose Metabolism (pages 179–206): Stanley M. Hileman and Christian Bjorb?k
Chapter eight courting among fats Distribution and Insulin Resistance (pages 207–235): Philip G. McTernan, Aresh Anwar and Sudhesh Kumar
Chapter nine PPAR? and Glucose Homeostasis (pages 237–267): Robert okay. Semple and Stephen O'Rahilly
Chapter 10 Adipokines and Insulin Resistance (pages 269–295): Daniel ok. Clarke and Vidya Mohamed?Ali
Chapter eleven nutritional components and Insulin Resistance (pages 297–316): Jeremy Krebs and Susan Jebb
Chapter 12 actual task and Insulin Resistance (pages 317–400): Nicholas J. Wareham, Soren Brage, Paul W. Franks and Rebecca A. Abbott
Chapter thirteen Genetics of the Metabolic Syndrome (pages 401–450): George Argyropoulos, Steven Smith and Claude Bouchard
Chapter 14 Insulin Resistance and Dyslipidaemia (pages 451–466): Benoit Lamarche and Jean?Francois Mauger
Chapter 15 Insulin Resistance, high blood pressure and Endothelial disorder (pages 467–483): Stephen J. Cleland and John M. C. Connell
Chapter sixteen Insulin Resistance and Polycystic Ovary Syndrome (pages 485–509): Neus Potau
Chapter 17 Syndromes of serious Insulin Resistance (SSIRs) (pages 511–533): David Savage and Stephen O'Rahilly
Chapter 18 healing ideas for Insulin Resistance (pages 535–560): Harpal S. Randeva, Margaret Clarke and Sudhesh Kumar
Chapter 19 Drug remedy for Insulin Resistance – a glance on the destiny (pages 561–585): Bei B. Zhang and David E. Moller
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Extra resources for Insulin Resistance: Insulin Action and Its Disturbances in Disease
Example text
2001) Specificity in ligand binding and intracellular signalling by insulin and insulin-like growth factor receptors. Biochem Soc Trans 29, 513–525. 10. Gammeltoft, S. (1984) Insulin receptors: binding kinetics and structure–function relationship of insulin. Physiol Rev 64, 1321–1378. 11. , Blithe, D. , Crettaz, M. and Kahn, C. R. (1982) Insulin stimulates tyrosine phosphorylation of the insulin receptor in a cell-free system. Nature 298, 667–669. 12. , Ou, J. , Kan, Y. , Goldfine, I. , Roth, R.
284, 311 – 313 The 14–3–3 proteins are a family of abundant, widely expressed proteins that bind to phospho-serine-containing motifs (particularly favouring those in a PKB consensus). The consequences of 14–3–3 binding vary with different proteins, and can include either positive or negative effects on function. Most simply, binding of 14–3–3 may inhibit dephosphorylation or proteolysis, thus extending the lifetime of activated targets. 314 Some of these binding partners (such as PKCζ and Grb10) may be relevant to insulin action, although their functional significance remains to be determined.
They are expressed primarily in lymphocytes and myeloid cells, where their functions may include coupling Fcγ RIIb and other receptors to inhibition of MAP kinases. 198 Importantly, Gabs have the potential to make additional interactions through other tyrosine-based motifs and proline-rich regions. Gabs are substrates for multiple tyrosine kinases and interact particularly with Met receptors. 208, 209 There are several members of the Shc family, of which ShcA is most widely expressed. This exists as three isoforms of approximate Mr 46, 52 and 66 kDa, p52 being the major isoform in most cells.