Insulin Resistance presentations about Insulin Resistance EB with interest for Insulin Resistance Validating Insulin Resistance content Free registration form / enregistrement gratuit
1
2
  Français - August 16, 2011
Welcome to the #1 online source of information for Diabetes Specialists! An international online community of more than 10,000 Diabetes Specialists.

CME on Diabetes is a website built to transmit top-level CME conferences given by international experts in endocrinology, insulin resistance, prediabetes, metabolic syndrome and type 2 diabetes. More than 2.6 million slides have been viewed since the website launch. Thank you for your continued support and commitment!
 Presentation

"Metabolic Syndrome and Insulin Resistance"

Prof. Philipp Scherer (biography)
English - 2005-05-06 - 83 minutes
(47 slides)
(30 slides)
(12 questions)

Summary :
Obesity is an important component of the metabolic syndrome, and in this presentation Prof. Scherer describes the role of adipocyte-derived peptide hormones and their impact on energy metabolism, with a focus on adiponectin, and the contribution of the adipocyte towards systemic inflammation.

Leptin, adiponectin and resistin are peptide hormones that are secreted by adipocytes, and they have been implicated in insulin sensitivity and energy homeostasis. Adiponectin although secreted by fat cells exhibits high circulating levels in lean individuals, and low adiponectin levels have been associated with increased diabetes (1) and CV (2) risk.

Adiponectin levels can be increased by weight loss or treatment with PPAR gamma agonists. The TRIPOD study showed that changes in insulin sensitivity did not correlate well with changes in total adiponectin levels after TZD treatment, but did correlate with changes in the ratio of high molecular weight (HMW) adiponectin to total adiponectin. It is primarily the HMW form of adiponectin that seems to be metabolically responsive, and this complex is primarily induced by TZDs.

Different mouse models are available for research that either have adiponectin knocked out or overexpressed. For example, in ob/ob transgenic mice overexpressing wildtype adiponectin by 2-3 fold, improvements were seen in fasting glucose levels, glucose tolerance, fasting insulin levels, triglyceride levels and postprandial triglyceride clearance, though these ob/ob mice overexpressing adiponectin showed more weight gain. In another study, transgenic mutant (cys39ser) adiponectin ob/ob wildtype-adiponectin-null mice having low level expression of the transgene showed improvements in liver triglyceride content and plasma triglyceride and glucose levels, although again the transgenic mice had increased fat mass.

Clinical and experimental studies indicate the liver to be an important target tissue of adiponectin for improvement of insulin sensitivity. Resistin has the opposite effect on insulin sensitivity compared to adiponectin. It has been shown experimentally for example that resistin infusion causes a decrease in hepatic insulin sensitivity.

Similar to what happens in vascular endothelium, hyperglycaemia induces high levels of mitochondrially-derived reactive oxygen species (ROS) in fat cells. Increased ROS levels induce inflammation via NFkB activation leading to induction of proteins such as IL-6, and local insulin resistance. Changes in ROS levels affect glutathione levels in the secretory pathway, changing the redox potential, and this in turn affects the rates of secretion and the molecular forms secreted, of proteins such as adiponectin and resistin. TZDs act at the level of the mitochondria, and induce adiponectin as well as critical chaperones which affect the handling of adiponectin and the secretion of its HMW complexes.

FAT-ATTAC (FAT Apoptosis Through Triggered Activation of Caspase-8) mice are useful in their ability to become fatless in an acute setting. Activation of caspase-8 causing apoptosis of fat cells in these mice is followed by a disappearance of circulating adiponectin. Also, insulin levels are relatively suppressed in caspase-8-activated FAT-ATTAC ob/ob mice compared to their ob/ob counterparts. Prof. Scherer further describes the effects of beta3 adrenergic receptor activity in adipose tissue, and concludes the presentation with a look at the contribution of the adipocyte towards systemic inflammation.

Copyright © 2005 MULTIWEBCAST "State-of-the-Art Webcast Services"

Learning objectives :
After viewing this presentation the participant will be able to discuss:

- Metabolic effects of adipocyte-secreted peptide hormones;
- Effects of hyperglycaemia-induced reactive oxygen species in the adipocyte;
- Mechanisms of PPAR gamma agonist action in the adipocyte;
- Contributions of the adipocyte to systemic inflammation.

Bibliographic references :
1. R. Retnakaran*, A. J. G. Hanley*, N. Raif, P. W. Connelly, M. Sermer§ and B. Zinman Hypoadiponectinaemia in South Asian women during pregnancy: evidence of ethnic variation in adiponectin concentration Diabetic Medicine. Volume 21 Issue 4 Page 388 - April 2004.

2. Tobias Pischon, MD, MPH; Cynthia J. Girman, DrPH; Gokhan S. Hotamisligil, MD, PhD; Nader Rifai, PhD; Frank B. Hu, MD, PhD; Eric B. Rimm, ScD. Plasma Adiponectin Levels and Risk of Myocardial Infarction in Men JAMA. 2004;291:1730-1737.

   


  Login
  Username :
  Password :
   
  Lost your password?


  Search our website
  Would you like to know more about insulin resistance? Are you looking for information pertaining to Type 2 Diabetes? You can find what you are looking for in over 2000 references available on CMEonDiabetes.
 

  Social
  Let others know about this presentation.

 Del.icio.us
 Digg!



MULTILEARNING - MULTIWEBCAST - MULTIEPOSTER - MULTIEPORTAL

Copyright © 2002-2015 MULTILEARNING Group INC.. All rights reserved.  Disclaimer
Powered by Multiwebcast - webcast services


USER ACKNOWLEDGES AND AGREES THAT ALL DECISIONS MADE WITH THE ASSISTANCE OR USE OF THE SOFTWARE AND/OR THE WEBSITE AND/OR BASED ON CONTENT FOUND HEREIN WILL BE EXCLUSIVELY THE RESPONSIBILITY OF THE USER.
insulin resistanceC-Reactive Protein (CRP)CRP, C-Reactive ProteinADHD ADDdiabetes insulin