Mar 2007
Journal Club | May 2007 | Feb 2007

IRIG: Ceramide in insulin resistance in "Cell Metabolism"

03/16/2007 00:27
Although it is generally accepted that FFA is a risk factor for insulin resistance, it is quite controversial about the signaling molecules for FFA-induced insulin resistance. Ceramide and DAG are two derivatives of FFA. It has been confusing about which of the two FFA derivatives is the "dominant player" in the translation of FFA signal into insulin resistance. Each molecule is supported by multiple published studies of many labs. In the current issue of "Cell Metabolism", a study using transgenic and pharmacological approaches demonstrated that ceramide is the "dominant player". Inhibition of ceramide  led to blocking of insulin resistance in three models: glucocorticoid, FFA and obesity. In these conditions, DAG level was not changed by ceramide inhibition. See attache PDF file.    
     
     Regarding adiponectin receptor knockout mice, there are two additional studies published in "Diabetes" and Endocrinology" this month along with the one in "Nature Medicine". It seems that the metabolic phenotypes are not consistent among the three independent studies. Attached are the PDF files from Diabetes and Endocrinology. These two papers are recommended by Drs. Lu Cai at the University of Louisville, and Jianhua Shao at the University of Kentucky.   
 
by Jianping at PBRC

—-----------------------------       
 
Jianping Ye, MD
Professor of Molecular Biology
Pennington Biomedical Research Center
Louisiana State University System
6400 Perkins Road
Baton Rouge, LA 70808
Phone: (225) 763-3163
Fax: (225) 763-2525
E-mail: yej@pbrc.edu
|

IRIG: Adiponectin receptor knockout in "Nature Medicine"

03/07/2007 21:27
The metabolic activities of adiponectin have been well known for some times. However, its nature of hormone or cytokine is challenged by its high protein concentration (mg level) in the blood. Cloning of its receptor and identification of the receptor signaling pathways support the hormone/cytokine nature of adiponectin. Now, this consensus is enforced by a knockout study of the adiponectin receptor in the current issue of Nature Medicine. This issue also has another exciting study to provide evidence that TZD (PPARg) acts on Beta-cells through ABCA1. Following are links to these papers.       
        
Targeted disruption of AdipoR1 and AdipoR2 causes abrogation of adiponectin binding and metabolic actions pp332 - 339
Toshimasa Yamauchi et al.
10.1038/nm1557
Abstract: http://ealerts.nature.com/cgi-bin24/DM/y/ecoP0SohGc0HjT0BNem0EP
Article: http://ealerts.nature.com/cgi-bin24/DM/y/ecoP0SohGc0HjT0BNen0EQ
 
[beta]-cell ABCA1 influences insulin secretion, glucose homeostasis and response to thiazolidinedione treatment pp340 - 347
Liam R Brunham et al.
10.1038/nm1546
Abstract: http://ealerts.nature.com/cgi-bin24/DM/y/ecoP0SohGc0HjT0BNeo0ER
Article: http://ealerts.nature.com/cgi-bin24/DM/y/ecoP0SohGc0HjT0BNep0ES
 
The ABCs of [beta]-cell dysfunction in type 2 diabetes pp241 - 242
Cholesterol toxicity may damage pancreatic [beta]-cells, leading to decreased insulin secretion and impaired glucose tolerance (pages 340-347).
Manu V Chakravarthy and Clay F Semenkovich
10.1038/nm0307-241
http://ealerts.nature.com/cgi-bin24/DM/y/ecoP0SohGc0HjT0BNd50ES
 
By Jianping at PBRC

—-------------------------------------

 
Jianping Ye, MD
Professor of Molecular Biology
Pennington Biomedical Research Center
Louisiana State University System
6400 Perkins Road
Baton Rouge, LA 70808
Phone: (225) 763-3163
Fax: (225) 763-2525
E-mail: yej@pbrc.edu
|