Clinical Chemistry
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


Clinical Chemistry 53: 5-7, 2007; 10.1373/clinchem.2006.080432
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by van Dam, R. M.
Right arrow Articles by Hu, F. B.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by van Dam, R. M.
Right arrow Articles by Hu, F. B.
Related Collections
Right arrow Proteomics and Protein Markers
(Clinical Chemistry. 2007;53:5-7.)
© 2007 American Association for Clinical Chemistry, Inc.


Editorials

Lipocalins and Insulin Resistance: Etiological Role of Retinol-Binding Protein 4 and Lipocalin-2?

Rob M. van Dam1,a and Frank B. Hu2

1 Departments of Nutrition and Epidemiology, Harvard School of Public Health, Boston MA
2 Channing Laboratory, Brigham and Women’s Hospital, and Harvard Medical School, Boston, MA

aAddress correspondence to this author at: Department of Nutrition, Harvard School of Public Health, 665 Huntington Ave., Bldg II, Boston, MA 02115. Fax 617-432-2435; e-mail rvandam@hsph.harvard.edu.

The first 300 words of the full text of this article appear below.

The prevalence of type 2 diabetes is increasing dramatically worldwide. Excess adiposity is an important contributor to the development of type 2 diabetes and cardiovascular diseases (1). Insulin resistance, inflammation, hypertension, and dyslipidemia, components of the metabolic syndrome, have been implicated in the effects of adiposity on type 2 diabetes and cardiovascular diseases, but the mechanisms responsible for these detrimental effects of adiposity have not been fully elucidated.

Two paradigms are currently areas of intense study: one focused on ectopic fat and the other on the endocrine function of adipose tissue (2). Ectopic fat is present in nonadipose tissues such as the liver, muscle, and probably pancreatic ß-cells. Both lipodystrophy (failure to develop adipose tissue) and obesity with full adipose cells are characterized by a lack of fat-storage capacity, resulting in overflow to other tissues of triglycerides and free fatty acids in the form of ectopic fat. Normal physiological processes can be disrupted by this ectopic fat, leading to insulin resistance and impaired insulin secretion. The endocrine function of adipose tissue is an important regulatory process throughout the body that is carried out by signaling proteins secreted by adipose tissue. These signaling proteins are called adipocytokines or adipokines, and they include leptin, adiponectin, resistin, tumor necrosis factor-{alpha}, and interleukin-6.

Members of the lipocalin family of proteins have large sequence differences but share a common tertiary structure formed by segments termed lipocalin folds (3). Lipocalin folds consist of 8 antiparallel ß-sheets that surround a hydrophobic pocket and allow lipocalins to function as transport or carrier proteins. Several human lipocalins have been identified, including retinol-binding protein 4 (RBP4), which has recently been added to the list of adipokines that may link obesity and insulin resistance (4)(5). In this issue of Clinical . . . [Full Text of this Article]




The following articles in journals at HighWire Press have cited this article:


Home page
Clin. Chem.Home page
C. Kanaka-Gantenbein, A. Margeli, P. Pervanidou, S. Sakka, G. Mastorakos, G. P. Chrousos, and I. Papassotiriou
Retinol-Binding Protein 4 and Lipocalin-2 in Childhood and Adolescent Obesity: When Children Are Not Just "Small Adults"
Clin. Chem., July 1, 2008; 54(7): 1176 - 1182.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 2007 by the American Association for Clinical Chemistry.