| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
Central Arkansas Veterans Healthcare System and Department of Medicine, Division of Endocrinology, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205
Address all correspondence and requests for reprints to: Philip A. Kern, M.D., Central Arkansas Veterans Healthcare System, 598/151 LR, 4300 West 7th Street, Little Rock, Arkansas 72205. E-mail: kernphilipa{at}uams.edu.
The perilipins are highly phosphorylated adipocyte proteins that are localized at the surface of the lipid droplet. With activation by protein kinase A, perilipins translocate away from the lipid droplet and allow hormone-sensitive lipase to hydrolyze the adipocyte triglycerides to release nonesterified fatty acids (NEFA). Because of the potential importance of adipocyte lipolysis to obesity and insulin resistance, we measured perilipin protein and mRNA levels in nondiabetic subjects with varying degrees of insulin resistance. By Northern and Western blotting, we could detect perilipin A, but not perilipin B. Perilipin A protein and mRNA levels were quantitated and were highly correlated with each other. There was a significant positive relationship between perilipin expression and obesity (r = 0.55; P < 0.01, perilipin mRNA vs. percent body fat). However, there was no significant relationship between perilipin expression and blood NEFA, nor was there a significant relationship between perilipin expression and insulin resistance, using the insulin sensitivity index derived from the iv glucose tolerance test with minimal modeling. In addition, there was no significant relationship between perilipin and adipocyte or systemic inflammatory markers, such as TNF
, IL-6, and adiponectin. Thus, perilipin was elevated in obese subjects, perhaps as a compensatory mechanism to limit basal lipolysis. However, there was no relationship between perilipin and insulin resistance.
This work was supported by a Merit Review Grant from the Veterans Administration, Grant M01-RR-14288 from the General Clinical Research Center, and NIH Grant DK-39176.
Abbreviations: BMI, Body mass index; NEFA, nonesterified fatty acid; SI, insulin sensitivity index.
This article has been cited by other articles:
![]() |
S. Fernandez-Veledo, I. Nieto-Vazquez, J. de Castro, M. P. Ramos, S. Bruderlein, P. Moller, and M. Lorenzo Hyperinsulinemia Induces Insulin Resistance on Glucose and Lipid Metabolism in a Human Adipocytic Cell Line: Paracrine Interaction with Myocytes J. Clin. Endocrinol. Metab., July 1, 2008; 93(7): 2866 - 2876. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. Kovsan, R. Ben-Romano, S. C. Souza, A. S. Greenberg, and A. Rudich Regulation of Adipocyte Lipolysis by Degradation of the Perilipin Protein: NELFINAVIR ENHANCES LYSOSOME-MEDIATED PERILIPIN PROTEOLYSIS J. Biol. Chem., July 27, 2007; 282(30): 21704 - 21711. [Abstract] [Full Text] [PDF] |
||||
![]() |
D. Corella, L. Qi, J. V. Sorli, D. Godoy, O. Portoles, O. Coltell, A. S. Greenberg, and J. M. Ordovas Obese Subjects Carrying the 11482G>A Polymorphism at the Perilipin Locus Are Resistant to Weight Loss after Dietary Energy Restriction J. Clin. Endocrinol. Metab., September 1, 2005; 90(9): 5121 - 5126. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Endocrinology | Endocrine Reviews | J. Clin. End. & Metab. |
| Molecular Endocrinology | Recent Prog. Horm. Res. | All Endocrine Journals |