HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: EJE-09-0419v1 161/6/837    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Kanety, H. Articles by Laron, Z. PubMed PubMed Citation Articles by Kanety, H. Articles by Laron, Z.

Total and high molecular weight adiponectin are elevated in patients with Laron syndrome despite marked obesity

¹ Institute of Endocrinology, Chaim Sheba Medical Center, Tel-Hashomer 52621, Israel² Endocrinology and Diabetes Research Unit, Schneider Childrens Medical Center of Israel, Petah Tikva, Israel; both affiliated to the Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel³ The Mina and Everard Goodman Faculty of Life Sciences, Bar-Ilan University, Ramat-Gan, Israel⁴ Department of Metabolic Medicine, Graduate School of Medicine, Osaka University, Osaka, Japan

(Correspondence should be addressed to H Kanety; Email: hkanety{at}sheba.health.gov.il)

Objective: Patients with Laron syndrome (LS; primary GH insensitivity) caused by molecular defects of the GH receptor gene, are characterized by dwarfism, profound obesity, and hyperlipidemia. The aim of the current study was to evaluate adiponectin levels in LS, as obesity is known to be associated with low adiponectin.

Design and methods: We studied nine untreated LS adult patients (5 males, 4 females) and six girls with LS receiving once-daily treatment by IGF1. Total and high molecular weight (HMW) adiponectin levels, adiponectin multimers distribution, and metabolic indices were analyzed in serum samples obtained during several years of follow-up.

Results: Adiponectin levels in the severely obese adult LS patients (percent body fat; females 61.0±2.5%, males 40.6±8.1%) were two- to three-fold higher than those reported for subjects of corresponding age, gender and degree of adiposity. Total adiponectin was significantly higher in females compared with males (21.4±3.5 vs 10.2±4.6 µg/ml, P<0.001). The elevated adiponectin in LS subjects was associated with an increased abundance of the HMW isoform, and positively correlated with body fat percentage (r=0.65, P=0.017) and leptin (r=0.65, P=0.012). There was no correlation between adiponectin levels (total and HMW) and the degree of insulin resistance in LS subjects or their blood lipids levels. Adiponectin was also high in young girls with LS (22.9±7.4 µg/ml) and did not change during long-term IGF1 replacement therapy.

Conclusion: Adiponectin hypersecretion in LS, despite profound obesity, suggests that GH activity may negatively impact adiponectin secretion from adipocytes.