Serum leptin activity in obese and lean patients

被引:16
作者
Friedman-Einat, M
Camoin, L
Faltin, Z
Rosenblum, CI
Kaliouta, V
Eshdat, Y
Strosberg, AD
机构
[1] Agr Res Org, Volcani Ctr, Inst Anim Sci, IL-50250 Bet Dagan, Israel
[2] Inst Cochin Genet Mol, F-75014 Paris, France
[3] Agr Res Org, Volcani Ctr, Inst Hort, IL-50250 Bet Dagan, Israel
[4] Merck Res Labs, Dept Obes Res, Rahway, NJ 07065 USA
关键词
leptin; leptin-receptor; (LEPR; OB-R); bioassay; luciferase; human serum;
D O I
10.1016/S0167-0115(02)00259-8
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Blood levels of the satiety hormone leptin are directly correlated to fat stores in obese and lean people. Therefore, leptin resistance is the logical explanation for the phenomenon of common obesity. However, the important question of whether or not the intrinsic leptin activity could differ between obese and lean people has not been examined before. In the present study, serum leptin activity was measured by an in vitro assay of leptin signaling in a modified culture of HEK-293 cells. The system is based on activation of a luciferase reporter gene through a leptin receptor-dependent activation of the signal transducer and activator of transcription (STAT3). Serum samples from 20 obese and 20 non-obese individuals with leptin levels ranging from 3 to 75 ng/ml, as determined by radioimmunoassay (RIA), were used. A high correlation was observed for each serum sample between leptin RIA values and leptin activity in the bioassay. The results indicate that obesity in the 20 obese patients among the 40 individuals examined cannot be accounted for by alterations in leptin activity in our assay. The assay system provides a tool to screen for possible rare cases exhibiting alteration in leptin activity either due to a change in leptin itself or through interaction with other serum factors. (C) 2002 Elsevier Science B.V. All rights reserved.
引用
收藏
页码:77 / 82
页数:6
相关论文
共 36 条
[1]  
Arcuri P, 2000, INT J MOL MED, V6, P97
[2]   Leptin enters the brain by a saturable system independent of insulin [J].
Banks, WA ;
Kastin, AJ ;
Huang, WT ;
Jaspan, JB ;
Maness, LM .
PEPTIDES, 1996, 17 (02) :305-311
[3]   Leptin transport across the blood-brain barrier: Implications for the cause and treatment of obesity [J].
Banks, WA .
CURRENT PHARMACEUTICAL DESIGN, 2001, 7 (02) :125-133
[4]   The role of SOCS-3 in leptin signaling and leptin resistance [J].
Bjorbæk, C ;
El-Haschimi, K ;
Frantz, JD ;
Flier, JS .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1999, 274 (42) :30059-30065
[5]  
Boado RJ, 1996, J NEURAL TRANSM-SUPP, P275
[6]   Obesity is associated with a decreased leptin transport across the blood-brain barrier in rats [J].
Burguera, B ;
Couce, ME ;
Curran, GL ;
Jensen, MD ;
Lloyd, RV ;
Cleary, MP ;
Poduslo, JF .
DIABETES, 2000, 49 (07) :1219-1223
[7]   Decreased cerebrospinal-fluid/serum leptin ratio in obesity: A possible mechanism for leptin resistance [J].
Caro, JF ;
Kolaczynski, JW ;
Nyce, MR ;
Ohannesian, JP ;
Opentanova, I ;
Goldman, WH ;
Lynn, RB ;
Zhang, PL ;
Sinha, MK ;
Considine, RV .
LANCET, 1996, 348 (9021) :159-161
[8]   Disappearance of body fat in normal rats induced by adenovirus-mediated leptin gene therapy [J].
Chen, GX ;
Koyama, K ;
Yuan, X ;
Lee, Y ;
Zhou, YT ;
ODoherty, R ;
Newgard, CB ;
Unger, RH .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1996, 93 (25) :14795-14799
[9]   Serum immunoreactive leptin concentrations in normal-weight and obese humans [J].
Considine, RV ;
Sinha, MK ;
Heiman, ML ;
Kriauciunas, A ;
Stephens, TW ;
Nyce, MR ;
Ohannesian, JP ;
Marco, CC ;
McKee, LJ ;
Bauer, TL ;
Caro, JF .
NEW ENGLAND JOURNAL OF MEDICINE, 1996, 334 (05) :292-295
[10]   Central leptin gene therapy suppresses body weight gain, adiposity and serum insulin without affecting food consumption in normal rats: a long-term study [J].
Dhillon, H ;
Kalra, SP ;
Prima, V ;
Zolotukhin, S ;
Scarpace, PJ ;
Moldawer, LL ;
Muzyczka, N ;
Kalra, PS .
REGULATORY PEPTIDES, 2001, 99 (2-3) :69-77