Relationship between muscle sympathetic nerve activity and plasma leptin concentration

被引:86
作者
Snitker, S [1 ]
Pratley, RE [1 ]
Nicolson, M [1 ]
Tataranni, PA [1 ]
Ravussin, E [1 ]
机构
[1] AMGEN INC, THOUSAND OAKS, CA 91320 USA
来源
OBESITY RESEARCH | 1997年 / 5卷 / 04期
关键词
sympathetic nervous system; adrenergic fibers; electrophysiology; obesity; microneurography;
D O I
10.1002/j.1550-8528.1997.tb00561.x
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
In humans, basal muscle sympathetic nerve activity (MSNA), a direct measure of sympathetic nervous outflow, is correlated with percentage of body fat. The underlying physiological mechanism is unknown. On the basis of the observation that leptin increases sympathetic nervous outflow in the ob/ob mouse, we hypothesized that leptin, a hormone secreted by the adipose tissue, may act as a peripheral signal to increase sympathetic nervous outflow from the central nervous system. We therefore tested whether basal MSNA is correlated with plasma leptin concentration. Fasting plasma samples and recordings of basal MSNA in the peroneal nerve were obtained from 37 healthy, nondiabetic men (35 white and 2 Mexican-Americans; 29 +/- 7 years, 86 +/- 14 kg, 24 +/- 10% body fat; mean +/- SD) who were fed a weight-maintenance diet on a metabolic ward. As expected, plasma leptin concentration (geometric mean, 6.4 ng/mL; 95% confidence interval, 4.6 ng/mL to 9.0 ng/mL) correlated with % body fat (r=0.93, p<0.001). Basal MSNA was 31.6 +/- 10.0 bursts/min and correlated with % body fat (r=0.53, p<0.001) and with plasma leptin concentration (r=0.44, p<0.01). In conclusion, the results demonstrate a correlation between MSNA and plasma leptin concentration of a magnitude similar to that between MSNA and % body fat. Leptin may therefore be the peripheral signal explaining the correlation between MSNA and % body fat. A full understanding of the relationship between leptin and the activity of the sympathetic nervous system requires further studies, including the administration of leptin in humans.
引用
收藏
页码:338 / 340
页数:3
相关论文
共 16 条
[1]   CONTRIBUTION OF BAT AND SKELETAL-MUSCLE TO THERMOGENESIS INDUCED BY EPHEDRINE IN MAN [J].
ASTRUP, A ;
BULOW, J ;
MADSEN, J ;
CHRISTENSEN, NJ .
AMERICAN JOURNAL OF PHYSIOLOGY, 1985, 248 (05) :E507-E515
[2]  
BRAY GA, 1989, VITAM HORM, V45, P1
[3]   Role of leptin in fat regulation [J].
Collins, S ;
Kuhn, CM ;
Petro, AE ;
Swick, AG ;
Chrunyk, BA ;
Surwit, RS .
NATURE, 1996, 380 (6576) :677-677
[4]   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
[5]   WEIGHT-REDUCING EFFECTS OF THE PLASMA-PROTEIN ENCODED BY THE OBESE GENE [J].
HALAAS, JL ;
GAJIWALA, KS ;
MAFFEI, M ;
COHEN, SL ;
CHAIT, BT ;
RABINOWITZ, D ;
LALLONE, RL ;
BURLEY, SK ;
FRIEDMAN, JM .
SCIENCE, 1995, 269 (5223) :543-546
[6]   Reduced expression of the leptin gene (ob) by catecholamine through a G(s) protein-coupled pathway in 3T3-L1 adipocytes [J].
Kosaki, A ;
Yamada, K ;
Kuzuya, H .
DIABETES, 1996, 45 (12) :1744-1749
[7]   LEPTIN LEVELS IN HUMAN AND RODENT - MEASUREMENT OF PLASMA LEPTIN AND OB RNA IN OBESE AND WEIGHT-REDUCED SUBJECTS [J].
MAFFEI, M ;
HALAAS, J ;
RAVUSSIN, E ;
PRATLEY, RE ;
LEE, GH ;
ZHANG, Y ;
FEI, H ;
KIM, S ;
LALLONE, R ;
RANGANATHAN, S ;
KERN, PA ;
FRIEDMAN, JM .
NATURE MEDICINE, 1995, 1 (11) :1155-1161
[8]   Activation of beta(3) adrenergic receptors suppresses leptin expression and mediates a leptin-independent inhibition of food intake in mice [J].
Mantzoros, CS ;
Qu, DQ ;
Frederich, RC ;
Susulic, VS ;
Lowell, BB ;
MaratosFlier, E ;
Flier, JS .
DIABETES, 1996, 45 (07) :909-914
[9]   EFFECTS OF THE OBESE GENE-PRODUCT ON BODY-WEIGHT REGULATION IN OB/OB MICE [J].
PELLEYMOUNTER, MA ;
CULLEN, MJ ;
BAKER, MB ;
HECHT, R ;
WINTERS, D ;
BOONE, T ;
COLLINS, F .
SCIENCE, 1995, 269 (5223) :540-543
[10]   Cerebrospinal fluid leptin levels: Relationship to plasma levels and to adiposity in humans [J].
Schwartz, MW ;
Peskind, E ;
Raskind, M ;
Boyko, EJ ;
Porte, D .
NATURE MEDICINE, 1996, 2 (05) :589-593