Skip to main content

Lund University Publications

LUND UNIVERSITY LIBRARIES

Testosterone and diurnal rhythmicity of leptin, TNF-alpha and TNF-II receptor in insulin-resistant myotonic dystrophy patients

Johansson, A ; Ahrén, Bo LU ; Forsberg, H and Olsson, T (2002) In International Journal of Obesity 26(10). p.1386-1392
Abstract
OBJECTIVE: To investigate the leptin and TNF systems in relation to testosterone in insulin resistant myotonic dystrophy (DM1) subjects. DESIGN AND SUBJECTS: Fasting morning samples and diurnal sampling during 24 h. Forty-two DM1 subjects (20 women and 22 men; age 41.5 (28.5-58.7)y, body mass index (BMI) 23.3 (18.6-29.2)kg/m(2); median and 10th and 90th percentile, respectively). Fifty healthy volunteers (23 women and 27 men; age 42 (27.0-56.9)y, BMI 24.0 (20.7-29.7) kg/m(2)). Nine men with DM1 and nine healthy men participated in diurnal sampling. MEASUREMENTS: Body composition was measured by bioelectric impedance analysis. Circulating levels of leptin, TNF-alpha, TNFR-II, insulin, testosterone and lipids were measured. The number of CTG... (More)
OBJECTIVE: To investigate the leptin and TNF systems in relation to testosterone in insulin resistant myotonic dystrophy (DM1) subjects. DESIGN AND SUBJECTS: Fasting morning samples and diurnal sampling during 24 h. Forty-two DM1 subjects (20 women and 22 men; age 41.5 (28.5-58.7)y, body mass index (BMI) 23.3 (18.6-29.2)kg/m(2); median and 10th and 90th percentile, respectively). Fifty healthy volunteers (23 women and 27 men; age 42 (27.0-56.9)y, BMI 24.0 (20.7-29.7) kg/m(2)). Nine men with DM1 and nine healthy men participated in diurnal sampling. MEASUREMENTS: Body composition was measured by bioelectric impedance analysis. Circulating levels of leptin, TNF-alpha, TNFR-II, insulin, testosterone and lipids were measured. The number of CTG triplet repeats was analysed. RESULTS: Basal as well as median 24 h levels of leptin and TNFR-II were significantly increased in DM1 patients, independent of body fat mass. This was associated with higher insulin and lower testosterone levels in DM1 patients. The genetic defect was related to leptin and TNFR-II levels in DM1 patients. CONCLUSION: Hyperleptinemia in DM1 is clearly linked to the concomitant hypogonadism. The genetic defect may directly or indirectly contribute to increased leptin levels. Increased exposure of cytokines may contribute to insulin resistance and other hormonal disturbances in DM1. (Less)
Please use this url to cite or link to this publication:
author
; ; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
resistance, insulin, testosterone, TNF receptor, TNF, myotonic dystrophy, leptin
in
International Journal of Obesity
volume
26
issue
10
pages
1386 - 1392
publisher
Nature Publishing Group
external identifiers
  • wos:000178571300015
  • pmid:12355336
  • scopus:0036799745
ISSN
1476-5497
DOI
10.1038/sj.ijo.0802078
language
English
LU publication?
yes
id
d262892e-2ae8-40a3-a83c-fda935d66170 (old id 325645)
date added to LUP
2016-04-01 12:30:59
date last changed
2024-01-08 23:10:13
@article{d262892e-2ae8-40a3-a83c-fda935d66170,
  abstract     = {{OBJECTIVE: To investigate the leptin and TNF systems in relation to testosterone in insulin resistant myotonic dystrophy (DM1) subjects. DESIGN AND SUBJECTS: Fasting morning samples and diurnal sampling during 24 h. Forty-two DM1 subjects (20 women and 22 men; age 41.5 (28.5-58.7)y, body mass index (BMI) 23.3 (18.6-29.2)kg/m(2); median and 10th and 90th percentile, respectively). Fifty healthy volunteers (23 women and 27 men; age 42 (27.0-56.9)y, BMI 24.0 (20.7-29.7) kg/m(2)). Nine men with DM1 and nine healthy men participated in diurnal sampling. MEASUREMENTS: Body composition was measured by bioelectric impedance analysis. Circulating levels of leptin, TNF-alpha, TNFR-II, insulin, testosterone and lipids were measured. The number of CTG triplet repeats was analysed. RESULTS: Basal as well as median 24 h levels of leptin and TNFR-II were significantly increased in DM1 patients, independent of body fat mass. This was associated with higher insulin and lower testosterone levels in DM1 patients. The genetic defect was related to leptin and TNFR-II levels in DM1 patients. CONCLUSION: Hyperleptinemia in DM1 is clearly linked to the concomitant hypogonadism. The genetic defect may directly or indirectly contribute to increased leptin levels. Increased exposure of cytokines may contribute to insulin resistance and other hormonal disturbances in DM1.}},
  author       = {{Johansson, A and Ahrén, Bo and Forsberg, H and Olsson, T}},
  issn         = {{1476-5497}},
  keywords     = {{resistance; insulin; testosterone; TNF receptor; TNF; myotonic dystrophy; leptin}},
  language     = {{eng}},
  number       = {{10}},
  pages        = {{1386--1392}},
  publisher    = {{Nature Publishing Group}},
  series       = {{International Journal of Obesity}},
  title        = {{Testosterone and diurnal rhythmicity of leptin, TNF-alpha and TNF-II receptor in insulin-resistant myotonic dystrophy patients}},
  url          = {{http://dx.doi.org/10.1038/sj.ijo.0802078}},
  doi          = {{10.1038/sj.ijo.0802078}},
  volume       = {{26}},
  year         = {{2002}},
}