Epidemiological evidence against a role for C-reactive protein causing leptin resistance
(2013) In European Journal of Endocrinology 168(1). p.101-106- Abstract
- Objective: It has been suggested that elevated levels of C-reactive protein (CRP) might interfere with leptin signalling and contribute to leptin resistance. Our aim was to assess whether plasma levels of CRP influence leptin resistance in humans, and our hypothesis was that CRP levels would modify the cross-sectional relationships between leptin and measures of adiposity. Design and methods: We assessed four measures of adiposity: BMI, waist circumference, fat mass and body fat (%) in 2113 British Regional Heart Study (BRHS) men (mean (S.D.) age 69 (5) years), with replication in 760 (age 69 (6) years) European Male Ageing Study (EMAS) subjects. Results: In BRHS subjects, leptin correlated with CRP (Spearman's r=0.22, P<0.0001). Leptin... (More)
- Objective: It has been suggested that elevated levels of C-reactive protein (CRP) might interfere with leptin signalling and contribute to leptin resistance. Our aim was to assess whether plasma levels of CRP influence leptin resistance in humans, and our hypothesis was that CRP levels would modify the cross-sectional relationships between leptin and measures of adiposity. Design and methods: We assessed four measures of adiposity: BMI, waist circumference, fat mass and body fat (%) in 2113 British Regional Heart Study (BRHS) men (mean (S.D.) age 69 (5) years), with replication in 760 (age 69 (6) years) European Male Ageing Study (EMAS) subjects. Results: In BRHS subjects, leptin correlated with CRP (Spearman's r=0.22, P<0.0001). Leptin and CRP correlated with all four measures of adiposity (r value range: 0.22-0.57, all P<0.0001). Age-adjusted mean levels for adiposity measures increased in relation to leptin levels, but CRP level did not consistently influence the beta-coefficients of the regression lines in a CRP-stratified analysis. In BRHS subjects, the BMI vs leptin relationship demonstrated a weak statistical interaction with CRP (P=0.04). We observed no similar interaction in EMAS subjects and no significant interactions with other measures of adiposity in BRHS or EMAS cohorts. Conclusion: We have shown that plasma CRP has little influence on the relationship between measures of adiposity and serum leptin levels in these middle-aged and elderly male European cohorts. This study provides epidemiological evidence against CRP having a significant role in causing leptin resistance. European Journal of Endocrinology 168 101-106 (Less)
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- author
- organization
- publishing date
- 2013
- type
- Contribution to journal
- publication status
- published
- subject
- in
- European Journal of Endocrinology
- volume
- 168
- issue
- 1
- pages
- 101 - 106
- publisher
- Society of the European Journal of Endocrinology
- external identifiers
-
- wos:000312985200018
- scopus:84871952153
- pmid:23047304
- ISSN
- 1479-683X
- DOI
- 10.1530/EJE-12-0348
- language
- English
- LU publication?
- yes
- id
- 8fd8eccd-5b7a-435f-8904-e3668c1ddfbe (old id 3481072)
- date added to LUP
- 2016-04-01 10:45:54
- date last changed
- 2022-04-11 12:19:29
@article{8fd8eccd-5b7a-435f-8904-e3668c1ddfbe,
abstract = {{Objective: It has been suggested that elevated levels of C-reactive protein (CRP) might interfere with leptin signalling and contribute to leptin resistance. Our aim was to assess whether plasma levels of CRP influence leptin resistance in humans, and our hypothesis was that CRP levels would modify the cross-sectional relationships between leptin and measures of adiposity. Design and methods: We assessed four measures of adiposity: BMI, waist circumference, fat mass and body fat (%) in 2113 British Regional Heart Study (BRHS) men (mean (S.D.) age 69 (5) years), with replication in 760 (age 69 (6) years) European Male Ageing Study (EMAS) subjects. Results: In BRHS subjects, leptin correlated with CRP (Spearman's r=0.22, P<0.0001). Leptin and CRP correlated with all four measures of adiposity (r value range: 0.22-0.57, all P<0.0001). Age-adjusted mean levels for adiposity measures increased in relation to leptin levels, but CRP level did not consistently influence the beta-coefficients of the regression lines in a CRP-stratified analysis. In BRHS subjects, the BMI vs leptin relationship demonstrated a weak statistical interaction with CRP (P=0.04). We observed no similar interaction in EMAS subjects and no significant interactions with other measures of adiposity in BRHS or EMAS cohorts. Conclusion: We have shown that plasma CRP has little influence on the relationship between measures of adiposity and serum leptin levels in these middle-aged and elderly male European cohorts. This study provides epidemiological evidence against CRP having a significant role in causing leptin resistance. European Journal of Endocrinology 168 101-106}},
author = {{Rutter, M. K. and Sattar, N. and Tajar, A. and O'Neill, T. W. and Lee, D. M. and Bartfai, G. and Boonen, S. and Casanueva, F. F. and Finn, J. D. and Forti, G. and Giwercman, Aleksander and Han, T. S. and Huhtaniemi, I. T. and Kula, K. and Lean, M. E. J. and Pendleton, N. and Punab, M. and Silman, A. J. and Vanderschueren, D. and Lowe, G. and O'Rahilly, S. and Morris, R. W. and Wu, F. C. and Wannamethee, S. G.}},
issn = {{1479-683X}},
language = {{eng}},
number = {{1}},
pages = {{101--106}},
publisher = {{Society of the European Journal of Endocrinology}},
series = {{European Journal of Endocrinology}},
title = {{Epidemiological evidence against a role for C-reactive protein causing leptin resistance}},
url = {{http://dx.doi.org/10.1530/EJE-12-0348}},
doi = {{10.1530/EJE-12-0348}},
volume = {{168}},
year = {{2013}},
}