Document Detail


Inflammation-associated insulin resistance: differential effects in rheumatoid arthritis and systemic lupus erythematosus define potential mechanisms.
MedLine Citation:
PMID:  18576352     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
OBJECTIVE: Insulin resistance is increased by inflammation, but the mechanisms are unclear. The present study was undertaken to test the hypothesis that decreased insulin sensitivity is differentially associated with mediators of inflammation by studying 2 chronic inflammatory diseases of different pathogenesis, systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA).
METHODS: We measured fasting insulin, glucose, and lipid levels, erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), interleukin-6 (IL-6), tumor necrosis factor alpha (TNFalpha), and coronary artery calcification in 103 patients with SLE and in 124 patients with RA. Insulin sensitivity was measured using the homeostasis model assessment (HOMA) index.
RESULTS: The HOMA value was higher in RA patients (median 2.05 [interquartile range (IQR) 1.05-3.54]) than in SLE patients (1.40 [0.78-2.59]) (P = 0.007). CRP and ESR did not differ significantly in RA and SLE patients. Body mass index (BMI) was significantly correlated with the HOMA index in both RA (rho = 0.20) and SLE (rho = 0.54), independently of age, sex, race, and current use of corticosteroids. In RA patients, the HOMA index was also significantly positively correlated with IL-6 (rho = 0.63), TNFalpha (rho = 0.50), CRP (rho = 0.29), ESR (rho = 0.26), coronary calcification (rho = 0.26), and Disease Activity Score in 28 joints (rho = 0.21); associations adjusted for age, sex, race, BMI, and current use of corticosteroids remained significant (P < 0.05). In SLE patients, the HOMA index was also significantly correlated with ESR (rho = 0.35) and CRP (rho = 0.25), but not with other variables. The association between the ESR and the HOMA value in patients with SLE remained significant after adjustment for confounding covariates (P = 0.008). In multivariable models, the major contributing factors to the HOMA index were the BMI in SLE patients, and IL-6 and TNFalpha levels in RA patients.
CONCLUSION: The pathogenesis of insulin resistance and its contribution to atherogenesis varies in different inflammatory settings.
Authors:
Cecilia P Chung; Annette Oeser; Joseph F Solus; Tebeb Gebretsadik; Ayumi Shintani; Ingrid Avalos; Tuulikki Sokka; Paolo Raggi; Theodore Pincus; C Michael Stein
Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, N.I.H., Extramural    
Journal Detail:
Title:  Arthritis and rheumatism     Volume:  58     ISSN:  0004-3591     ISO Abbreviation:  Arthritis Rheum.     Publication Date:  2008 Jul 
Date Detail:
Created Date:  2008-07-15     Completed Date:  2008-08-08     Revised Date:  2014-09-18    
Medline Journal Info:
Nlm Unique ID:  0370605     Medline TA:  Arthritis Rheum     Country:  United States    
Other Details:
Languages:  eng     Pagination:  2105-12     Citation Subset:  AIM; IM    
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MeSH Terms
Descriptor/Qualifier:
Adult
Arthritis, Rheumatoid / immunology*,  physiopathology
Blood Glucose
Blood Sedimentation
C-Reactive Protein / analysis,  immunology
Calcinosis / blood,  immunology
Coronary Artery Disease / blood,  immunology
Female
Humans
Inflammation / blood,  physiopathology*
Insulin / blood
Insulin Resistance / immunology*
Interleukin-6 / blood,  immunology
Lupus Erythematosus, Systemic / immunology*,  physiopathology
Male
Middle Aged
Tumor Necrosis Factor-alpha / blood,  immunology
Grant Support
ID/Acronym/Agency:
GM5-M01-RR-00095/GM/NIGMS NIH HHS; HL-04012/HL/NHLBI NIH HHS; HL-65082/HL/NHLBI NIH HHS; HL-67964/HL/NHLBI NIH HHS; K24 HL004012/HL/NHLBI NIH HHS; K24 HL004012-09/HL/NHLBI NIH HHS; R01 HL065082/HL/NHLBI NIH HHS; R01 HL065082-08/HL/NHLBI NIH HHS; R01 HL067964/HL/NHLBI NIH HHS; R01 HL067964-04/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Blood Glucose; 0/Insulin; 0/Interleukin-6; 0/Tumor Necrosis Factor-alpha; 9007-41-4/C-Reactive Protein
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