Elevated plasma interleukin-18 is a marker of insulin-resistance in type 2 diabetic and non-diabetic humans
Elevated plasma IL-18 is present in several conditions sharing insulin-resistance as common trait, but the association with insulin-resistance per se is not established. Plasma/serum IL-6, IL-18, TNF-α, soluble TNF receptor II (sTNFR2), and C-reactive protein (CRP) were measured in 97 patients with...
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| Vydáno v: | Clinical Immunology Ročník 117; číslo 2; s. 152 - 160 |
|---|---|
| Hlavní autoři: | , , , , |
| Médium: | Journal Article |
| Jazyk: | angličtina |
| Vydáno: |
San Diego, CA
Elsevier Inc
01.11.2005
Elsevier |
| Témata: | |
| ISSN: | 1521-6616, 1521-7035, 1365-2567 |
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| Abstract | Elevated plasma IL-18 is present in several conditions sharing insulin-resistance as common trait, but the association with insulin-resistance per se is not established. Plasma/serum IL-6, IL-18, TNF-α, soluble TNF receptor II (sTNFR2), and C-reactive protein (CRP) were measured in 97 patients with type 2 diabetes (DM) and 84 non-diabetic controls (CON). The association with insulin-resistance—estimated using the homeostasis model assessment (HOMA-IR)—was analyzed using multivariate linear and logistic regression. Compared to CON, DM demonstrated higher plasma levels of IL-18 (
P = 0.001), IL-6 (
P < 0.001), sTNFR2 (
P = 0.005), and CRP (
P < 0.001), while TNF-α was lower (
P = 0.017). Plasma IL-18 increased across HOMA-IR quartiles in both DM and CON, both with and without adjustment for confounders (all
P < 0.05). In contrast, neither IL-6, TNF-α, sTNFR2, nor CRP was associated with HOMA-IR in CON when adjusting for confounders. Accordingly, 50% increase of IL-18 corresponded to a marked increase of HOMA-IR in both DM and CON (DM: 26%,
P = 0.014; CON: 25%,
P = 0.003) after adjustment for confounders. Our results show that plasma IL-18 was associated with HOMA-IR independent of obesity and type 2 diabetes. |
|---|---|
| AbstractList | Elevated plasma IL-18 is present in several conditions sharing insulin-resistance as common trait, but the association with insulin-resistance per se is not established. Plasma/serum IL-6, IL-18, TNF-α, soluble TNF receptor II (sTNFR2), and C-reactive protein (CRP) were measured in 97 patients with type 2 diabetes (DM) and 84 non-diabetic controls (CON). The association with insulin-resistance—estimated using the homeostasis model assessment (HOMA-IR)—was analyzed using multivariate linear and logistic regression. Compared to CON, DM demonstrated higher plasma levels of IL-18 (
P = 0.001), IL-6 (
P < 0.001), sTNFR2 (
P = 0.005), and CRP (
P < 0.001), while TNF-α was lower (
P = 0.017). Plasma IL-18 increased across HOMA-IR quartiles in both DM and CON, both with and without adjustment for confounders (all
P < 0.05). In contrast, neither IL-6, TNF-α, sTNFR2, nor CRP was associated with HOMA-IR in CON when adjusting for confounders. Accordingly, 50% increase of IL-18 corresponded to a marked increase of HOMA-IR in both DM and CON (DM: 26%,
P = 0.014; CON: 25%,
P = 0.003) after adjustment for confounders. Our results show that plasma IL-18 was associated with HOMA-IR independent of obesity and type 2 diabetes. Elevated plasma IL-18 is present in several conditions sharing insulin-resistance as common trait, but the association with insulin-resistance per se is not established. Plasma/serum IL-6, IL-18, TNF- alpha , soluble TNF receptor II (sTNFR2), and C-reactive protein (CRP) were measured in 97 patients with type 2 diabetes (DM) and 84 non-diabetic controls (CON). The association with insulin-resistance-estimated using the homeostasis model assessment (HOMA-IR)-was analyzed using multivariate linear and logistic regression. Compared to CON, DM demonstrated higher plasma levels of IL-18 (P = 0.001), IL-6 (P < 0.001), sTNFR2 (P = 0.005), and CRP (P < 0.001), while TNF- alpha was lower (P = 0.017). Plasma IL-18 increased across HOMA-IR quartiles in both DM and CON, both with and without adjustment for confounders (all P < 0.05). In contrast, neither IL-6, TNF- alpha , sTNFR2, nor CRP was associated with HOMA-IR in CON when adjusting for confounders. Accordingly, 50% increase of IL-18 corresponded to a marked increase of HOMA-IR in both DM and CON (DM: 26%, P = 0.014; CON: 25%, P = 0.003) after adjustment for confounders. Our results show that plasma IL-18 was associated with HOMA-IR independent of obesity and type 2 diabetes. Elevated plasma IL-18 is present in several conditions sharing insulin-resistance as common trait, but the association with insulin-resistance per se is not established. Plasma/serum IL-6, IL-18, TNF-alpha, soluble TNF receptor II (sTNFR2), and C-reactive protein (CRP) were measured in 97 patients with type 2 diabetes (DM) and 84 non-diabetic controls (CON). The association with insulin-resistance-estimated using the homeostasis model assessment (HOMA-IR)-was analyzed using multivariate linear and logistic regression. Compared to CON, DM demonstrated higher plasma levels of IL-18 (P = 0.001), IL-6 (P < 0.001), sTNFR2 (P = 0.005), and CRP (P < 0.001), while TNF-alpha was lower (P = 0.017). Plasma IL-18 increased across HOMA-IR quartiles in both DM and CON, both with and without adjustment for confounders (all P < 0.05). In contrast, neither IL-6, TNF-alpha, sTNFR2, nor CRP was associated with HOMA-IR in CON when adjusting for confounders. Accordingly, 50% increase of IL-18 corresponded to a marked increase of HOMA-IR in both DM and CON (DM: 26%, P = 0.014; CON: 25%, P = 0.003) after adjustment for confounders. Our results show that plasma IL-18 was associated with HOMA-IR independent of obesity and type 2 diabetes.Elevated plasma IL-18 is present in several conditions sharing insulin-resistance as common trait, but the association with insulin-resistance per se is not established. Plasma/serum IL-6, IL-18, TNF-alpha, soluble TNF receptor II (sTNFR2), and C-reactive protein (CRP) were measured in 97 patients with type 2 diabetes (DM) and 84 non-diabetic controls (CON). The association with insulin-resistance-estimated using the homeostasis model assessment (HOMA-IR)-was analyzed using multivariate linear and logistic regression. Compared to CON, DM demonstrated higher plasma levels of IL-18 (P = 0.001), IL-6 (P < 0.001), sTNFR2 (P = 0.005), and CRP (P < 0.001), while TNF-alpha was lower (P = 0.017). Plasma IL-18 increased across HOMA-IR quartiles in both DM and CON, both with and without adjustment for confounders (all P < 0.05). In contrast, neither IL-6, TNF-alpha, sTNFR2, nor CRP was associated with HOMA-IR in CON when adjusting for confounders. Accordingly, 50% increase of IL-18 corresponded to a marked increase of HOMA-IR in both DM and CON (DM: 26%, P = 0.014; CON: 25%, P = 0.003) after adjustment for confounders. Our results show that plasma IL-18 was associated with HOMA-IR independent of obesity and type 2 diabetes. |
| Author | Perstrup, Lisbeth B. Berntsen, Annika Fischer, Christian P. Pedersen, Bente K. Eskildsen, Peter |
| Author_xml | – sequence: 1 givenname: Christian P. surname: Fischer fullname: Fischer, Christian P. email: cfischer@dadlnet.dk organization: Centre of Inflammation and Metabolism, The Department of Infectious Diseases and The Copenhagen Muscle Research Centre, Rigshospitalet and The Faculty of Health Sciences, University of Copenhagen, Blegdamsvej 9, Section M7641, DK-2100 Copenhagen, Denmark – sequence: 2 givenname: Lisbeth B. surname: Perstrup fullname: Perstrup, Lisbeth B. organization: The Department of Medicine, Roskilde County Hospital, Køge, Denmark – sequence: 3 givenname: Annika surname: Berntsen fullname: Berntsen, Annika organization: The Department of Medicine, Roskilde County Hospital, Køge, Denmark – sequence: 4 givenname: Peter surname: Eskildsen fullname: Eskildsen, Peter organization: The Department of Medicine, Roskilde County Hospital, Køge, Denmark – sequence: 5 givenname: Bente K. surname: Pedersen fullname: Pedersen, Bente K. organization: Centre of Inflammation and Metabolism, The Department of Infectious Diseases and The Copenhagen Muscle Research Centre, Rigshospitalet and The Faculty of Health Sciences, University of Copenhagen, Blegdamsvej 9, Section M7641, DK-2100 Copenhagen, Denmark |
| BackLink | http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=17206034$$DView record in Pascal Francis https://www.ncbi.nlm.nih.gov/pubmed/16112617$$D View this record in MEDLINE/PubMed |
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| Keywords | CRP SBP Type 2 diabetes Obesity OR Cytokines Inflammation Epidemiology IL-6 HDL HOMA-IR DBP TNF-α IL-18 sTNFR2 Insulin resistance TAG TZD Endocrinopathy Human Immunopathology Pancreatic hormone Cytokine Biological marker Metabolic diseases Insulin Interleukin 18 Blood plasma Target tissue resistance Immunology |
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| SubjectTerms | Biological and medical sciences Biomarkers - blood C-Reactive Protein - metabolism Case-Control Studies Cross-Sectional Studies Cytokines Diabetes Mellitus, Type 2 - blood Diabetes Mellitus, Type 2 - diagnosis Diabetes Mellitus, Type 2 - metabolism Epidemiology Female Fundamental and applied biological sciences. Psychology Fundamental immunology Humans Immunopathology Inflammation Insulin resistance Insulin Resistance - physiology Interleukin-18 - blood Interleukin-6 - blood Male Medical sciences Middle Aged Obesity Receptors, Tumor Necrosis Factor, Type II - blood Tumor Necrosis Factor-alpha - metabolism Type 2 diabetes |
| Title | Elevated plasma interleukin-18 is a marker of insulin-resistance in type 2 diabetic and non-diabetic humans |
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