Metabolic syndrome, insulin resistance and the inflammation markers C-reactive protein and ferritin

Abstract

Background: Patients with metabolic syndrome (MS) have above-average risk of developing atherosclerosis and cardiovascular disease. Inflammation plays a key role in the development of atherosclerosis. High levels of the acute phase reactants C-reactive protein (CRP) and ferritin have been reported to correlate with various components of MS. Patients and methods: The serum CRP, ferritin, glucose, insulin, triglycerides, HDL-cholesterol and total cholesterol concentrations of 598 obese or overweight patients were determined, together with relevant anthropometric parameters. Insulin resistance was evaluated by the HOMA method. MS was diagnosed using the ATP III criteria. Results: CRP levels were higher among patients with central obesity than in those without (5.8 vs 3.9 mg/l; P ¼ 0.003), and higher among those with fasting plasma glucose concentrations X110 mg/dl than in those with lower concentrations (7.4 vs 4.1 mg/l; P ¼ 0.01). Serum ferritin levels were higher among patients with triglyceride concentrations X150 mg/dl than in those with lower levels (76.8 vs 40.1 ng/ml; Po0.001), and higher among those with fasting plasma glucose concentrations X110 mg/dl than in those with lower concentrations (75.7 vs 41.7 ng/ml; P ¼ 0.005). The number of MS criteria that were satisfied increased with CRP and ferritin levels. Patients with insulin resistance also had higher CRP and ferritin levels than those without, 7.3 vs 4.3 mg/l for CRP (P ¼ 0.032) and 124.5 vs 80.1 ng/ml for ferritin (Po0.001). Conclusions: MS and insulin resistance are associated with elevated serum CRP and ferritin. Evaluation of subclinical chronic inflammation in patients with MS and/or insulin resistance by determination of these markers might aid in their evaluation as candidates for aggressive intervention against cardiovascular risk factors.

A Prospective Study ofTrans-Fatty Acid Levels in Blood and Risk of Prostate Cancer

“…This is a particularly important finding given that peroxisome proliferator-activated receptor-g can modulate both insulin resistance and inflammation (28) and is expressed in prostate tumors where its agonists have generally antiproliferative effects (28)(29)(30)(31). Moreover, the association between 18:2 trans fats and prostate cancer was apparently stronger among overweight and obese men, who may already be subject to increased insulin resistance and chronic inflammation (32,33), and among men who were not assigned to aspirin in the trial in our study and among carriers of the variant genotype of the RNASEL gene in other study (15), supporting the notion that trans-fatty acids may influence prostate carcinogenesis through these mechanisms.…”

Gamma-Glutamyl Transferase

“…Sialic acid (58) Uric acid (Salonen) (59) Ferritin (60,61) Ghrelin (62) Sex hormone-binding globulin (SHBG) (63) Triglycerides (50) Apolipoprotein CIII (64) Small LDL particles (50) Microalbuminuria (50) Soluble CD36 (65) Soluble CD40 ligand (66) Soluble P-selectin (66) *Inflammatory cytokines reported to be increased in in the metabolic syndrome include IL-6, IL-10, IL-18, and TNF alpha.…”

“…These include parameters of obesity and products released by adipose tissue, plasma insulin levels and insulin-like growth factors, liver enzymes, C-reactive protein and circulating metabolites, several components of circulating lipoproteins, microalbuminuria, and markers of increased cellular inflammation. [51][52][53][54][55][56][57][58][59][60][61][62][63][64][65][66] The status of these biomarkers as causative factors, either in generation of the metabolic syndrome or directly in atherogenesis, at present is uncertain. Some of them have been implicated as causes, but others as a reflection of a metabolic abnormality.…”

Postmenopausal Status as Independent Risk Factor for Metabolic Syndrome

“…Elevated levels of CRP are associated with an increased WC, 46 insulin resistance, 47 body mass index (BMI), and hyperglycemia 48 and increased with the number of MS components. It is more likely to be elevated in obese insulin-resistant, but not in obese insulin-sensitive subjects.…”