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To assess the relationships between insulin resistance and low-grade inflammation in subjects with type 1 diabetes mellitus (T1DM) who do not have clinical macrovascular complications. A total of 120 subjects diagnosed with T1DM 14 years before were evaluated for the following: (1) sex, age, body mass index, waist-to-hip ratio (WHR), blood pressure, smoking, alcohol intake, insulin dose, HbA1c and lipid profile; (2) microvascular complications; (3) plasma concentrations of soluble fractions of tumour necrosis factor-α receptors type 1 and 2, interleukin-6, adiponectin, leptin and high-sensitivity C-reactive protein (hs-CRP); and (4) insulin resistance (estimation of the glucose disposal rate-eGDR). Those subjects with an eGDR below the median of the same sex group were classified as insulin resistant and the others as insulin sensitive. Insulin-resistant men, compared to the insulin-sensitive, had higher WHR (0.89 ± 0.08 vs. 0.83 ± 0.05; P < 0.01), higher systolic [121 (118-125) vs. 114 (108-120) mmHg; P = 0.01] and diastolic [73 (66-80) vs. 67 (70-73) mmHg; P = 0.02] blood pressures, higher HbA1c values [8.7 (8.1-9.9) vs. 7.5 (7.2-8.0) %; P < 0.01] and higher hs-CRP concentrations [1.16 (0.61-3.20) vs. 0.49 (0.31-0.82) mg/dl; P = 0.01], but no other significant differences between groups were found. Insulin-resistant women had higher WHR and HbA1c values, compared to the insulin-sensitive, but they did not have any other differences. In men, hs-CRP correlated significantly with WHR and HbA1c (r = 0.363; P = 0.016 and r = 0.317; P = 0.036, respectively), after adjusting for age, alcohol intake, smoking and microvascular complications. Insulin-resistant men with T1DM have an increase in plasma concentrations of hs-CRP. Central obesity and HbA1c are its main determinants.

Objective: The objective of this study was to evaluate plasma visfatin levels in thyroid dysfunction and its relationship with inflammatory, anthropometric and insulin resistance parameters., Design and Patients: Twenty-four hyperthyroid and 27 hypothyroid patients were studied before and after treatment. Forty-five euthyroid subjects were used as control group., Measurements: Fasting plasma visfatin, IL-6, C reactive protein, adiponectin, thyroid hormones, waist-to-hip ratio, BMI, percentage of body fat and homeostasis model insulin resistance index (HOMA-IR) were measured., Results: Hyperthyroid patients showed increased insulin resistance, IL-6 and visfatin levels compared with controls (3.21 +/- 3.0 vs. 1.67 +/- 0.75, P = 0.022; 3.35 +/- 0.41 vs. 2.10 +/- 0.25 pg/ml, P = 0.016; and 37.4 +/- 5.81 vs. 23.79 +/- 4.2 ng/ml, P = 0.061 respectively). After normalization of thyroid function, IL-6 levels and HOMA-IR decreased (2.35 +/- 0.37 vs. 2.10 +/- 0.25 pg/ml, P = 0.045 and 3.21 +/- 0.60 vs. 2.28 +/- 0.38, P = 0.032 respectively), while body weight, adiposity and visfatin levels increased (26.1 +/- 1.2 vs. 26.7 +/- 1.2 kg/m(2), P = 0.049; 30.9 +/- 1.6 vs. 32.2 +/- 1.6%, P = 0.007; and 37.4 +/- 5.81 vs. 63.13 +/- 8.72 ng/ml, P = 0.047 respectively). C reactive protein and adiponectin levels were similar to those of the control group. Hypothyroid patients showed high visfatin levels (40.59 +/- 3.07 vs. 29.34 +/- 4.9 ng/ml, P = 0.049) that increased after treatment (81.4 +/- 9.2 ng/ml, P = 0.001) without changes in anthropometric or insulin resistance parameters. C reactive protein, IL-6 and adiponectin levels were similar to those of the control group. No correlations between visfatin and any analysed parameter were found in either hyper- or hypothyroidism., Conclusion: Visfatin exhibits a marked increase after normalization of thyroid function in both hyper and hypothyroid patients. We suggest that visfatin may play a role in the hormone stabilization process independent of anthropometric, inflammatory or insulin resistance variables.

Aims/hypothesis: Decreased sensing of the innate immune system may lead to chronic activation of the inflammatory cascade. We hypothesised that mannan-binding lectin (MBL) deficiency may confer risk of obesity and insulin resistance., Materials and Methods: We performed a cross-sectional study of MBL protein concentration (n=434) and MBL2 gene mutations (exon 1) (n=759) in association with obesity, markers of inflammation and insulin action (euglycaemic clamp, n=113), and a longitudinal study of MBL protein before and after weight loss in obese patients (n=10). We also studied the effects of MBL in vitro in muscle cells and circulating MBL-A (mouse equivalent of human MBL) in a mouse model., Results: Among 434 consecutive non-diabetic men, the age-adjusted serum MBL concentration was lower in obese subjects than in lean subjects (median: 959 microg/ml [interquartile range: 116.8-2,044 microg/ml] vs 1,365 [467-2,513] microg/ml; p=0.01) and was accompanied by increased serum inflammatory markers. Insulin action correlated significantly with serum MBL (r=0.49, p<0.0001). Serum MBL concentration increased by a median of 110.2% after weight loss. The change in serum concentration of MBL was positively associated with the increase in insulin sensitivity (r=0.713, p=0.021). At least one MBL2 gene mutation was present in 48.2% of obese vs 39.3% of non-obese subjects (p=0.037). The plasma concentration of MBL-A was lower in insulin-resistant obese ob/ob mice, as was the glucose/insulin ratio. Incubation of rat soleus muscle with human MBL markedly increased fatty acid oxidation., Conclusions/interpretation: These findings suggest that MBL, previously thought only to be involved in inflammation and immune system function, affects metabolic pathways.