Retinol Binding Protein-4 and Adiponectin Levels in Thyroid Overt and Subclinical Dysfunction.

Thyroid dysfunction is accompanied by numerous changes in intermediary metabolism. Retinol binding protein-4 (RBP-4) and adiponectin are 2 adipocytokines that have multiple metabolic functions. The aim of our study was to examine serum RBP4 and adiponectin levels in clinical (before and after therapy) and subclinical hyperthyroid and hypothyroid subjects as compared to controls.150 patients with thyroid dysfunction were recruited (65 hyperthyroid and 85 hypothyroid) while 28 euthyroid subjects served as a control group. We measured anthropometric, biochemical and hormonal (free T4, free T3, TSH, insulin) parameters in all participants. RBP-4 and adiponectin were measured using commercial ELISA kits.Mean baseline levels of RBP-4 were higher in patients with clinical hypothyroidism (29.0±10.2 ng/ml, 25.1±12.6 ng/ml, 38.8±16.5 ng/ml, 31.9±13.2 ng/ml, 20.4±8.2 ng/ml in patients with hyperthyroidism, subclinical hyperthryrodism, hypothyroidism, subclinical hypothyroidism and controls respectively, F=4.86, P<0.001) and decreased significantly in patients with clinical hyperthyroidism and hypothyroidism after normalization of thyroid hormones' levels (from 29.0±10.2 to 24.9±8.4 ng/ml, p=0.003 and from 38.8±16.5 to 29.0±10.8 ng/ml, p=0.001 respectively). We did not observe analogous changes in adiponectin levels in any of the studied groups.RBP-4 levels are higher in patients with clinical hypothyroidism and exhibit a marked decrease after normalization of thyroid function in both hyper and hypothyroid patients. We suggest that RBP-4 may play a role in the metabolic disturbances which accompany thyroid dysfunction.

Monocyte chemoattractant protein 1 is correlated with glycemic control and peripheral arterial disease in type 2 diabetic patients with metabolic syndrome.

We evaluated the serum levels of monocyte chemoattractant protein 1 (MCP-1) and their association with peripheral arterial disease (PAD) in 199 patients with type 2 diabetes mellitus (T2DM) and metabolic syndrome ([MetS], group A) in comparison with 109 healthy controls (group B). In group A, MCP-1 levels were significantly (P < .001) higher than group B and exhibited a positive correlation with HbA1c (P < .001) and a negative correlation with ankle-brachial index (P < .001). In the same group, patients with PAD had significantly higher MCP-1 levels compared with those without PAD (P < .001). In conclusion, T2DM patients with MetS exhibit higher serum MCP-1 levels. The latter is associated with worse glycemic control and PAD. These results suggest a potential contributory role for MCP-1 in the pathogenesis of PAD in the presence of hyperglycemia and MetS in T2DM.

Post-thyroidectomy thyroxine replacement dose in patients with or without compensated heart failure: the role of cytokines.

OBJECTIVE: To investigate the potential association between serum inflammatory cytokine levels and post-thyroidectomy thyroxine replacement dose in patients with or without compensated heart failure. PATIENTS AND METHODS: The study included 42 patients (group A: 20 men, mean age of 54.5+/-6.8 years) with NYHA I or II heart failure and 54 patients (group B: 25 men, mean age of 52.9+/-7.1 years) without heart failure. All patients had undergone total thyroidectomy and were euthyroid on a stable thyroxine replacement dose. Serum Interleukin-1b (IL-1b), Tumor Necrosis Factor alpha (TNF-alpha), Interleukin-6 (IL-6), TSH, T3, T4, fT3 and fT4 were measured. RESULTS: Both groups exhibited a significant positive correlation between IL-6 and levothyroxine replacement dosage (group A: r=0.708, p<0.001; group B: r=0.345, p=0.012) and a negative correlation between IL-6 and T3 (group A: r=-0.342, p=0.023, group B: r=-0.294, p=0.035). Significant independent predictors of levothyroxine replacement dosage were IL-6 (p<0.001) and TNF-alpha (p=0.007) in group A (58.3% of dosage variation) and only IL-6 (p=0.012) in group B (10.1% of dosage variation). CONCLUSIONS: In both groups, a significant positive correlation was observed between IL-6 and levothyroxine replacement dosage, but this correlation was stronger in group A. In the same group, there was evidence for a more pronounced influence of cytokines on levothyroxine dosage.

Serum magnesium levels in non-diabetic offspring of patients with Type 2 diabetes mellitus.

A tendency for magnesium deficiency in patients with diabetes mellitus is well established, which probably results from glycosuria-related hypermagnesiuria, nutritional factors or hyperinsulinaemia. Hypomagnesaemia is probably a secondary event but it can also lead to insulin resistance itself. The offspring of patients with Type 2 diabetes mellitus (T2DM) are at increased risk of developing diabetes and several metabolic abnormalities of the disease. The aim of this study was to determine if serum total magnesium levels in healthy offspring of T2DM patients underwent alterations and their relationship to indicators of glucose homeostasis. The sample consisted of two groups: 30 healthy offspring with at least one diabetic parent, and 30 age-matched healthy subjects with no family history of T2DM. None of the participants was on a diet. The mean serum magnesium concentration was 1.070 +/- 0.059 mmol/l in offspring and 1.075 +/- 0.084 mmol/l in controls (p=0.66). There was no statistically significant correlation between serum magnesium levels and parameters of glucose homeostasis in offspring. Our results support the conclusion that total serum magnesium probably has no relationship with the main indicators of glucose homeostasis in offspring of T2DM patients and is not likely to be a fundamental risk factor for the development of insulin resistance.