Atherogenic indices and prehypertension in obese and non-obese children.

We evaluate the relationship between different lipoproteins and atherogenic indices with pre-hypertension in 297 obese and 942 non-obese children with Tanner stage 1 enrolled in a multicentre, community-based cross-sectional study. Height, weight, fasting glucose and insulin levels, total cholesterol, triglycerides, high-density lipoprotein cholesterol (HDL-c), low-density lipoprotein cholesterol (LDL-c), non-HDL-c, LDL/HDL-c, triglycerides/cholesterol and total cholesterol/HDL-c ratios were measured. Mean age was 8.4 ± 1.2 years; pre-hypertension was identified in 104 (8.4%) participants, 46 (15.5%) obese and 58 (6.1%) non-obese children. The pre-hypertensive non-obese children show a high proportion of family history of hypertension (41.6 and 24.7%, p = 0.002) and elevation of insulin at a relatively low body mass index. The triglycerides:HDL-c ratio, but not other lipoproteins or atherogenic indices, was associated with pre-hypertension in obese (1.15, 95% confidence intervals 1.06-1.26) and non-obese children (1.38 95% confidence intervals 1.22-1.57). The triglycerides:HDL-c ratio is related to pre-hypertension in children; the family history of hypertension seems to be a risk factor in developing pre-hypertension.

Changes in the antioxidant defence and in selenium concentration in tissues of vanadium exposed rats.

Vanadium is an element whose role as a micronutrient for humans is not yet completely established, but which has been shown to possess hypoglycaemic properties in diabetes. In an earlier study, we showed that in STZ-diabetic rats, exposure to 1 mg V per day has no effect on glycaemia or on antioxidant status. When the exposure was raised to 3 mg V per day there was a hypoglycaemic effect, together with reduced Se in the tissues, which reduced antioxidant defences. The aim of the present study was to examine whether exposure to 1 mg V per day modifies Se nutritional status and/or antioxidant defences in healthy rats. Two groups of rats were examined: control and vanadium-treated. Vanadium, as bis(maltolato)oxovanadium(iv), was supplied in the drinking water. The experiment had a duration of five weeks. Selenium was measured in excreta, serum, skeletal muscle, kidneys, liver, heart, femur and adipose tissue. Number of red (RBC) and white (WBC) blood cells and haemoglobin (Hb) were determined in samples of whole blood. Glutathione peroxidase (GPx), glutathione transferase (GST), catalase (CAT) and NAD(P)H:quinine-oxidoreductase1 (NQO1) activity, and malondialdehyde (MDA) in the liver were evaluated. Treatment significantly reduced food intake, produced an anaemic state, and decreased Se absorption and Se content in serum, kidneys and the liver. GPx, GST and NQO1 activity were decreased in the liver, while MDA levels rose. We conclude that healthy rats are more sensitive than diabetic ones to the effects of V. This should be taken into account for populations that are particularly exposed to V for environmental reasons, and/or that consume V as a nutritional supplement.

Effect of bis(maltolato)oxovanadium (IV) (BMOV) on selenium nutritional status in diabetic streptozotocin rats.

The role of V as a micronutrient, and its hypoglycaemic and toxicological activity, have yet to be completely established. The present study focuses on changes in the bioavailability and tissue distribution of Se in diabetic streptozotocin rats following treatment with V. The following four study groups were examined: control; diabetic (DM); diabetic treated with 1 mg V/d (DMV); diabetic treated with 3 mg V/d (DMVH). V was supplied in the drinking water as bis(maltolato)oxovanadium (IV). The experiment had a duration of 5 weeks. Se was measured in food, faeces, urine, serum, muscle, kidney, liver and spleen. Glucose and insulin serum were studied, together with glutathione peroxidase (GSH-Px), glutathione reductase (GR), glutathione transferase (GST) activity and malondialdehyde (MDA) levels in the liver. In the DM group, we recorded higher levels of food intake, Se absorbed, Se retained, Se content in the kidney, liver and spleen, GSH-Px and GST activity, in comparison with the control rats. In the DMV group, there was a significant decrease in food intake, Se absorbed, Se retained and Se content in the liver and spleen, and in GSH-Px and GST activity, while fasting glycaemia and MDA remained unchanged, in comparison with the DM group. In the DMVH group, there was a significant decrease in food intake, glycaemia, Se absorbed, Se retained, Se content in the kidney, liver and spleen, and in GSH-Px and GST activity, and increased MDA, in comparison with the DM and DMV groups. We conclude that under the experimental conditions described, the treatment with 3 mg V/d caused a tissue depletion of Se that compromised Se nutritional status and antioxidant defences in the tissues.

Severe hypomagnesemia and low-grade inflammation in metabolic syndrome.

To evaluate the association between severe hypomagnesemia and the low-grade inflammatory response in subjects with metabolic syndrome (MetS), ninety-eight individuals with new diagnosis of MetS were enrolled in a cross-sectional study. Pregnancy, smoking, alcohol intake, renal damage, hepatic disorders, infectious or chronic inflammatory diseases, malignancy, use of diuretics, statins, calcium antagonist, antioxidants, vitamins, anti-inflammatory drugs, or previous oral magnesium supplementation were exclusion criteria. According serum magnesium levels, participants were assigned to the following groups: 1) severe hypomagnesemia (≤1.2 mg/dL); 2) hypomagnesemia (>1.2≤1.8 mg/dL); 3) Normal serum magnesium levels (>1.8 mg/dL). The low-grade inflammatory response was defined by elevation of serum levels of (hsCRP >1.0 ≤10.0 mg/L) or TNF-alpha (TNF-α ≥3.5 pg/mL). Severe hypomagnesemia, hypomagnesemia, and normomagnesemia were identified in 21 (21.4%), 38 (38.8%), and 39 (39.8%) individuals. The ORs, adjusted by WC, showed that severe hypomagnesemia (OR: 8.1; CI 95%: 3.6-19.4 and OR: 3.7; CI 95%: 1.1-12.1), but not hypomagnesemia (OR: 1.8; CI 95%: 0.9-15.5 and OR: 1.6; CI 95%: 0.7-3.6), was strongly associated with elevated hsCRP and TNF-α levels, and that normomagnesemia exhibited a protective role (OR: 0.32; CI 95%: 0.1-0.7 and OR: 0.28; CI 95%: 0.1-0.6) for elevation of CRP and TNF-α. Results of this study show that, in subjects with MetS, severe hypomagnesemia, but not hypomagnesemia, is associated with elevated concentrations of CRP and TNF-α.