Vanadium methyl-bipyridine organoligand and its influence on energy balance and organs mass

In the treatment of lifestyle diseases, including metabolic syndrome and type 2 diabetes, it is important to lower body mass and fat tissue, and consequently, to increase insulin-sensitivity. Unfortunately, it often happens that low- energy diet which would lower overweight is not observed and, thus, it does not bring the expected effects. This paper discusses the influence of three diets — control, high-fructose, and high-fatty diet — on absorption of energy from food in order to transform it into body mass. The kJ/g ratio which describes this process has been calculated. In the tested diets, the addition of fructose (79.13±2.47 kJ/g) or fat (82.48± 2.28 kJ/g) results in higher transformation of energy into body mass than in the case of control diet (89.60±1.86 kJ/g). The addition of Na[VO(O 2 ) 2 (4,4 ′ -Me 2 -2,2 ′ -bpy)] • 8H 2 O (where 4,4 ′ -Me 2 -2,2 ′ -bpy=4,4 ′ -dimethyl-2,2 ′ -bipyridine) results in sta- tistical increase of that ratio: fruct ose diet (86.88±0.44 kJ/g), fat diet (104.68±3.01 kJ/g), and control diet (115.98±0.56 kJ/g), respectively. Fat diet statistically influences the decrease of kidney mass in comparison to th e other diets. The application of the tested vanadium compound results also in the statistical decrease of the fatty liver caused by fructose and fat diet

Investigation of the influence of vanadium compounds treatment in NZO mice model : preliminary study

New Zealand obese mice (NZO) are characterized by symptoms similar to human metabolic syn- drome. Vanadium in different investigations showed anti-diabetic activity but until now an NZO mice model has not been tested with this element. The aim of this study was to investigate anti-diabetic activity of three vanadium compounds (VOSO 4 , VO(mal) 2 and Na(VO(O 2 ) 2 bpy)◊8H 2 O) in the NZO model. Metabolic syn- drome was induced by special diet (1.5% of cholesterol and 15% of saturated fatty acids) during 8 weeks. In the next 5 weeks, the tested vanadium compounds were administered once daily, in a dose of 0.063 mmol/kg of body mass. At the end of the experiment, glucose, cholesterol, triglycerides and alanine transaminase were measured in the serum. The obtained results showed that the glucose level was decreased nearly to the healthy NZO mice in comparison to the NZO mice with metabolic syndrome. In all groups on the diet with cholesterol, the level of this parameter was statistically higher in comparison to the group without cholesterol addition. Vanadium treatment in a dose 0.063 mmol/kg of body mass does not influence cholesterol, triglycerides and alanine transaminase activity

Alterations of bio-elements, oxidative, and inflammatory status in the zinc deficiency model in rats

Our previous study showed that dietary zinc restriction induces depression-like behavior with concomitant up-regulation of the N-methyl-d-aspartate receptor (NMDAR). Because metal ions, oxidative stress, and inflammation are involved in depression/NMDAR function, in the present study, bio-elements (zinc, copper, iron, magnesium, and calcium), oxidative (thiobarbituric acid-reactive substances; protein carbonyl content), and inflammatory (IL-1α, IL-1β) factors were measured in serum, hippocampus (Hp), and prefrontal cortex (PFC) of male Sprague–Dawley rats subjected to a zinc-adequate (ZnA) (50 mg Zn/kg) or a zinc-deficient (ZnD) (3 mg Zn/kg) diet for 4 or 6 weeks. Both periods of dietary zinc restriction reduced serum zinc and increased serum iron levels. At 4 weeks, lowered zinc level in the PFC and Hp as well as lowered iron level in the PFC of the ZnD rats was observed. At 6 weeks, however, iron level was increased in the PFC of these rats. Although at 6 weeks zinc level in the PFC did not differ between the ZnA and ZnD rats, extracellular zinc concentration after 100 mM KCl stimulation was reduced in the PFC of the ZnD rats and was accompanied by increased extracellular iron and glutamate levels (as measured by the in vivo microdialysis). The examined oxidative and inflammatory parameters were generally enhanced in the tissue of the ZnD animals. The obtained data suggest dynamic redistribution of bio-elements and enhancement of oxidative/inflammatory parameters after dietary zinc restriction, which may have a link with depression-like behavior/NMDAR function/neurodegeneration