Does type 1 diabetes mellitus affect bone quality in prepubertal children?

Type 1 diabetes mellitus [T1DM] in children often starts before the achievement of peak bone mass. This may constitute a landmark in predicting bone fracture risk later in their lives. This study aims to determine the serum levels of bone markers in children with T1DM in combination with their bone mineral density [BMD]. Children diagnosed with T1DM for 3 years or more without signs of puberty were included in the diabetic group. Another group of age-matched healthy non-diabetic controls was recruited froma local school. The serum levels of a group of biochemical markers for bone formation and resorption were determined in both study groups, and BMD was measured by ultrasound absorptiometry. Thirty six children with T1DM and 39 normal children were included in this study. The results showed that 24/36 [66.7%] diabetic children had a Z score below zero. Of these, five scored below -1. In contrast, 12/39 [30.8%] children from the control group had a Z score below zero, but none had a score below -1. Significantly lower levels of osteocalcin and procollagen N-terminal peptide were detected in the diabetic group. The serum levels of bone resorption markers were significantly higher in the diabetic group. T1DM decreases BMD and some bone formation and increases some bone resorption biomarkers. BMD and bone markers are useful diagnostic tools for the early detection of alterations in the bone quality of children with T1DM. This, if treated in a timely manner, may decrease future bone fracture susceptibility

Changes in the expression of hepatic cytochrome P450 isoenzymes 2E1, 2B1/2, 4A, and 2C6 in mice infected with different levels of schistosoma mansoni cercariae

Most xenobiotic agents are metabolized by cytochrome P450 system. In the present study, Western blotting was used to investigate the effect of different levels of Schistosoma mansoni infection on the expression of somr cytochrome P450 isozymes [CYP 2E1, 2B1/2, 2C6, 4A], and to enzyme assay their related metabolic functions in mouse liver microsomes. Male mice were infected with 60, 120, 180, 300, and 600 S. mansoni cercariae per mouse for 33 days and compared with control. The signal intensity for CYP 2E1 was greatly increased over the control at 60,120, 180, and 300 cercariae/mouse with no change at the last level of S. mansoni infection. Also, the expression of CYP 4A was potentially induced at all levels of S. mansoni infection. A significant induction of CYP 2B1/2 expression was observed at all levels of S. mansoni infection with loss of signal at 180 cercariae/mouse. In contrast, CYP 2C6 expression was induced at the first two levels and such expression was decreased at the last three levels. In addition, Infection of mouse with 60, 120, and 180 cercariae/mouse decreased; [1] 7-methoxycoumarin O-demethylase activity by 36, 54, and 58% respectively; [2] 7-ethoxycoumarin O-deethylase activity by 33, 40, and 57% respectively; [3] coumarin hydroxylase activity by 35, 45, and 55% respectively. However, 300 and 600 cercariae/mouse induced: [1] 7-methoxycoumarin O-demethylase activity by 45 and 97% respectively; [2]; 7-ethoxycoumarin O-deethylase activity by 26 and 90% respectively; [3] coumarin hydroxylase activity by 100 and 200% respectively. In addition, all levels of S. mansoni infection decreased the sleeping time caused by hexobarbital. It is concluded that different levels of S. mansoni infection change the expression of different CYP isozymes and that these alterations could enhance the carcinogenicity of N-nitrosamines which is mainly dependent on CYP 2E1. The alterations in the expression of CYP 2E1, 4A and 2B1/2 isozymes as a result of S. mansoni infection may change the therapeutic actions of drugs that are primarily metabolized by the P450 system, when administered to patients with schistosomiasis

Multiplicity of Schistosoma mansoni infection changed the activity of ATPases and the levels of free radical in the liver of male mice

The present study was carried out to investigate the influence of Schistosoma mansoni infection on the levels of thiobarbituric acid- reactive substances [TBARS] as free radicals and on the activity of Na+, K+ -ATPase and Ca+2, Mg+2 -ATPase in the livers and brains of male mice after 33 days of infection with 60, 120, 180 and 300 cercariae/mouse. The study showed that the levels of free radicals increased with increasing the intensity of S. mansoni infection. There was a correlation between the increment of free radical levels and the inhibition of different types of ATPase activity of S. mansoni-infected mice. In addition, this study also provided a new possible mechanism of liver damage caused by schistosome through induction of free radical levels. The results demonstrated that the activity of ATPase decreased and the level of free radicals [TBARS] increased at all levels of S. mansoni infection. The deleterious effect of free radicals on the liver and other possible organs could be increased, especially at higher intensity of S. mansoni infection. These alterations might be one of the factors associated with the etiology of liver damage, which are commonly encountered in schistosomal patients