ABSTRACT
Adiponectin and resist in are fat cell-derived hormones, which are thought to be respectively protective and disadvantageous with regard to the development of cardiovascular disease and diabetes mellitus type 2. The aim is to study the relationship between insulin resistance and serum adiponectin and resistin in obese children. A total of 60 obese and 30 nonobese children were enrolled and serum levels of adiponectin and resistin were measured by enzyme immunoassay. Compared with controls, higher insulin resistance by homeostasis model [HOMA-lR] and lower whole body insulin sensitivity index [WBISI] were found in obese children [all p=0.000]. The acliponectin levels in obese children and controls were 3.41 +/- 1.93 and 5.21 +/- 3.1 micro g/L with a significant difference [p=0. 001], while the difference of resistin levels was not significant [p=0.963]. Significant correlations between insulin resistance parameters [HOMA-lR and WBISI] and age, sexual development, body mass index, serum triglyceride, HDL-cholesterol, LDL-cholesterol, alanine aminotransferase, uric acid, or adiponectin levels [all p<0.05] were noted. On the other hand there was no significant correlation between insulin resistance parameters and serum levels of resistin[p>0.05]. In conclusion, These results suggest that adiponectin may play a protective role in obese children through decreasing insulin resistance
Subject(s)
Humans , Male , Female , Adiponectin/blood , Resistin/blood , Child , Insulin Resistance , Body Mass Index , Cholesterol/blood , Triglycerides/bloodABSTRACT
Antenatal carnitine administration has been shown to induce fetal lung maturity by increasing pulmonary surfactant in animal and human studies. In this study, the aim was to investigate the status of carnitine in maternal and neonatal plasma of preterm infants with respiratory distress syndrome [RDS] in the first hours of life. We also aimed to characterize the carnitine status in these neonates with respect to sex, gestational age, birth weight, mode of delivery, and antenatal corticosteroid administration. Maternal plasma-free carnitine levels were determined before delivery and neonatal plasma-free carnitine levels were determined within 2 h of birth in preterm infants = 34 weeks gestational age] who developed RDS in the first 6 h of life and in the control group. The results showed that the mean neonatal plasma-free carnitine level was significantly lower in preterm infants with RDS than in the control group [19.96 +/- 5.77 micro mol/L, and 37.9 +/- 5.77 micro mol/L, respectively; p = 0.001] while the mean maternal plasma-free carnitine levels were similar in both groups [33.28 +/- 9.58 micro mol/L, and 37.3 +/- 9.55 micro mol/L, respectively; p = 0.168]. Neonatal plasma-free carnitine levels correlated negatively with gestational age and birth weight in the RDS group [r = -0.512; p = 0.009 and r = -0.476; p = 0.016], and in the control group [r = -0.869; p = 0.0001 and r = -0.810; p-0.0001]. Sex, mode of delivery, and antenatal corticosteroid administration had no statistically significant effect on the level of plasma-free carnitine in the studied preterm infants. Low neonatal plasma-free carnitine levels in preterm infants with RDS maybe due to decreased maternal-fetal transfer of carnitine or to increased consumption of carnitine in fetal lung tissue for surfactant synthesis. This could be contributing factor in the pathogenesis of RDS in preterm infants
Subject(s)
Humans , Male , Female , Infant, Premature , Carnitine/blood , Gestational Age , Birth WeightABSTRACT
Management of short bowel syndrome is a challenge in the postoperative period due to defect in the absorptive surface area which leads to diarrhea with loss of a large amount of fluids and nutrients that necessitates specific enteral and parenteral nutrition. These manifestations improve when the process of intestinal adaptation starts. There is a controversy about the role of growth hormone in accelerating the process of intestinal adaptation. In this study, 24 patients with short bowel syndrome were divided into two groups. The first group consists of 14 patients received growth hormone and a second group consists of 10 patients that didn't receive growth hormone. In both groups, enteral and parenteral nutrition, loperamide to delay intestinal motility and ranitidine in the first week to decrease gastric hypersecretion were given. The beginning of intestinal adaptation beside histological examination of the intestine was compared in both groups. Growth hormone appeared to have a positive effect on accelerating the intestinal adaptation in short bowel syndrome clinically. The histological examination which was done 3-6 months postoperatively revealed increase of the length of the villi with thickened mucosa in both groups without significant difference because, most probably, the histological study was done after the intestinal adaptation has started in both groups