Insulin sensitivity indices: Fasting versus glucose-stimulated ýndices in pediatric non-alcoholic fatty liver disease

OBJECTIVE: We aimed to compare insulin sensitivity indices, fasting vs glucose stimulated, in children and adolescents with non-alcoholic fatty liver disease. PATIENTS AND METHODS: Two hundredeleven obese children with median age of 11.24 ± 2.65 years were evaluated. After initial clinical and anthropometric examination, B-mode ultrasonography (USG) was performed and all subjects underwent Oral Glucose Tolerance Test (OGTT). Quantitative insulin sensitivity check index (QUICKI), homeostatic model assessment for insulin resistance (Homa-IR), the insulinogenic index (IGI), the Matsuda index, and the oral glucose insulin sensitivity (OGIS) model were used to determine peripheral insulin sensitivity. RESULTS: 59.24% (68 boys, 57 girls) of obese children had NALFD. The prevalence of FLD in obese adolescents was significantly higher than in prepubertal children (65.8% vs. 51.5%). Fasting glucose, insulin, Homa-IR, QUICKI, and OGIS and Matsuda were significantly different between subjects with and without NALFD. Insulin and glucose indices were not found to be significantly different in the prepubertal group, whereas Homa-IR, QUICKI, Matsuda, and OGIS were significantly different in the pubertal group. Age, waist circumference, and OUICKI were found to be risk factors associated with the presence of NALFD in the logistic-regression analysis. CONCLUSIONS: Age, waist circumference, and OUICKI were found to be risk factors associated with NALFD. As the value of QUICKI decreases, the probability of having steatosis increases. Although OGTT results gave the information about the glucose tolerance of a subject, indices derived from OGTT were not found to be superior to the traditional surrogates such as Homa-IR or QUICKI

Mutations in FGF17, IL17RD, DUSP6, SPRY4, and FLRT3 Are Identified in Individuals with Congenital Hypogonadotropic Hypogonadism

Congenital hypogonadotropic hypogonadism (CHH) and its anosmia-associated form (Kallmann syndrome [KS]) are genetically heterogeneous. Among the >15 genes implicated in these conditions, mutations in FGF8 and FGFR1 account for ∼12% of cases; notably, KAL1 and HS6ST1 are also involved in FGFR1 signaling and can be mutated in CHH. We therefore hypothesized that mutations in genes encoding a broader range of modulators of the FGFR1 pathway might contribute to the genetics of CHH as causal or modifier mutations. Thus, we aimed to (1) investigate whether CHH individuals harbor mutations in members of the so-called "FGF8 synexpression" group and (2) validate the ability of a bioinformatics algorithm on the basis of protein-protein interactome data (interactome-based affiliation scoring [IBAS]) to identify high-quality candidate genes. On the basis of sequence homology, expression, and structural and functional data, seven genes were selected and sequenced in 386 unrelated CHH individuals and 155 controls. Except for FGF18 and SPRY2, all other genes were found to be mutated in CHH individuals: FGF17 (n = 3 individuals), IL17RD (n = 8), DUSP6 (n = 5), SPRY4 (n = 14), and FLRT3 (n = 3). Independently, IBAS predicted FGF17 and IL17RD as the two top candidates in the entire proteome on the basis of a statistical test of their protein-protein interaction patterns to proteins known to be altered in CHH. Most of the FGF17 and IL17RD mutations altered protein function in vitro. IL17RD mutations were found only in KS individuals and were strongly linked to hearing loss (6/8 individuals). Mutations in genes encoding components of the FGF pathway are associated with complex modes of CHH inheritance and act primarily as contributors to an oligogenic genetic architecture underlying CHH

Inaugural Charles River World Congress on Animal Models in Drug Discovery and Development

https://deepblue.lib.umich.edu/bitstream/2027.42/138112/1/12967_2017_Article_1274.pd

A Type of Pyles Metaphyseal Dysplasia (Or Simulation Questionable) - a Case-Report

WOS: A1983QQ2870011

A Case-Report - a Variety of Pyles Metaphyseal Dysplasia Or Simulating

WOS: A1983QP3420011

The effects of thiamine on glucose consumption in normal and malnourished infants

This study was done on 10 normal (in view of their nutritional and vitamin supplementation) children and 10 children with expected thiamine deficiency. The cases were between 3 and 25 mth of age. In these 2 groups an oral glucose loading of 1.75 gm./Kg. of body weight was done and 2 hr later blood glucose, lactic and pyruvic acids, blood gases and pH values were determined in the venous blood. Once again the next day the same determinations were made 2 hr after an equal amount of glucose loading together with an i.m. injection of 100 mg. of thiamine. The statistical analysis of the results is given. When oral glucose loadings were done together with the injection of thiamine it was seen that glucose is used in the body more conservatively. In normal children and in children with thiamine deficiency after an oral glucose loading with thiamine (parenterally) the results were found altered. In malnourished children pH and blood gas analysis showed that glucose utilization and formation of basic constituents and metabolites from glucose are less than they are in normal children. (Journal received: 17 MAY 1974

The effect of pyridoxine on glucose consumption in normal and malnourished infants

[No abstract available

One hour effect of vitamin D2 in normal children and in children with rickets - I. (Alterations in the renal venous and arterial blood)

Before and one hour after the administration of 600,000 i. u. of calciferol heparinized renal venous and arterial blood samples are drawn from 15 normal and 25 rachitic children. Hematocrit, plasma proteins, sodium, potassium, chloride and CO2 determinations are done and the alterations in the water and electrolyte balance are investigated. A non significant decrease of 1-2% in the hematocrit values of all the cases and the significant decrease of the plasma proteins in the rachitic cases in the renal venous blood show that Vitamin D is effective on the water and electrolyte equilibria in rickets within a one hour period. The arteriovenous difference of chloride is significant in the group of normals before Vitamin D and a chloride filtration at the renal level is demonstrated. In cases of mild rickets the arteriovenous difference is significant and a sodium filtration at the renal level is demonstrated. After the administration of Vitamin D this loss of sodium disappears. The arteriovenous alterations in the plasma CO2 confirm the failure in the acidification capacity in cases of mild rickets. This increase in CO2 in the systemic blood with the 1 hour effect of Vitamin D is shown to be due to the displacement of bicarbonate by phosphate in the labile compartment on the crystal surface. Renal disorder in the acid-base metabolism in cases of mild rickets is seen. The 1 hour effect of vitamin D demonstrates some alterations at the renal level. A pre renal event which increases the plasma CO2 is suggested