Early atherogenesis and visceral fat in obese adolescents.

BACKGROUND/OBJECTIVES: Little information is available as to the cause of increased thickening of the intima-media of the carotid artery (cIMT) in the pediatric population. Therefore, cIMT was compared in obese adolescents and normal-weight controls, and associations between cIMT and lipid and non-lipid cardiovascular risk factors were assessed. SUBJECTS/METHODS: Subjects included 61 obese non-diabetic male and female volunteers aged 12-18 years inclusive with a body mass index (BMI) >95th percentile for age and 2-h blood glucose <200 mg dl(-1) matched to 25 normal-weight control volunteers with normal glucose levels. Each subject underwent a 2-h glucose tolerance test and measurement of hemoglobin A1c, ultrasensitive C-reactive protein, fasting insulin, blood lipids, visceral, subcutaneous abdominal and hepatic fat, and cIMT. RESULTS: Maximum cIMT was 0.647±0.075 mm in the obese subjects versus 0.579±0.027 mm in normal-weight controls (P<0.001). There was no difference in maximum cIMT between male and female subjects. There were significant correlations between maximum cIMT and BMI z-score, 2-h glucose, fasting insulin, homeostasis model assessment (HOMA), total low-density lipoprotein (LDL) cholesterol, very LDL cholesterol, high-density lipoprotein (HDL) cholesterol, HDL2 cholesterol, HDL3 cholesterol, triglycerides, remnant lipoprotein cholesterol, intermediate-density lipoprotein cholesterol, lipoprotein(a), apoprotein B100, abdominal subcutaneous fat volume, visceral fat volume and hepatic phase difference. On multiple regression analysis, visceral fat was the most significant predictor of maximum cIMT. Two-hour blood glucose, HOMA and systolic blood pressure were also significant predictors of maximum cIMT. CONCLUSIONS: cIMT was increased in the obese adolescents compared with the normal-weight-matched controls. Visceral fat was a key predictor of arterial wall thickening in these subjects. The results suggest that the focus of cardiovascular disease prevention in the adolescent obese should be visceral obesity, and not blood lipids or lipid subclasses.

Fatty liver disease, glucose tolerance and insulin resistance in obese adolescents.

BACKGROUND/OBJECTIVES: Adult studies suggest that intra-hepatic fat predicts 2-h blood glucose levels and type 2 diabetes, and may have a role in the development of insulin resistance. Our study objective was to explore relationships between intra-hepatic fat and (i) blood glucose levels and (ii) insulin resistance determined by homeostasis model assessment (HOMA) in a group of obese adolescents. METHODS: Subjects were 61 obese non-diabetic male and female volunteers aged 12-18 years inclusive with a body mass index >95th percentile for age and 2-h blood glucose <200 mg dL(-1) . Each subject underwent 2-h glucose tolerance testing and measurement of haemoglobin A1c, ultrasensitive C-reactive protein and fasting insulin. Visceral, subcutaneous abdominal and intra-hepatic fat were determined by magnetic resonance imaging. Intra-hepatic fat was measured by gradient echo chemical shift imaging. RESULTS: Alanine aminotransferase levels and hepatic phase difference were not significant correlates of fasting or 2-h glucose. In a multiple regression model including hepatic phase difference and visceral fat volume, visceral fat volume was the sole predictor of HOMA. CONCLUSIONS: This study provides no support to the notion that intra-hepatic fat has a role in the regulation of fasting blood glucose, 2-h postprandial blood glucose or systemic insulin resistance.

Availability of antenatal and perinatal care in an ICDS area.

PIP: During March-April 1991, in the Chaksu rural Integrated Child Development Services (ICDS) block near Jaipur, India, interviews were conducted with all lactating mothers living near the anganwadi centers of Kothoon, Shivdaspur, and Dehlala (subcenter level) and of Mahadevpura, Kareda-Khurz, and Sawai Jai Singh Pura (peripheral level) to determine availability of prenatal and perinatal care. 93.4% of the mothers were between 18 and 35 years old. 72.8% of all mothers received prenatal care with assistant nurse-midwives providing most of the prenatal care (39.7% of all mothers). 11% of mothers received their first prenatal care checkup during the first trimester. The figures for the second and third trimesters were 39.7% and 22.1%, respectively. 66.2% of all mothers received the tetanus toxoid (either 2 doses or a booster dose) during pregnancy. All mothers received labor and delivery care, mainly from untrained traditional birth attendants (54.4%) and from others (28.7%). 78.6% of deliveries occurred at home. 28.3% of mothers began breast feeding after 48 hours postpartum. Only 17.2% began breast feeding within 6 hours of birth. Only 11.7% received any postnatal care at all, with medical officers providing most of it (8.8% of all mothers). Most mothers did not receive any supplementary nutrition during pregnancy (64.7%) and during lactation (71.3%). Only 8.8% and 12.5% received supplementary nutrition regularly during pregnancy and during lactation, respectively. 50% of mothers received iron folic acid during pregnancy. Yet only 33.8% received it regularly. These findings suggest that prenatal checkups and complete tetanus toxoid immunization were adequate, but initiation of breast feeding and postnatal care were poor in this rural ICDS area.^ieng

Hereditary elliptocytosis due to both qualitative and quantitative defects in membrane skeletal protein 4.1.

Protein 4.1 is an important structural component of the membrane skeleton that helps determine erythrocyte morphology and membrane mechanical properties. In a previous study we identified a case of human hereditary elliptocytosis (HE) in which decreased membrane mechanical stability was due to deletion of 80 amino acids encompassing the entire 10-Kd spectrin-actin binding domain. A portion of this domain (21 amino acids) is encoded by an alternatively spliced exon that is expressed in late but not early erythroid cells. We now report a case of canine HE in which the abnormal phenotype is caused by failure to express this alternative peptide in the mature red blood cell (RBC) membrane skeleton, in conjunction with quantitative deficiency of protein 4.1. Western blotting of RBC membranes from a dog with HE showed a truncated protein 4.1 that did not react with antibodies directed against the alternative peptide. In addition, sequencing of cloned reticulocyte protein 4.1 cDNA showed a precise deletion of 63 nucleotides comprising this exon. Normal dog reticulocytes did express this exon. Expression of this 21 amino acid peptide during erythroid maturation is therefore essential for proper assembly of a mechanically competent membrane skeleton, because RBCs lacking this peptide have unstable membranes.