Kapriel Danadian

Determination of body composition in African-American children: validation of bioelectrical impedence with dual energy X-ray absorptiometry.

Body compositional differences between Black and White adults are well-known. It has become increasingly apparent that these racial variations may begin in childhood. Previously, our group validated tetrapolar bioelectrical impedance (BIA) measurements against H2(18O) dilution method to develop prediction formulas of fat free mass (FFM) in healthy White-American children: FFM = 0.524 Ht2/R + 0.415 Wt 0.32. In the present study we used BIA to establish a FFM prediction equation for forty African-American children (19 males and 21 females). Of the females, six were diagnosed with polycystic ovary syndrome (PCOS) and were obese. FFM was determined by dual energy X-ray absorptiometry (DEXA). Impedence measurements by BIA showed a strong correlation with FFM determined by DEXA. In healthy Black children, FFM = 0.84 Ht2/R + 1.10 with a standard error of estimate (SEE) of 1.47 kg (R2 = 0.97). In Black females with PCOS, FFM = 0.62 Ht2/R + 0.21 Wt - 1.94 with a SEE of 1.43 kg (R2 = 0.99). The observed differences in the prediction equations of FFM between White-American and African-American children underline the importance of using race-specific formulas in evaluating body composition. With the overall increase in rates of childhood obesity and more so in the Black race, BIA is an easy and useful tool for the assessment and follow up of body compositional changes with lifestyle interventions.

Insulin resistance of puberty in African-American children: lack of a compensatory increase in insulin secretion

Abtract: Type 2 diabetes has been increasing in children, mostly affecting minority populations at around the age of puberty. Despite a multitude of studies demonstrating pubertal insulin resistance/hyperinsulinemia in white children, data are almost non‐existent in African‐American children. The aim of the present study was to investigate the impact of puberty on glucose metabolism, insulin sensitivity and secretion in African‐American children. Twenty prepubertal and 16 pubertal African‐American subjects participated. All underwent a 3‐h hyperinsulinemic (40 mU/m2/min) euglycemic clamp to determine insulin‐stimulated glucose disposal, and a 2‐h hyperglycemic (12.5 mmol/L) clamp to assess first‐ and second‐phase insulin secretion. Body composition was assessed by dual energy X‐ray absorptiometry (DEXA) and visceral and subcutaneous abdominal adiposity with computed tomography (CT) scan at L4–L5. Total glucose disposal, glucose oxidation and non‐oxidative glucose disposal were significantly lower in the pubertal group compared with the prepubertal one (53.8 ± 3.9 vs. 72.2 ± 5.0 µmol/kg/min, p = 0.009; 23.3 ± 1.1 vs. 31.6 ± 1.7 µmol/kg/min, p = 0.001; and 30.0 ± 3.3 vs. 40.5 ± 3.9 µmol/kg/min, p = 0.049, respectively). Insulin sensitivity was ∼30% lower in the adolescents compared with the prepubertal children. However, first‐ and second‐phase insulin secretions were not different between the two groups (971.4 ± 180.6 vs. 1044.0 ± 191.4 pmol/L and 999.6 ± 159.6 vs. 955.8 ± 142.2 pmol/L, respectively). In conclusion, despite ∼30% lower insulin sensitivity in African‐American adolescents compared with prepubertal children, insulin secretion is not higher. This is in contrast to published findings in white children in whom insulin secretion is higher during puberty. These racial differences in physiologic adaptation to puberty could play a role in the higher prevalence of type 2 diabetes in African‐American children at the time of puberty.

Insulin Secretion, Insulin Sensitivity and Diabetes in Black Children

Historically, type 2 diabetes has been considered rare in the pediatric population. However, over the last decade, there has been a disturbing upswing in the rate of non-type 1 diabetes in the pediatric age group, particularly adolescents, with a greater proportion of Black children being affected. In this review, the following questions will be addressed: (1) what are the clinical characteristics of youth-onset atypical diabetes, (2) how common is it, (3) what are the risk factors, and (4) how should it be treated?

LEPTIN IN AFRICAN-AMERICAN CHILDREN

Leptin, the protein product of the obesity gene, produced by adipose tissue, regulates body weight and energy expenditure through CNS feedback mechanisms. In obesity, leptin levels are elevated suggestive of leptin resistance. Because of increased prevalence of obesity in African-Americans, the aim of this study was to assess leptin and its relationship to adiposity in African-American children. We measured plasma leptin levels in 42 African-American children (23 M, 19 F), age 11.8 +/- 0.3 yr, and compared them with 30 American-White children matched for age, body composition and puberty. Body composition was assessed by bioelectrical impedance and plasma leptin by RIA. Data are presented as means +/- SEM and statistical significance is implied by p < 0.05. There was no racial difference in plasma leptin levels (Blacks: 9.8 +/- 1.6, Whites 9.8 +/- 1.9 ng/ml). Leptin correlated with %BF in Black (r = 0.75, p = 0.005) and White (r = 0.79, p = 0.005) children. There were no gender or puberty related differences in leptin levels in African-American children. We concluded that leptin levels are comparable between African-American and American White children of similar body composition. The major determinant of serum leptin levels in these children is degree of adiposity with no gender or puberty related differences. Longitudinal studies are needed to assess leptins role during puberty in both genders.

GH Treatment in Adolescents with Non-GH Deficient Short Stature (NGHD-SS): Physical, Biochemical and Metabolic Changes

GH Treatment in Adolescents with Non-GH Deficient Short Stature (NGHD-SS): Physical, Biochemical and Metabolic Changes

Hyperglycemic Clamp: A Single Experiment to Simultaneously Assess Insulin Secretion and Insulin Sensitivity in Children † 420

Hyperglycemic Clamp: A Single Experiment to Simultaneously Assess Insulin Secretion and Insulin Sensitivity in Children † 420

Short-term pharmacologically induced growth study of ontogenetic allometry of oxygen uptake in children.

Background: A range of allometric coefficients have been proposed in describing the maximal oxygen uptake (VO2max): body mass relation in children using weight-bearing ergometry. However, a wide deviation in the allometric coefficients for VO2max may be apparent when selected pediatric cohorts are studied in conjunction with clinical intervention for growth abnormalities. Aim: The purpose of this study was to determine the allometric coefficients for VO2max after short-term pharmacologically induced growth in pre- and early pubescent children. Subjects and methods: The treatment group consisted of nine subjects with non-growth hormone (GH)-deficient short stature and one with GH-deficient short stature (mean age: 13.7 ± 1.7 years). Ten pre- and early pubescent children matched for age, height, weight, VO2max and body mass index (BMI) were controls. The treatment group were evaluated before (Pre-GH) and after (Post-GH) 4 months of subcutaneous GH therapy (0.05 mg kg−1day−1 × 6 days week−1). Results: The mean ontogenetic coefficient for the treatment group was 1.50 ± 0.20 and for the control group was 0.77 ± 0.34. The mean allometric coefficient for body mass relative to VO2max was significantly higher in the treatment group compared with the control group (p<0.05). Height, weight, fat free mass (FFM), VO2max indexed to body mass (mL kg−1 min−1) and FFM (mL kgFFM−1 min−1) increased (p<0.05) with GH therapy. GH therapy also increased insulin-like growth factor-I (IGF-I) and served as a biochemical marker of GH therapy (p<0.05). The control group had no significant differences in all the variables tested (p<0.05). Conclusion: The scaling for oxygen uptake (VO2) for body mass varies with GH treatment and the increase in VO2max that commonly occurs in conjunction with physical growth in the pre-and early pubescent individual may be linked to an increase in FFM and linear size. Résumé. Arrière plan: Une gamme de coefficients d’allométrie a été proposée pour décrire la relation entre consommation d’énergie maximum (VO2max) et masse corporelle, chez des enfants examinés par ergométrie avec charge pondérale. On observe cependant qu’une large déviation des coefficients d’allométrie pour le VO2max peut apparaître lorsque des cohortes pédiatriques sont étudiées pour les anomalies de la croissance, en conjonction avec une intervention clinique. But: Le but de cette étude est de déterminer les coefficients d’allométrie pour le VO2max à la suite d’une courte poussée de croissance induite par pharmacologie chez des enfants prépubères ou de puberté récente. Sujets et méthodes: Le groupe sous traitement consiste en neuf sujets de stature courte sans déficience d’hormone de croissance (HC) et d’un sujet de stature courte suite suite à une déficience de l’hormone de croissance (âge moyen : 13,7 ± 1,7 ans). On a pris comme contrôles, dix enfants prépubères et de puberté récente appariés pour l’âge, la stature, le poids, le VO2max et l’IMC. Le groupe en traitement a été évalué avant (Pré-HC) et après (post-HC) quatre mois d’injections d’HC sous cutanée (0,05 mg kg−1 jour−1 × 6 jours semaine−1). Résultats: Le coefficient ontogénique moyen pour le groupe sous traitement est de 1,50 ± 0,20 et pour le groupe de contrôle 0,77 ± 0,34. Le coefficient allométrique moyen pour la masse corporelle en rapport avec VO2max est significativement plus élevé dans le groupe traité que dans le groupe contrôle (p<0,05). La stature, le poids, la masse maigre, le VO2max rapporté à la masse corporelle (mL kg−1 min−1) et à la masse maigre (mL kg−1 min−1) s’accroissent avec la thérapie par HC (p < 0,05). La thérapie HC accroît également le facteur I de croissance insulino mimétique, lequel sert de marqueur biochimique de la thérapie HC (p < 0,05). Le groupe de contrôle ne présente pas de différence significative pour toutes les variables examinées (p < 0,05). Conclusion: L’échelle de VO2 en fonction de la masse corporelle, varie avec les traitement par HC et l’augmentation en VO2max qui se produit en général en conjonction avec la croissance physique chez l’individu prépubère ou pubère récent, peut être liée à l’accroissement de la masse maigre et de la taille linéaire. Zusammenfassung. Hintergrund: Eine Vielzahl allometrischer Koeffizienten ist vorgeschlagen worden, um die Relation von maximaler Sauerstoffaufnahme (VO2max) zu Körpermasse im Kindesalter unter Verwendung von gewichtsbezogener Ergometrie zu beschreiben. Allerdings wird eine weite Abweichung allometrischer Koeffizienten für VO2max offensichtlich, wenn ausgewählte pädiatrische Stichproben in Verbindung mit klinischen Interventionen bei Wachstumsstörungen untersucht werden. Ziel: Sinn dieser Studie war die Bestimmung von allometrischen Koeffizienten für VO2max nach kurzzeitigem medikamenteninduzierten Wachstum bei präpubertären Kindern und Kindern in der frühen Pubertät. Probanden und Methoden: Die Behandlungsgruppe bestand aus neun Probanden mit nicht-wachstumshormonbedingtem Kleinwuchs und einem Patienten mit Kleinwuchs aufgrund eines Wachstumshormonmangels (mittleres Alter: 13,7 ± 1,7 Jahre). Die Kontrollgruppe bestand aus zehn gleichaltrigen präpubertären Kindern und Kindern in der frühen Pubertät von vergleichbarer Körperhöhe und vergleichbarem Gewicht, VO2max und BMI. Die Behandlungsgruppe wurde vor (prä-GH) und nach (post-GH) 4-monatiger subkutaner Wachstumshormontherapie (0,05 mg kg−1 Tage–1 × 6 Tage Woche−1) untersucht. Ergebnisse: Der mittlere ontogenetische Koeffizient für die Behandlungsgruppe war 1,50 ± 0,20 und für die Kontrollgrupp.,77 ± 0,34. Der mittlere allometrische Koeffizient für Körpermasse relativ zu VO2max war in der Behandlungsgruppe signifikant höher als in der Kontrollgruppe (p < 0,05). Körperhöhe, Gewicht, fettfreie Masse (FFM), VO2max in Bezug zu Körpermasse (mL kg−1 min−1) und FFM (mL kg FFM−1 min−1) stiegen mit Wachstumshormontherapie (p < 0,05). Die Wachstumshormontherapie führte auch zu einem Anstieg des Insulin-like Growth Factor-I (IGF-I) und diente als biochemischer Marker der Wachstumshormontherapie (p < 0,05). Die Kontrollgruppe zeigte keine signifikanten Unterschiede bei den getesteten Variablen (p < 0,05). Zusammenfassung: Die Anpassung von VO2 an Körpermasse variiert mit der Wachstumshormontherapie, und der Anstieg von VO2max, der üblicherweise in Verbindung mit körperlichem Wachstum vor und zu Beginn der Pubertät auftritt, könnte mit einer Vermehrung von FFM und Körperlänge verknüpft sein. Resumen. Antecedentes: Se ha propuesto un rango de coeficientes alométricos para describir la relación entre el consumo máximo de oxígeno (VO2max) y la masa corporal en niños, utilizando la prueba de esfuerzo (ergometría “weight-bearing”). Sin embargo, puede ponerse de manifiesto una amplia desviación de los coeficientes alométricos para el VO2max cuando se estudian las cohortes pediátricas seleccionadas junto con la intervención clínica para las anomalías del crecimiento. Objetivo: El objetivo de este estudio fue determinar los coeficientes alométricos para el VO2max tras un crecimiento a corto plazo inducido farmacológicamente en niños pre-puberales y con pubertad temprana. Sujetos y métodos: El grupo de tratamiento consistió en nueve individuos con baja estatura no deficientes de hormona de crecimiento (GH) y uno con baja estatura y deficiente para la GH (edad media: 13,7 ± 1,7 años). Diez niños pre-puberales y con pubertad temprana de la misma edad, estatura, peso, VO2max e IMC fueron los controles. El grupo de tratamiento fue evaluado antes (Pre-GH) y después (Post-GH) de 4 meses de terapia subcutánea con GH (0,05 mg kg−1 día–1 × 6 días por semana−1). Resultados: El coeficientes ontogénico medio para el grupo de tratamiento fue de 1,50 ± 0,20 y para el grupo de control de 0,77 ± 0,34. El coeficiente alométrico medio para la masa corporal respecto al VO2max fue significativamente mayor en el grupo que recibía tratamiento que en el grupo control (p < 0,05). La estatura, el peso, la masa libre de grasa (FFM), el VO2max indexado para la masa corporal (mL kg−1 min−1) y la FFM (mL kg FFM−1 min−1) aumentaban (p < 0,05) con la terapia con GH. Esta terapia también incrementaba el factor de crecimiento semejante a la insulina tipo I (IGF-I) y sirvió como un marcador bioquímico de la terapia con GH (p < 0,05). El grupo de control no mostró diferencias significativas en ninguna de las variables testadas (p < 0,05). Conclusión: la escala del VO2max para la masa corporal varía con el tratamiento con GH; el incremento en el VO2max que ocurre habitualmente junto con el crecimiento físico en los individuos pre-puberales y de pubertad temprana puede estar asociado con un incremento de la FFM y del tamaño lineal.

Insulin Sensitivity in African-American Children with and without Family History of Type 2 Diabetes

OBJECTIVE African-Americans are at increased risk for type 2 diabetes. We have previously demonstrated that African-American children are hyperinsulinemic and insulin resistant compared with their white American peers. The aim of the present investigation was to assess the impact of family history of type 2 diabetes on insulin sensitivity in African-American children. RESEARCH DESIGN AND METHODS A total of 13 prepubertal healthy children with negative family history (FH-) and 9 with positive family history (FH+) of type 2 diabetes underwent a 3-h hyperinsulinemic (40 mU x m(-2) x min(-1))-euglycemic clamp study to assess insulin sensitivity. The groups were comparable for age, pubertal status, total body adiposity determined by dual-energy X-ray absorptiometry, abdominal adiposity assessed by computed tomography scan at the level of L4-5 lumbar vertebra, and physical fitness measured by maximal oxygen consumption (VO2max). RESULTS The FH+, compared with the FH-, group had lower insulin-stimulated glucose disposal (10.9+/-1.2 vs. 14.2+/-0.9 mg x kg(-1) x min(-1), P = 0.035) and lower nonoxidative glucose disposal (5.7+/-0.8 vs. 8.3+/-0.6 mg x kg(-1) x min(-1), P = 0.015), with no differences in rates of glucose oxidation, fat oxidation, or insulin-mediated free fatty acid suppression. Fasting hepatic glucose production assessed with [6,6-2H2]glucose and basal rates of glucose and fat oxidation were not different between the two groups. CONCLUSIONS These data suggest that in African-American children, family history of type 2 diabetes is a risk factor for insulin resistance. These children manifest important metabolic alterations, including impaired insulin-stimulated total and nonoxidative glucose disposal early in the first decade of life. We propose that this familial tendency, combined with environmental influences, could lead to type 2 diabetes decades later.

Sex Hormone Binding Globulin (SHBG) and Insulin-Like Growth Factor Binding Protein-1 (IGF-BP1) in Children with Acanthosis Nigricans: A Marker for Insulin Resistance and/or Hyperinsulinemia? † 452

Sex Hormone Binding Globulin (SHBG) and Insulin-Like Growth Factor Binding Protein-1 (IGF-BP1) in Children with Acanthosis Nigricans: A Marker for Insulin Resistance and/or Hyperinsulinemia? † 452

Central Adiposity and Insulin Sensitivity in Healthy African-American Children |[bull]| 411

Abdominal adiposity has been implicated as a risk factor for insulin resistance and NIDDM in adults. African-Americans (AA) are at increased risk for obesity, CVD, hypertension and NIDDM. We have shown that healthy AA children are insulin resistant and have higher insulin secretion compared with their White peers (J Pediatr 129:1996; J Clin Endocrinol Metab 82:1997). Moreover, AA children are more obese with central distribution of fat compared with their White peers. Therefore, the aim of the present investigation was to study the relationship of central obesity to insulin resistance in AA children. We studied 19 (10M, 9F) healthy AA prepubertal children, age (9.8±0.2 yrs), BMI (19.6±1.0 kg/m2). Body composition was assessed with DEXA, and abdominal adiposity by CT scan at the level of L4-5with measurements of subcutaneous adipose tissue (SAT) and visceral adipose tissue (VAT). Insulin action was assessed by a 3hr hyperinsulinemic (40mu/m2/min)-euglycemic clamp. Insulin stimulated glucose disposal (Rd) was calculated over the last 30 min of the clamp. Results: (mean ± SEM) However, in a multiple regression analysis SAT was the only significant determinant of Rd explaining 64% of its variability independent of%BF. Table