Raquel Burrows

Effect of glycemic index on whole-body substrate oxidation in obese women

BACKGROUND:Glycemic index is hypothesized to determine fuel partitioning through serum plasma insulin modifications induced by dietary carbohydrates, thereby modulating fat accretion or oxidation.OBJECTIVE:To assess the glycemic effects on postprandial fuel oxidation and blood response.DESIGN:In all, 12 obese women were fed on a randomized crossover design with two test meals (breakfast+lunch). High- or low-glycemic meals were provided on separate days. Energy intake on high-glycemic meal was 7758±148 kJ and for low-glycemic meal was 7806±179 kJ. Carbohydrates supplied were 273±5 and 275±6 g, respectively. Macronutrient distribution was 55% carbohydrates, 30% fat and 15% protein. Fuel oxidation was measured continuously in a respiratory chamber for 10 h. Serum glucose, free fatty acids (FFA), insulin and glucagon samples were taken for 5 h after breakfast.RESULTS:Glucose AUC changed significantly in response to different glycemic breakfast. Low- vs high-glycemic breakfast was 211±84 and 379±164 mmol/l (P<0.05). Similarly, insulin changed from 94±37 and 170±87 nmol/l (P<0.05), respectively. The rate of increment for serum glucose and insulin reached by the high- vs low-glycemic meal was 1.8 times more with the high-glycemic breakfast. Serum FFA were similarly suppressed by both meal types by 3 h after meal intake, but then raised significantly more with the low-glycemic meal by the fourth and fifth hour (P<0.05). Plasma glucagon did not show a significant variation with glycemic index. Carbohydrate and fat oxidation was not modified by glycemic meal characteristics, being virtually the same for low- vs high-glycemic comparisons in the 5 h following breakfast and lunch (P=NS).CONCLUSION:This study demonstrates that dietary glycemic characteristics were unable to modify fuel partitioning in sedentary obese women.

Adolescent Metabolic Syndrome Risk Is Increased with Higher Infancy Weight Gain and Decreased with Longer Breast Feeding

Background. Prevalence of the metabolic syndrome is increasing in pediatric age groups worldwide. Meeting the criteria for the metabolic syndrome puts children at risk for later cardiovascular and metabolic disease. Methods. Using linear regression, we examined the association between infant weight gain from birth to 3 months and risk for the metabolic syndrome among 16- to 17-year-old Chilean adolescents (n = 357), accounting for the extent of breastfeeding in infancy and known covariates including gender, birth weight, and socioeconomic status. Results. Participants were approximately half male (51%), born at 40 weeks of gestation weighing 3.5 kg, and 48% were exclusively breastfed for ≥90 days. Factors independently associated with increased risk of metabolic syndrome in adolescence were faster weight gain in the first 3 months of life (B = 0.16, P < 0.05) and male gender (B = 0.24, P < 0.05). Breastfeeding as the sole source of milk for ≥90 days was associated with significantly decreased risk of metabolic syndrome (B = −0.16). Conclusion. This study adds to current knowledge about early infant growth and breastfeeding and their long-term health effects.

Melanocortin-4 receptor gene variants in Chilean families: association with childhood obesity and eating behavior

Abstract Objective: To screen for mutations in the coding region of the melanocortin-4 receptor (MC4R) gene and to assess the association between the rs17782313 variant near MC4R with childhood obesity and eating behavior. Subjects and methods: A cross-sectional sample of 221 obese Chilean children and 268 parents were incorporated in the study to assemble 134 case–parent trios. We performed direct sequencing of the MC4R coding region while the rs17782313 variant was genotyped by a Taqman assay. Eating behavior scores were calculated using the Child Eating Behavior and Three Factor Eating Questionnaires adapted for Chilean families. Results: A low frequency of genetic variation in the coding region of MC4R was found in Chilean obese children (Thr150Ile mutation and polymorphisms Ile251Leu and Val103Ile). The rs17782313 variant is possibly associated with satiety responsiveness (P = 0.01) and enjoyment of food scores (P = 0.03). Conclusion: The rs17782313 variant may influence eating behavior in obese children.

Melanocortin-3 receptor gene variants: Association with childhood obesity and eating behavior in Chilean families

OBJECTIVE To evaluate the association between melanocortin-3 receptor common genetic polymorphisms with childhood obesity and eating behavior in Chilean families. METHODS Two hundred twenty-nine obese children (6-12 y old, body mass index >95th percentile of Centers for Disease Control and Prevention/National Center for Health Statistics, 2000) and 270 parents were selected. Genotypes for MC3R genetic markers -239A>G, 17C>A (Thr6Lys), 241G>A (Val81Ile), +2138InsCAGACC, and microsatellite D20s32e were determined. Eating behavior scores were computed using the Child Eating Behavior Questionnaire and a shorter version of the Three Factor Eating Questionnaire adapted for evaluating eating inclinations in children. Genotype-obesity associations were assessed by the Transmission Disequilibrium Test. Non-parametric tests were used to compare eating behavior scores across study groups. RESULTS Allelic frequencies of -239G, 17A, 241A, and +2138InsCAGACC were estimated as 4.5%, 5.9%, 5.6%, and 17.6%, respectively, in obese children. The Transmission Disequilibrium Test in case-parent trios revealed no significant associations between childhood obesity and genetic markers, including the microsatellite D20s32e. In girls, we found significantly higher scores of the emotional eating subscale in carriers of the +2138InsCAGACC compared with non-carriers (P=0.04). In boys, carriers of 17A and 241A showed lower scores for the emotional eating subscale (P=0.01), whereas carriers of +2138InsCAGACC showed significantly lower scores for the enjoyment of food subscale compared with non-carriers (P=0.04). CONCLUSIONS There is not sufficient evidence to support the contribution for common melanocortin-3 receptor variants in childhood obesity. However, our results are concordant for a role of melanocortin-3 receptor variants in some dimensions of eating behavior such as emotional eating and enjoyment of food.

Healthy Chilean Adolescents with HOMA-IR ≥ 2.6 Have Increased Cardiometabolic Risk: Association with Genetic, Biological, and Environmental Factors

Objective. To determine the optimal cutoff of the homeostasis model assessment-insulin resistance (HOMA-IR) for diagnosis of the metabolic syndrome (MetS) in adolescents and examine whether insulin resistance (IR), determined by this method, was related to genetic, biological, and environmental factors. Methods. In 667 adolescents (16.8 ± 0.3 y), BMI, waist circumference, glucose, insulin, adiponectin, diet, and physical activity were measured. Fat and fat-free mass were assessed by dual-energy X-ray absorptiometry. Family history of type 2 diabetes (FHDM) was reported. We determined the optimal cutoff of HOMA-IR to diagnose MetS (IDF criteria) using ROC analysis. IR was defined as HOMA-IR values above the cutoff. We tested the influence of genetic, biological, and environmental factors on IR using logistic regression analyses. Results. Of the participants, 16% were obese and 9.4 % met criteria for MetS. The optimal cutoff for MetS diagnosis was a HOMA-IR value of 2.6. Based on this value, 16.3% of participants had IR. Adolescents with IR had a significantly higher prevalence of obesity, abdominal obesity, fasting hyperglycemia, and MetS compared to those who were not IR. FHDM, sarcopenia, obesity, and low adiponectin significantly increased the risk of IR. Conclusions. In adolescents, HOMA-IR ≥ 2.6 was associated with greater cardiometabolic risk.

Relationship of Adiposity and Insulin Resistance Mediated by Inflammation in a Group of Overweight and Obese Chilean Adolescents

The mild chronic inflammatory state associated with obesity may be an important link between adiposity and insulin resistance (IR). In a sample of 137 overweight and obese Chilean adolescents, we assessed associations between high-sensitivity C-reactive protein (hs-CRP), IR and adiposity; explored sex differences; and evaluated whether hs-CRP mediated the relationship between adiposity and IR. Positive relationships between hs-CRP, IR and 2 measures of adiposity were found. Hs-CRP was associated with waist circumference (WC) in boys and fat mass index (FMI) in girls. Using path analysis, we found that hs-CRP mediated the relationship between adiposity (WC and FMI) and the homeostatic model assessment of insulin resistance (HOMA-IR) (p < 0.05) in both sexes. Our novel finding is that inflammation statistically mediated the well described link between increased adiposity and IR.

High HOMA-IR, adjusted for puberty, relates to the metabolic syndrome in overweight and obese Chilean youths

Burrows RA, Leiva LB, Weisstaub G, Lera LM, Albala CB, Blanco E, Gahagan S. High HOMA‐IR, adjusted for puberty, relates to the metabolic syndrome in overweight and obese Chilean youths.

Obesity is associated with acute inflammation in a sample of adolescents

Obesity is associated with a mild chronic inflammatory response, which has been suggested to be pivotal in the development of cardiometabolic alterations of obesity. However, little is known about the involvement of acute inflammation.

The hypothalamic-pituitary-adrenal axis in infantile malnutrition.

We studied the circadian rhythm and the response of the hypothalamic‐pituitary‐adrenal (HPA) axis to ovine corticotrophin releasing hormone (oCRH) stimulation and dexamethasone suppression in 32 children with grade II‐III marasmus. Children were studied prior to and after nutritional rehabilitation. Mean baseline plasma cortisol concentrations were elevated at admission and decreased significantly after nutritional rehabilitation. Mean±SEM plasma cortisol response to oCRH increased from a basal of 480 ±41 to a peak of 582 ± 58 nmol/1 at the time of admission, and from a basal of 234±27 to a peak of 532±41 nmol/1 after caloric rehabilitation. Dexamethasone suppression in the malnourished group was associated with a decrease in the mean±SEM basal plasma cortisol concentration from 397±44 to 171 ±44 nmol/1. After caloric rehabilitation, basal cortisol levels decreased from 259±27 to 22±5 nmol/l following dexamethasone. Our results support the concept that malnutrition is associated with decreased responsiveness to oCRH and incomplete dexamethasone suppression, and that these abnormalities are restored after nutritional rehabilitation.

Effect of calcium and vitamin D supplementation on bone mineral density of celiac children

Abstract We were interested in detecting the changes in bone mineral density (BMD) in prepuberal and puberal celiac children after 24 months of supplementation with 1000 mg of calcium and 400 U of vitamin D daily. 19 celiac children (16 females, and 3 males, age 6 to 15 years) with good compliance to the gluten free diet for at least two years, paired with 19 healthly children of the same age and sex were studied. Celiac patients had mean calcium intakes of 739 mg per day, that increased to 1444 mg per day after nutritional supplementation, with 84 and 74% of compliance during the first and second years of supplementation. Celiac patients did not show significant changes in stature and nutritional status during supplementation. The whole group of celiac subjects showed a significant increase in z score of WB-BMD and FN-BMD from the start and until 24 months of supplementation, compared to the controls (WB-BMD: −0.24±0.40 and −0.80±0.59 vs 0.49±0.62 and 0.62±0.83. FN-BMD:−0.41±0.96 and 0.04±1.12 vs 0.58±1.29 and 0.36±1.15 respectively) Total group and pubertal celiac patients showed a significantly greater variation (delta z score) of hip BMD (FN-BMD 0.53 ± 0.85 p