Dara Schuster

Childhood obesity: a risk factor for injuries observed at a level-1 trauma center

PURPOSE Obesity is an independent risk factor in trauma-related morbidity in adults. The purpose of this study was to investigate the effect of obesity in the pediatric trauma population. METHODS All patients (6-20 years) between January 2004 and July 2007 were retrospectively reviewed and defined as non-obese (body mass index [BMI] <95th percentile for age) or obese (BMI > or =95th percentile for age). Groups were compared for differences in demographics, initial vital signs, mechanisms of injury, length of stay, intensive care unit stay, ventilator days, Injury Severity Score, operative procedures, and clinical outcomes. RESULTS Of 1314 patients analyzed, there were 1020 (77%) nonobese patients (mean BMI = 18.8 kg/m(2)) and 294 (23%) obese patients (mean BMI = 29.7 kg/m(2)). There was no significant difference in sex, heart rate, length of stay, intensive care unit days, ventilator days, Injury Severity Score, and mortality between the groups. The obese children were significantly younger than the nonobese children (10.9 +/- 3.3 vs 11.5 +/- 3.5 years; P = .008) and had a higher systolic blood pressure during initial evaluation (128 +/- 17 vs 124 +/- 16 mm Hg, P < .001). In addition, the obese group had a higher incidence of extremity fractures (55% vs 40%; P < .001) and orthopedic surgical intervention (42% vs 30%; P < .001) but a lower incidence of closed head injury (12% vs 18%; P = .013) and intraabdominal injuries (6% vs 11%; P = .023). Evaluation of complications showed a higher incidence of decubitus ulcers (P = .043) and deep vein thrombosis (P = .008) in the obese group. CONCLUSION In pediatric trauma patients, obesity may be a risk factor for sustaining an extremity fracture requiring operative intervention and having a higher risk for certain complications (ie, deep venous thrombosis [DVT] and decubitus ulcers) despite having a lower incidence of intracranial and intraabdominal injuries. Results are similar to reports examining the effect(s) of obesity on the adult population.

Pathogenetic Mechanisms of Impaired Glucose Tolerance and Type II Diabetes in African-Americans: The significance of insulin secretion, insulin sensitivity, and glucose effectiveness

OBJECTIVE To examine the significance of alterations in insulin sensitivity index (S1), glucose effectiveness (Sg), and β-cell function in the pathogenesis of type II diabetes in African-Americans with varying degrees of glucose intolerance. RESEARCH DESIGN AND METHODS A total of 154 African-Americans residing in Franklin County, Ohio, were studied. There were 101 subjects with normal glucose tolerance (NGT), 36 with impaired glucose tolerance (IGT), and 17 with type II diabetes. An oral glucose tolerance test (OGTT) was performed on each subject. S1 and Sg were measured by insulin-modified, frequently sampled intravenous glucose tolerance test (FSIGT). RESULTS The mean fasting and postprandial serum glucose levels were significantly greater in the diabetic groups when compared with the IGT and NGT groups. In contrast, while fasting serum insulin and C-peptide levels tended to be greater in the type II diabetic and IGT groups, the postprandial responses were blunted at 30 min in the IGT and type II diabetic groups when compared with the NGT group. The mean acute first-phase insulin release after intravenous glucose was blunted also in the IGT and type II diabetic groups when compared with the NGT group. The S1 was significantly lower in the IGT (1.51 ± 0.19) and type II diabetic (0.61 ± 0.15) groups when compared with the NGT group (2.94 ± 0.20 × 10−4 · min−1 · μU−1 · ml−1). The Sg was not significantly different in the NGT (2.90 ± 0.20), IGT (2.47 ± 0.19), and the type II diabetic (2.35 ± 0.15 × 10−2/min) groups. The glucose effectiveness at theoretical zero insulin concentration (GEZI) followed similar patterns as the Sg. Furthermore, the basal insulin effect (BIE) was significantly lower in the IGT and type II diabetic groups compared with the NGT group. In addition, the glucose decay constant (Kg) was significantly lower (P < 0.001) in the IGT (1.21 ± 0.13) and the type II diabetic (1.07 ± 0.12) groups when compared with the NGT group (2.03 ± 0.10% per minute). CONCLUSIONS Our present study demonstrates that African-American patients with IGT and mild type II diabetes have significant reduction in β-cell function, insulin sensitivity, and BEI but have normal and intact Sg and GEZI when compared with NGT subjects. We conclude the following: 1) a reduction in Sg does not appear to play a significant role in the pathogenetic mechanism of IGT and type II diabetes in African-American patients, and 2) the intact Sg in the IGT and type II diabetic groups could serve as a compensatory mechanism for hyperglycemia in African-Americans.

Race and ethnicity determine serum insulin and C-peptide concentrations and hepatic insulin extraction and insulin clearance : Comparative studies of three populations of West African ancestry and white Americans

We examined the importance of ethnicity in terms of beta-cell secretion and hepatic insulin extraction (HIE) and insulin clearance (IC) to peripheral insulin levels before and after stimulation in three populations of West African ancestry, namely African-Americans, Ghanaian immigrants, and native Ghanaians living in diverse environments, and white Americans. Following 10 to 12 hours of overnight fasting, each subject ingested a 75-g oral glucose load. Blood samples for determination of serum glucose, insulin, and C-peptide were obtained at baseline and after the oral glucose load at 30-minute intervals for 240 minutes. Basal HIE and IC were calculated as the molar ratios of C-peptide and insulin concentrations at basal steady state, and postprandial values as molar ratios of the incremental integrated C-peptide and insulin areas. Clinical characteristics of the patients were not significantly different among the four groups. During the fasting and postprandial state, serum glucose levels were not significantly different among the four groups. Surprisingly, the mean fasting insulin concentration was significantly greater in native Ghanaians (21.19 +/- 0.93 microU/mL, P < .05) than in African-Americans (11.90 +/- 1.02,microU/ML), Ghanaian immigrants (8.14 +/- 0.96 microU/mL), and white Americans (7.03 +/- 0.78 microU/mL). Following the oral glucose load, the mean serum peak and incremental integrated areas of insulin were significantly (P < .05) greater in native Ghanaians, African-Americans, and Ghanaian immigrants compared with white Americans. In contrast, there were no significant differences in postprandial serum insulin responses among the three groups of West African ancestry, irrespective of country of origin or residence. Despite the higher insulin concentrations in blacks of West African ancestry compared with whites, the corresponding basal and postprandial serum C-peptide levels were not significantly different among the four groups. Mean basal and postprandial HIE and IC were significantly (P < .05 to .01) reduced (25% to 52%) in the three populations of West African ancestry compared with the white Americans, but these values were not significantly different among the West African descendants. When comparing metabolic responses in obese (body mass index [BMI] > 27 kg/m2) and non-obese (BMI < 27 kg/m2) native Ghanaians, we found no significant differences in fasting insulin, C-peptide, and basal HIE or IC. Also, there were no significant relations between fasting and postprandial serum insulin, obesity indices, and HIE and IC in any of the groups. In summary, our study demonstrates that glucose-tolerant native Ghanaians, Ghanaian immigrants, and African-Americans of West African ancestry manifest hyperinsulinemia and a decreased HIE and IC compared with white Americans. We conclude that race and ethnicity may be the major determinants of the mechanism(s) of beta-cell secretion, insulin action, and peripheral insulin levels and HIE or IC in humans. We speculate that the lower HIE and IC in blacks of West African descent appears to be a highly conserved metabolic trait irrespective of the country of residence.

Effects of race and ethnicity on insulin sensitivity, blood pressure, and heart rate in three ethnic populations : Comparative studies in African-Americans, African immigrants (Ghanaians), and white Americans using ambulatory blood pressure monitoring

We sought to examine the association of insulin, insulin sensitivity, and blood pressure using ambulatory blood pressure monitor in three ethnically distinct populations. The study population comprised the following. Group 1 (n = 31): African-Americans; Group 2 (n = 27): recent African immigrants; and Group 3 (n = 31): white Americans who were residing in Franklin County, Ohio. Quantitative insulin sensitivity index (Si) was obtained using the minimal model method in both groups of African ancestry and white Americans. The mean insulin sensitivity index (Si) was similar in the African-Americans (3.23 +/- 0.47 x (10)-4 x [min-l x microU/mL (-1)])(-l) and African immigrants (2.53 +/- 0.27). However, these Si values were significantly (P < .01) lower in people of African ancestry than in white Americans (6.56 +/- 1.07). The mean systolic (SBP) and diastolic blood pressure (DBP) and heart rates (HR) during 24-h and daytime periods were not significantly different in the African-Americans and African immigrants. During the night, whereas the mean SBP was not different in the three groups, DBP and HR were significantly (P < .05) higher in both groups of African ancestry than in white Americans. However, we found no significant relationships among serum insulin levels, insulin sensitivity, and ambulatory blood pressure (systolic and diastolic and mean arterial pressure) and heart rates in any of the groups. In summary, our present study demonstrates that people of African ancestry manifest 1) significantly lower insulin sensitivity indices and 2) blunted physiologic reduction in nocturnal DBP and HR when compared to white Americans who reside in the same environment. We speculate that these chronobiological alterations in BP and HR in blacks appear to be genetically determined.

Cardiovascular Effects of Type 1 Diabetes Mellitus in Children

Previous studies have shown that type 1 diabetes mellitus (DM) is associated with cardiovascular abnormalities. Early detection and treatment of these abnormalities may help to prevent the natural progression of the disease. The present study was undertaken to define early cardiovascular abnormalities in children with type 1 DM. Simultaneous evaluation of multiple cardiovascular parameters was performed in 14 children with type 1 DM and 14 age- and gender-matched normal subjects. Measurements of carotid artery intima-media thickness (cIMT, echocardiography), carotid and aortic (ascending and abdominal) distensibility (echocardiography, brachial artery blood pressure), aortic pulse wave velocity (carotid to femoral artery, Doppler), and left ventricular dimensions, mass, and function (echocardiography) were performed. Diabetic children demonstrated a greater cIMT (0.36 ±0.04 mm vs 0.31 ±0.03 mm, p=0.002) and decreased carotid artery distensibility (4.4 ±1.6 cm2·dynes-1·10-6 vs 6.0 ±1.9 cm2·dynes-1·10-6, p<0.01) compared to control. Aortic pulse wave velocity was increased in DM (6.70 ±0.39 vs 6.30 ±0.31, p=0.02) compared to control. Left ventricular diameters, mass, and systolic and diastolic function did not differ between the 2 groups. Simultaneous assessment of multiple cardiovascular parameters in children with type 1 DM revealed impaired carotid artery structure and function, and decreased elastic properties of the aorta, before demonstrable changes in left ventricular structure and function could be detected.

Differential Impact of Obesity on Glucose Metabolism in Black and White American Adolescents

BACKGROUND The authors have previously demonstrated abnormalities in glucose and insulin metabolism in nondiabetic black American (BA) adults versus white American (WA) adults. Whether similar glucoregulatory alterations extend to BA adolescents remain unknown. In addition, obesity, a known risk factor for insulin resistance and hyperinsulinemia, occurs in a greater proportion of BA adults and children when compared to WA. The objective of the present study was to examine the differential effects of obesity on glucose homeostasis in BA and WA adolescents. METHODS We examined glucose homeostasis in BA and WA adolescents using oral glucose tolerance test (OGTT), intravenous glucose tolerance test (IVGTT), and [6,6-2H2]-glucose infusion. The study consisted of four age-, sex-, and pubertal stage-matched groups: 15 lean BA, 29 lean WA, 7 obese BA, and 9 obese WA. RESULTS Both obese groups had significantly increased insulin and C-peptide area under the curve (AUC) during OGTT and IVGTT when compared to their same-race lean counterparts. During OGTT, obese BA demonstrated greater insulin and C-peptide when compared to obese WA. During IVGTT, first- and second-phase insulin were significantly greater in obese BA versus obese WA. CONCLUSION In summary, BA adolescents demonstrated insulin resistance which is markedly exaggerated in the face of obesity when compared to WA adolescents, implying a differential impact for obesity on glucose homeostasis that is unique to the obese BA adolescent group. In conclusion, there is a need for early aggressive weight management in obese BA adolescents.

The Impact of Socioeconomic Status on Cardiovascular Risk Factors in African-Americans at High Risk for Type II Diabetes: Implications for syndrome X

OBJECTIVE The rate of type II diabetes in African-Americans is reaching epidemic proportions. African-Americans with type II diabetes suffer from more cardiovascular diseases (CVDs) associated with diabetes than the general population. Lower socioeconomic status (SES) and family history are often cited as contributory factors to the premature development of diabetes and CVDs in the general population. However, we are not aware of any study that has examined the relationships between SES and CVD risk factors (i.e., syndrome X) in a genetically enriched African-American population at high risk for type II diabetes. RESEARCH DESIGN AND METHODS We studied 200 healthy first-degree relatives of African-American patients with type II diabetes (age 25–65 years, mean 42.5 ± 8.4 years; 42 men, 158 women). Standard oral glucose tolerance test, metabolic, and anthropometric parameters, as well as questionnaires on SES, demographic characteristics, and physical activity, were obtained for each subject. SES was divided into quartiles based on annual income. To assess the impact of insulin on CVD risk, we examined clinical characteristics and metabolic parameters according to quartiles of fasting insulin concentrations. RESULTS Clinical characteristics, including mean age, BMI, waist-to-hip ratio (WHR), percentage body fat and lean body mass, and blood pressure were not statistically different among SES quartiles. There were no significant differences in any of the metabolic, blood pressure, lipid and lipoprotein, or anthropometric parameters among SES quartiles. When examined by insulin quartile, BMI, WHR, and body fat content tended to be greatest in the fourth quartile. Similarly, fasting and postprandial serum C-peptide and glucose levels were significantly higher in the fourth quartile. We observed greater levels of very low density lipoprotein (VLDL) cholesterol and triglycerides and lower levels of HDL cholesterol in the fourth compared with the first through third insulin quartiles. Serum cholesterol and LDL cholesterol were not associated with increasing insulin concentration assessed by quartiles. We found similar systolic and diastolic blood pressure, irrespective of insulin quartiles. We found relationships between fasting insulin and systolic blood pressure (r = 0.181, P < 0.05) and triglycerides (r = 0.247, P < 0.01), VLDL cholesterol (r = 0.237, P < 0.01), WHR (r = 0.268, P < 0.005), BMI (r = 0.308, P < 0.001), and percentage of body fat (r = 0.237, P < 0.01). CONCLUSIONS The present study demonstrates no SES/income effect on CVD risk factors or syndrome × in African-Americans at high risk for type II diabetes. Clustering of several components of syndrome × was seen in individuals in the highest quartiles compared with the lowest quartiles of insulin in our high-risk African-American population. We conclude that the well-established conventional risk factors for CVD in genetically enriched African-Americans are found only in individuals with the highest insulin levels, independent of SES.

The effect of glycaemic control and glycaemic variability on mortality in patients hospitalized with congestive heart failure

Diabetes and CHF are common comorbidities in hospitalized patients but the relationship between glycaemic control, glycaemic variability, and mortality in patients with both conditions is unclear.

Early metabolic improvement following bariatric surgery in morbidly obese adolescents

Bariatric surgery results in durable weight loss and improved comorbidities. The objectives of this study were to examine the efficacy of gastric bypass in reducing comorbid burden and improving metabolic status among morbidly obese adolescents. The medical records of 15 gastric bypass patients were retrospectively reviewed. Changes in metabolic markers were determined at baseline, 1 and 2 years post‐operatively. Comparative analysis demonstrated significant improvement in weight, BMI, insulin, HbA1C, C‐peptide, %B, %S, IR, cholesterol, percentile cholesterol, TG, percentile TG, HDL, percentile HDL, LDL, percentile LDL, and VLDL. Results support bariatric surgery as a treatment for morbidly obese adolescents with comorbidities. Pediatr Blood Cancer 2012; 58: 112–116.

History of Gestational Diabetes Leads to Distinct Metabolic Alterations in Nondiabetic African-American Women With a Parental History of Type 2 Diabetes

OBJECTIVE Gestational diabetes mellitus (GDM) and positive parental history of type 2 diabetes are predictors of the future development of type 2 diabetes in several populations. However, the relative importance of parental history of diabetes and/or history of GDM as risk factors for the pathogenesis of diabetes in African-Americans remains unknown. Thus, the objectives of the present study were 1) to characterize the glucose homeostatic regulations and 2) to examine the contribution of parental history of type 2 diabetes to the potential metabolic alterations found in nondiabetic African-American women with a history of GDM (HGDM). RESEARCH DESIGN AND METHODS We evaluated β-cell secretion, insulin sensitivity (SI), and glucose-dependent glucose disposal (SG) in 15 glucose-tolerant African-American women with a parental history of type 2 diabetes and prior GDM (HGDM) and 35 women with a parental history of type 2 diabetes but without prior GDM (NHGDM). Fifteen healthy nonobese nondiabetic subjects without a family history of diabetes served as control subjects. Body composition was determined by bioelectrical impedance analyzer, and body fat distribution pattern was determined by waist-to-hip ratio (WHR). Insulin-modified frequently sampled intravenous glucose tolerance (FSIGT) test was performed in each subject. SI and SG were determined by the minimal model method. RESULTS The mean age, BMI, percent body fat content, and lean body mass were not different between the subgroups of relatives with and without a history of GDM, but were greater than those of the healthy control subjects. Mean fasting and postchallenge serum glucose levels were slightly but significantly greater in the HGDM versus NHGDM subjects and the healthy control subjects. However, the 2-h glucose levels were greater in the relatives with and without GDM when compared with the healthy control subjects. In contrast, mean postprandial serum insulin responses were significantly lower between t = 30 and 120 min in the HGDM versus NHGDM groups and the healthy control subjects. The mean serum insulin levels were not different in the NHGDM subjects and healthy control subjects. During the FSIGT test, acute first-phase insulin release (t = 0–5 min) was significantly lower in the HGDM versus NHGDM groups and healthy control subjects. Mean SI was significantly (P < 0.05) lower in the HGDM versus NHGDM subjects and healthy control subjects (1.87 ± 0.47 vs. 2.87 ± 0.35 and 3.09 ± 0.27 × 10−4 · min−1.[μU/ml]−1, respectively). SG was significantly lower in HGDM than NHGDM subjects and healthy control subjects (2.11 ± 0.15 vs. 3.25 ± 0.50 and 2.77 ± 0.22 × 10−2) · min−1, respectively). Mean glucose effectiveness at zero insulin concentrations (GEZI) was significantly lower in the HGDM subjects when compared with the NHGDM and healthy control subjects. CONCLUSIONS The present study demonstrates that in African-American women with a parental history of type 2 diabetes and GDM, defects in early-phase β-cell secretion, as well as a decreased SI, SG, and GEZI, persist when compared with those without GDM. We suggest that African-American women with a positive history of GDM have additional genetic defects that perhaps differ from that conferred by a parental history of diabetes alone. Alternatively, the metabolic and hormonal milieu during GDM may be associated with permanent alterations in β-cell function, SI, and glucose effectiveness in African-American women. These defects could play a significant role in the development of GDM, and perhaps in the subsequent development of type 2 diabetes, in African-American women.