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PubMed1983

Age-related changes in lipid and carbohydrate metabolism of the genetically obese mouse.

Obese mice (C57BL/6J ob/ob) and their lean controls were studied longitudinally from immediately post-weaning until 62 wk of age, at which time the experiment was terminated. The dynamic nature of the metabolic aberrations of the obese mouse syndrome was clearly demonstrated. Obese mice were hyperinsulinemic at all ages yet the concentration of glucose in plasma was elevated only at 5-20 wk and 63 wk of age, but was similar to that of lean mice at 20-60 wk of age. Triacylglycerols accumulated in the liver of obese mice between 5 and 18 wk of age to a level that was 20-fold greater than that found in the age-matched lean control. A decreased concentration of DNA/g of liver was also found in 5-18 wk-old obese mice, indicative of an enlarged hepatocyte. With the exception of 5-wk-old animals, total DNA per liver was increased in obese mice when compared to the lean control throughout the profile. Following the peak in 18-wk-old mice, the hepatic content of triacylglycerols precipitously fell so that at 45 wk of age its concentration in obese mice was similar to that of the lean control. Plasma free fatty acid levels as well as liver glycogen content were comparable in obese mice and their lean controls throughout the profile. In obese mice older than 45 wk of age, the content of triacylglycerols in plasma was significantly lower than that of the age-matched lean control while an accumulation of liver triacylglycerols was again found in obese mice. Myocardial triacylglycerols were elevated in obese mice when compared to the lean control at all ages. The longitudinal metabolic profile of the obese mouse developed in the present study clearly demonstrates the dynamic nature of the deviations in carbohydrate and lipid metabolism in this animal model of human obesity and insulin resistance.

Aging↗
PubMed1992

Relation of serum lipoprotein lipids and apolipoproteins to obesity in children: the Bogalusa Heart Study.

BACKGROUND: The relationship of serum lipoprotein lipids and apolipoproteins to obesity was studied in a biracial sample of 2,816 children of ages 5-17 in Bogalusa, Louisiana. METHODS: Two measures of obesity were used: fatness (subscapular skinfold thickness) and fat centrality (the ratio of subscapular to triceps skinfold thickness). Plasma insulin and glucose were included as metabolic markers related to obesity. RESULTS: The obesity associations were relatively strong with insulin (rs = 0.29, P less than 0.001, skinfold; rs = 0.15, P less than 0.001, skinfold ratio) and triglycerides (rs = 0.25, P less than 0.001, skinfold; rs = 0.19, P less than 0.001, skinfold ratio). The relationships of serum low-density lipoprotein cholesterol (LDL-C) (rs = 0.17, P less than 0.001, skinfold; rs = 0.13, P less than 0.001, skinfold ratio) and apolipoprotein (apo) B (rs = 0.16, P less than 0.001, skinfold; rs = 0.13, P less than 0.001, skinfold ratio) with the obesity measures were of lesser magnitude, but persisted after adjustment for insulin and triglycerides. The inverse association of obesity to serum high-density lipoprotein cholesterol (HDL-C) (rs = -0.13, P less than 0.001, both skinfold and skinfold ratio) and apo A-I (rs = -0.04, P = 0.03, skinfold; rs = -0.05, P = 0.004, skinfold ratio) was significant only before adjustment for insulin and serum triglycerides. Multiple linear regression of obesity measures showed that, like insulin, serum triglycerides had consistently higher standardized coefficients than LDL-C, HDL-C, apo B, and apo A-I. Apo A-I and apo B added only a small amount (less than 2%) of information to the relationship of serum lipoproteins with obesity measures. CONCLUSION: These results indicate that serum very-low-density lipoprotein (VLDL) levels are directly and independently related to obesity. The well-known inverse association between obesity and serum HDL-C is not independent, but secondary to the elevated VLDL or triglyceride levels associated with obesity. While associations of obesity and lipoprotein cholesterol are found, far fewer occur with apolipoproteins, especially Apo A-I. Interesting race and sex differences in the relationship of obesity to serum lipoproteins and apoproteins are noted, being greater among white children and more consistent in white males.

Adolescent↗
PubMed1992

Plasma islet amyloid polypeptide levels in obesity, impaired glucose tolerance and non-insulin-dependent diabetes mellitus.

We examined the response of plasma islet amyloid polypeptide (IAPP) to an oral glucose load in non-obese and obese subjects with normal glucose tolerance or impaired glucose tolerance (IGT), and in non-obese patients with non-insulin-dependent diabetes mellitus (NIDDM). Plasma IAPP response to intravenous glucagon injection in NIDDM patients was also studied. Plasma IAPP concentration was determined by a sensitive and specific radioimmunoassay. Basal levels of plasma IAPP in non-obese subjects with normal glucose tolerance, IGT and NIDDM were not significantly different from each other. Non-obese subjects with IGT showed delayed and higher plasma IAPP response to oral glucose load compared to normal non-obese subjects. In NIDDM patients, IAPP response to glucose was delayed and lower when compared to normal non-obese subjects. Basal levels of plasma IAPP in normal obese subjects and obese subjects with IGT were significantly higher than those in normal non-obese subjects. Plasma IAPP response to glucose load in these obese subjects was higher than that in normal non-obese subjects. Plasma IAPP response was decreased in diabetic patients treated with diet, oral hypoglycemic agents and insulin in that order. We conclude that the secretion of IAPP is reduced with progression of NIDDM, although it appears to be rather augmented in IGT compared to normal non-obese subjects.

Adult↗
PubMed1995

Effects of obesity and inheritance on the development of non-insulin-dependent diabetes mellitus in Otsuka-Long-Evans-Tokushima fatty rats.

We studied whether obesity or inheritance was the more important factor in the development of non-insulin-dependent diabetes mellitus (NIDDM) using female Otsuka-Long-Evans-Tokushima Fatty rats (OLETF) possessing one of the diabetic genes, ODB-1, and male Long-Evans-Tokushima-Otsuka rats (LETO) possessing no ODB-1, neither of which were diabetic when bred normally. Diabetes-resistant male LETO rats and female OLETF rats (4 weeks old) were assigned to three groups of 6 rats each, respectively; two groups in which obesity was induced by high calorie 'cafeteria' diet (D), or ventromedial hypothalamus lesions (V) with normal chow diet and a control group fed on normal chow (C). Six male OLETF rats were used as NIDDM positive controls. The mean daily energy intakes of obese male LETO and female OLETF rats were higher than those of the respective C groups. At 27 weeks of age, the average body weights of the obese LETO and female OLETF rats were significantly higher than those of the respective C groups and similar to that of the male OLETF group. Abdominal fat deposits of the obese groups were significantly higher than those of the respective C groups. At 28 weeks of age, the cumulative incidence of diabetes mellitus in obese LETO rats was 0% in group D and 17% in group V, while that of obese female OLETF rats in groups D and V were 100%. At 29 weeks of age, the plasma immunoreactive insulin (IRI) responses to glucose in obese female OLETF rats, groups D and V, were higher than that in group C. In obese LETO rats, insulin-stimulated glucose disposal in vivo was similar to that in group C, but in obese female OLETF rats, it was reduced to 41% in group D and 37% in group V of that in group C. Sections of islets of the pancreas of obese LETO rats appeared histologically normal, whereas those of obese female OLETF rats showed enlarged multilobulated fibrotic islets. These results demonstrate that obesity is necessary, but not sufficient alone for the development of NIDDM in these rat models.

Analysis of Variance↗
PubMed2003

[Prevention strategies of childhood obesity].

Considering the high prevalence and the increasing trends, obesity is now considered as a public health problem in numerous countries. The main aim of the National Program of Nutrition and Health is to stop the increasing prevalence of childhood obesity. In this frame work, a group of experts has established a new presentation of the corpulence curves, adapted for clinical practice, to define normal weight and obesity. Weight status is now currently assessed on the basis of weight and height measurements, after computing the Quetelet index or body mass index (BMI) corresponding to weight (m) divided by square of height (weight/height2). As body proportion varies during growth, age must be taken into account. Various curves were published. In 1982, based on the French sample of the international growth study, BMI curves were published. They were revised in 1991. The third and 97th centiles define the normal weight range. Overweight is defined by BMI values greater than the 97th centile. In the year 2000, a new international definition was established. Two centiles were constructed to define overweight and obesity. The new BMI charts adapted for clinical practice, proposed by the French National program of nutrition and health, include the French reference curves plus the centile defining obesity in the international definition. Thus, in the new French charts, the area above the 97th centile is split in two levels (degree 1 obesity and degree 2 obesity). Drawing the BMI curve for each child, like drawing weight and height curves, is a simple act which can be done routinely. The age at adiposity rebound (an indicator predicting the risk of adult obesity) can be read from the curve. It allows to identify an early phase of obesity development, even at the time when overweight is not yet clinically visible. When obesity appears clearly, the identification is easy. The use of BMI curves is particularly useful in two situations: (1) in very young overweight children, the curves allow to identify children who have a real risk of developing obesity. (2) By the age of 6 years, when due to normal physiological variations, clinical assessment can be misleading. The BMI curves allow to identify children at risk. When a child is identified as having a real risk of obesity, simple preventive measures, adapted for each subject, could avoid a development toward massive obesity, which may become difficult to reduce if managed too late.

Adolescent↗
PubMed2006

Obesity cardiomyopathy: is it a reality? An ultrasonic tissue characterization study.

Obesity is a well-established risk factor for congestive heart failure. Evidence has been provided indicating that insulin resistance could be the mediator between obesity and congestive heart failure, but the pathogenic mechanisms leading to myocardial alterations remain unclear. The aim of this study was to investigate, by ultrasonic integrated backscatter (IBS) analysis, subclinical alterations of left ventricular (LV) structure and function in severe obesity. Sixty consecutive, severely obese people, who were otherwise healthy (15 men, 45 women; mean age +/- SD = 31.8 +/- 7 years), were enrolled. A total of 48 sex- and age-matched nonobese healthy participants were recruited as control subjects. All participants underwent conventional 2-dimensional color Doppler echocardiography, pulsed wave Doppler tissue imaging at mitral annulus level, and IBS. The homeostasis model assessment insulin resistance index was used to assess insulin resistance; the index values in the obese group were significantly higher (mean +/- SD = 4.9 +/- 1.4) than in the control group (0.92 +/- 0.5, P < .0001). Obese patients had a greater LV mass index by height (58.5 +/- 14 g/m(2.7)) than did control subjects (37 +/- 8 g/m(2.7), P < .0001) because of compensation response to volume overload caused by a greater cardiac output (P < .02). Preload reserve was increased in obese patients, as demonstrated by the significant increase in left atrial dimension (P < .0001). This volumetric increase activated the Frank-Starling mechanism, and determined a significantly higher LV ejection fraction (P < .03) in obese patients as compared with control subjects. A slightly reduced LV diastolic function was demonstrated in obese patients (transmitral early to late peak diastolic transmitral flow velocities ratio = 1.1 +/- 0.7) as compared with control subjects (1.5 +/- 0.5, P < .02). Pulsed wave Doppler tissue imaging showed an impairment of diastolic LV longitudinal function and increased LV diastolic filling pressure. The IBS values at septum level, indexed by pericardium interface, were significantly higher for septum in the obese group (57.8 +/- 8%) than in the control group (42.3 +/- 9%, P < .0001). Additional IBS alterations were observed in the obese group, with a significantly lower cyclic variation index both at septum (P < .0001) and at posterior wall (P < .001) levels. A significant association was found between insulin resistance index and both the IBS index of myocardial reflectivity at septum level (expression of increased myocardial collagen content) or LV mass. In conclusion, this study demonstrates that obese patients exhibit myocardial structural and functional alterations related to insulin resistance and to LV volume overload, which could be considered the very early stage of incipient obesity cardiomyopathy.

Adult↗
PubMed2006

Effect of obesity on early morbidity and mortality following cardiac surgery.

BACKGROUND: The prevalence of obesity in most developed nations, including Australia, continues to rise and represent an increasing public health concern. Obesity has been considered a major risk factor in patients undergoing cardiac and other major surgery. METHODS: We retrospectively analysed prospectively collected data of consecutive patients undergoing cardiac surgery between June 2001 and February 2006 at two Australian public hospitals. Patients were divided into three groups by body mass index (BMI): non-obese (BMI 20-30), obese (BMI>30-40) and morbidly obese (BMI>40). Associations between early mortality and morbidity and obesity were assessed by univariate and multivariate methods. RESULTS: Out of 4053 patients, 85 were excluded for BMI<20. A total of 2743 patients were defined as non-obese, 1136 obese and 89 morbidly obese. There were no significant differences in operative mortality, stroke, pneumonia, new renal failure, atrial fibrillation, prolonged ventilation, reintubation, readmission to intensive care, prolonged length of hospital stay or readmission within 30 days. The morbidly obese group had increased rates of deep sternal infection by univariate (odds ratio [OR] 6.4, 95% confidence interval [CI] 2.1-19.1, p<0.001) and multivariate (OR 13.1, CI 3.4-50.7, p<0.001) analysis. The obese group had a lower rate of re-operation for bleeding by univariate (OR 0.61, CI 0.41-0.91, p=0.01) and multivariate (OR 0.64, CI 0.42-0.99, p=0.04) analysis. CONCLUSION: Apart from an increased rate of deep sternal wound infection, obesity is not associated with early mortality or other post-operative complications. The protective effect of obesity on re-operation for bleeding requires further study.

Aged↗
PubMed2005

Future and implications of reimbursement for obesity treatment.

Obesity has been defined as a distinct disease by the World Health Organization, National Institutes of Health, Centers for Disease Control and Prevention, and the American Dietetic Association. In the United States, a major reimbursement challenge is to promote acceptance of obesity as a chronic disease and acceptance of its treatment by health management organizations, private insurers, and the government. The United States health care system is focused on treating individual obesity-related diseases, but does not treat obesity as the underlying cause. Reimbursement of obesity treatments using "condition coverage" based on the presence of other diseases does not allow obesity to be treated independently as a disease in itself. It is necessary to make major investments in research to determine the best methods and to match the treatment with the individual, to prevent obesity in vulnerable populations, and to develop more effective drugs and treatments for those already overweight or obese. There should be a more detailed analysis of the cost of obesity, costs associated with obesity and obesity-related disease treatment, and costs of inaction. The obesity epidemic is too large to be ignored. Health care professionals have a duty to be informed about the disease and to advocate for patients who need help. Registered dietitians can be key players in delivering obesity treatment.

Cost-Benefit Analysis↗
PubMed2006

The impact of obesity on severely injured children and adolescents.

PURPOSE/BACKGROUND: In conjunction with the obesity epidemic in adults, we are starting to see an increase of obesity in children and adolescents. Obesity has been identified as risk factor for poor outcomes in adult trauma patients, but has not been investigated adequately in younger patients. The purpose of this study was to investigate the impact of obesity on the outcomes of a severely injured population of children and adolescents. METHODS: Retrospective review of traumatized children (age 6-12) and adolescents (age 13-19) admitted to the intensive care unit (ICU) at an urban, level I trauma center from 1998 to 2003. The trauma registry and ICU database were used for data acquisition. Height and weight were recorded for each patient upon admission to the ICU and used to calculate body mass index (BMI). Patients were categorized as either lean (BMI <95th percentile for age) or obese (BMI > or =95th percentile for age). The two groups were compared regarding admission demographics, vital signs, mechanism of injury, patterns of injury, Injury Severity Score, and operations required. Outcomes evaluated were need for and length of mechanical ventilation, complications, length of hospital and ICU stay, and mortality. RESULTS: There were 316 pediatric and adolescent trauma patients (262 [83%] lean, mean BMI = 23 kg/m2 and 54 [17%] obese, mean BMI = 33 kg/m2) admitted to the ICU. The lean and obese groups were similar regarding age, sex, mechanism of injury, admission vitals, injury severity, and operations required. Injury patterns were similar, except obese patients had less severe head injuries. Although there was no difference in mortality among obese (15%) and non-obese (9%) patients (P = .39), obese children did have more complications (41% vs 22%, P = .04). In addition, obese patients required longer ICU stays (8 +/- 9 vs 6 +/- 6 days, P = .05) after severe trauma. CONCLUSIONS: Despite similar admission characteristics and less severe head injuries, obese children and adolescents have more complications and require longer ICU stays than their lean counterparts.

Adolescent↗
PubMed2006

Obesity, and not obstructive sleep apnea, is responsible for metabolic abnormalities in a cohort with sleep-disordered breathing.

OBJECTIVE: To assess the profile of metabolic abnormalities in subjects with obstructive sleep apnea (OSA). PATIENTS AND METHODS: In a case-control study conducted in two years, from April 2003 to March 2005, data obtained from polysomnography study, lipid profile, fasting blood sugar, serum insulin, insulin resistance, leptin and adiponectin levels, were compared between the various groups. Included in the study were OSA subjects from a sleep laboratory and matched controls from the community. Those with recent myocardial infarction, upper airway surgery, class III/IV heart failure, pregnancy, acromegaly, chronic renal failure, or who were on treatment for hyperthyroidism, on systemic steroid treatment, or on hormonal replacement therapy, were excluded from the study. RESULTS: Forty apneic obese subjects (AHI=32.19, range 13-52.75) were compared with 40 non-apneic obese controls (AHI=1.3, range 0-2.45) and 40 normal weight control subjects (AHI=0.7, range 0-1). No significant difference was noted in levels of fasting blood sugar, insulin resistance (obese apneics 61.9, obese controls 47.8, non-obese controls 19.1), leptin (obese apneics 10.65 microg/L, obese controls 8.52 microg/L, non-obese controls 2.83 microg/L) or adiponectin (obese apneics 4959.3 ng/ml, obese controls 5706 ng/ml, non-obese controls 7412 ng/ml) in the OSA group compared to obese controls. CONCLUSIONS: OSA has no independent association with lipid abnormalities, insulin resistance, serum leptin and adiponectin levels. In multivariate analysis, obesity was the major determinant of metabolic abnormalities in this cohort.

Adolescent↗
PubMedDate not supplied

A comparison of weight histories in women with class III vs. class I-II obesity.

OBJECTIVE: To describe the weight histories of women with extreme or class III obesity (BMI >or= 40 kg/m2) in comparison with a sample of women with class I-II obesity (BMI < 40 kg/m2) and to provide reliability data for a clinical instrument that assesses weight history. RESEARCH METHODS AND PROCEDURES: Female patients (N = 149) with extreme obesity seeking bariatric surgery and 90 class I-II obese women seeking behavioral treatment completed the Weight and Lifestyle Inventory (WALI), a self-report instrument that assesses age of onset of obesity, maximum weight at different ages, family weight history, and weight changes related to pregnancy. Test-retest reliability data were obtained by administering the WALI to a subsample (n = 58) of class I-II obese participants at their initial visit and at another pretreatment visit 1 to 2 weeks later. RESULTS: Patients with extreme obesity had a significantly younger age of onset of obesity, were significantly heavier at all age ranges, reported significantly more weight gain with their first pregnancy, and had significantly heavier parents and siblings as compared with less obese patients. There were no significant differences between groups with respect to weight gain during second pregnancies or postpartum weight retention. Robust test-retest correlations were obtained for the weight history items on the WALI. DISCUSSION: Patients with extreme obesity report more indicators of a genetic predisposition to obesity as compared with less obese patients. The WALI appears to be a reliable instrument for the assessment of weight history in obese patients.

Adult↗
PubMed2003

Decreased energy levels can cause and sustain obesity.

Obesity has reached epidemic proportions and has become one of the major health problems in developed countries. Current theories consider obesity a result of overeating and sedentary life style and most efforts to treat or prevent weight gain concentrate on exercise and food intake. This approach does not improve the situation as may be seen from the steep increase in the prevalence of obesity. This encouraged us to reanalyse existing information and look for biochemical basis of obesity. Our approach was to ignore current theories and concentrate on experimental data which are described in scientific journals and are available from several databases. We developed and applied a Knowledge Discovery in Databases procedure to analyse metabolic data. We began with the contradictory information: in obesity, more calories are consumed than used up, suggesting that obese people should have excess energy. On the other side, obese people experience fatigue and decreased physical endurance that indicates diminished energy supply in the body. The result of our work is a chain of metabolic events leading to obesity. The crucial event is the inhibition of the TCA cycle at the step of aconitase. It disturbs energy metabolism and results in ATP deficiency with simultaneous fat accumulation. Further steps in obesity development are the consequences of diminished energy supply: inhibition of beta-oxidation, leptin resistance, increase in appetite and food intake and a decrease in physical activity. Thus, our theory shows that obesity does not have to be caused by overeating and sedentary life-style but may be the result of the "obese" change in metabolism which is forcing people to overeat and save energy to sustain metabolic functions of cells. This "obese" change is caused by environmental factors that activate chronic low-grade inflammatory process in the body linking obesity with the environment of developed countries.

Aconitate Hydratase↗
PubMed2000

JTT-501, a new oral hypoglycemic agent, reverses hypertriglyceridemia in Zucker fatty and ventromedial hypothalamus-lesioned obese rats.

JTT-501 is a new oral hypoglycemic agent that is reported to be effective in insulin-resistant diabetic animal models by improving insulin resistance. It also improves hypertriglyceridemia. We investigated the mechanism of the reversal of hypertriglyceridemia in two types of obese animals using JTT-501. In Zucker fatty obese rats, an animal model of genetic obesity, fasting plasma triglyceride and glucose significantly decreased after a single daily oral dose of JTT-501 (100 mg/kg) for 7 days. In ventromedial hypothalamus (VMH)-lesioned obese rats, an animal model of nongenetic obesity, fasting plasma triglycerides significantly decreased but fasting plasma glucose levels remained unchanged after treatment with this agent. In Sprague-Dawley (SD) rats, fasting plasma triglyceride and glucose levels remained unchanged. The JTT-501-treated Zucker fatty and VMH-lesioned obese rats showed a decrease in insulin, but it was not significant, while the treated SD rats showed a significant decrease in insulin. Postheparin plasma lipoprotein lipase (LPL) increased significantly in treated Zucker fatty obese and SD rats, but did not change in VMH-lesioned obese rats. The hepatic triglyceride secretion rate (TGSR) did not change in any species treated with JTT-501. There was a negative correlation between postheparin plasma LPL and plasma triglyceride levels in Zucker fatty obese rats, while no such correlation was observed in VMH-lesioned obese or SD rats. The fractional catabolic rate (FCR) for plasma triglyceride was increased significantly by JTT-501 in both Zucker fatty and VMH-lesioned obese rats. These results suggest that JTT-501 decreases plasma triglycerides mainly by increasing postheparin plasma LPL in Zucker fatty obese rats, while it ameliorates an impairment in the ability of adipose tissue to remove triglyceride from the circulation in VMH-lesioned obese rats.

Animals↗
PubMed2000

Pathogenic factors of glucose intolerance in obese Japanese adolescents with type 2 diabetes.

We attempted to identify the pathogenic factors involved in the progression to type 2 diabetes in obese Japanese adolescents. Subjects included 18 nondiabetic obese adolescents, 12 obese adolescents with type 2 diabetes on diet therapy, 10 obese adolescents with type 2 diabetes manifesting ketosis at onset or with a history of treatment with hypoglycemic agents, and 26 non-obese adolescent control subjects. The first-phase insulin response (FPIR), glucose disappearance constant (Kg), glucose effectiveness (Sg), and insulin sensitivity (S(I)) were obtained using an insulin-modified frequently sampled intravenous glucose tolerance test (FSIGT) and a minimal model analysis. The disposition index (DI, by FPIR x S(I)) was determined to assess any endogenous insulin effect. The results showed that Kg was decreased significantly (P = .0006) with the progression to severe diabetes in the obese groups. Although S(I) and Sg did not differ significantly among the 3 obese groups, both parameters were significantly lower in each obese group versus the non-obese controls. As a result of the significant decrease in FPIR (P < .0001), the DI decreased (P = .0006) with the progression to severe diabetes in the obese groups. In conclusion, an early manifestation of type 2 diabetes with occasional ketosis at onset may result from beta-cell dysfunction to glucose stimulation. This finding is demonstrated by the relatively low FPIR to decreased S(I) in obese Japanese adolescents, as well as the low Sg as a synergic role in glucose intolerance. The present findings from a Japanese population for pathogenic factors aside from obesity may help us to gain a better understanding of the progression to adolescent, early-onset, obese type 2 diabetes and its severity.

Adolescent↗
PubMed1997

Increases in high-density lipoprotein cholesterol with endurance exercise training are blunted in obese compared with lean men.

The effectiveness of endurance exercise training (without concomitant weight loss) for improving lipoprotein lipid levels in obese individuals remains controversial. The purpose of this study was to determine whether lipoprotein lipid responses to endurance exercise training are affected by obesity. Healthy middle-aged and older (57 +/- 2 years) lean (n = 16; body mass index [BMI], 22 to 26 kg/m2), moderately obese (n = 15; BMI, 27 to 30 kg/m2), and obese (n = 15; BMI, 31 to 37 kg/m2) men underwent a 9-month endurance exercise training program. The groups differed in the initial degree of obesity, waist circumference, and waist to hip ratio (WHR), but not in age or maximal aerobic capacity ( VO2max). The obese group had lower baseline levels of high-density lipoprotein cholesterol (HDL-C) and HDL2-C, and higher triglyceride (TG) levels than the lean group. Exercise training increased VO2max to a comparable degree in lean, moderately obese, and obese groups (18%, 24%, and 18%, respectively, P < .01). Exercise training significantly decreased TG levels in all groups, whereas total cholesterol and low-density lipoprotein cholesterol (LDL-C) decreased only in the obese group. Exercise training increased HDL-C and HDL2-C levels in lean (14% and 81%, respectively, P < .05) and moderately obese (7% and 59%, respectively, P < .05) men, whereas neither HDL-C nor HDL2-C changed in obese men. The change in HDL-C correlated negatively with initial BMI (r = -.42, P < .01) and waist circumference (r = -.43, P < .01). These results show that the effects of exercise training on HDL-C are blunted in obese middle-aged and older men, whereas improvements in TG occur independently of the degree of obesity.

Body Composition↗
PubMed1999

Circulating tumor necrosis factor alpha concentrations are higher in abdominal versus peripheral obesity.

Fat tissue is a significant source of endogenous tumor necrosis factor alpha (TNFalpha), the pluripotent cytokine that plays an important role as a mediator of the peripheral insulin resistance found in obesity. The majority of evidence for this role of TNFalpha is from studies in animal models of obesity. To explore further the role of TNFalpha in the pathogenesis of obesity-related insulin resistance in humans, we compared plasma levels of TNFalpha and the other main endocrine cytokine, interleukin-6 ([IL-6] both measured by enzyme-linked immunosorbent assay), in 26 obese women (body mass index [BMI] > 30 kg/m2) and 13 female controls (BMI < 26 kg/m2) without a history of recent or active infection. Glucose and insulin levels were measured at 0, 1, and 2 hours after a 75-g oral glucose load. There was no significant difference in plasma TNFalpha or IL-6 levels between obese and non-obese subjects overall (2.10 +/- 0.19 v 1.65 +/- 0.18 pg/mL and 2.06 +/- 0.29 v 1.50 +/- 0.17 pg/mL, respectively). However, TNFalpha levels were significantly elevated in obese subjects with a 2-hour glucose level more than 140 mg/dL (n = 8) compared with the other obese subjects (n = 18) and the non-obese controls (2.88 +/- 0.46 v 1.75 +/- 0.10 and 1.65 +/- 0.18 pg/mL, respectively, P < .01). Furthermore, the TNFalpha level correlated significantly with the waist to hip ratio ([WHR] r = .53, P < .01) and fasting and post-oral glucose tolerance test (OGTT) insulin levels (r = .47, P < .02), but not with the BMI, and was higher in obese women with a WHR more than 0.90 (n = 14) in comparison to those with a WHR less than 0.90 (n = 12, 2.47 +/- 0.29 v 1.66 +/- 0.18 pg/mL, respectively, P < .03). The corresponding plasma leptin level was significantly higher in obese women versus the control group (41.6 +/- 2.5 v22.3 +/- 2.9 ng/mL, P < .001) and was related to the BMI (r = .60, P < .01) but not to TNFalpha or the WHR. There were no significant differences in the corresponding IL-6 concentration between groups, and IL-6 did not correlate with TNFalpha, leptin, BMI, WHR, or insulin levels. In conclusion, circulating TNFalpha levels are higher in abdominal obesity compared with peripheral obesity, and may contribute to the insulin resistance that more commonly complicates the former pattern of fat distribution.

Abdomen↗
PubMed2001

Ethnic issues in the epidemiology of childhood obesity.

Childhood obesity may be seen as a marker for high-risk dietary and physical inactivity practices. Recent increases in the prevalence of overweight and obesity among American children are not limited to one age, gender, or ethnic group, which suggests that unique behaviors of the members of various racial or ethnic subgroups of the population are unlikely to be the major contributing factors. Rather, it seems that environmental changes promoting increased energy intake and decreased energy output are occurring and have widespread impact on children from various backgrounds. Although no ethnic group is immune from the current shift in energy balance, differential rates of overweight seem to exist among ethnic groups. National probability samples of African-American, Hispanic, and white children in the United States provide clear evidence that white children are at lower risk for childhood overweight than are African-American or Hispanic children. Of concern is the lack of national data on the prevalence of overweight and obesity for Native-American and Asian-American groups. Also of concern is the aggregation of racial and ethnic subgroups, which may render prevalence rates meaningless. This possibility is clearly true with some surveys of weight status that combine diverse populations, such as Asians and Pacific Islanders, into one group. The high rates of obesity in African-American, Hispanic, and Native-American children are of concern. Although parental SES is associated inversely with childhood obesity among whites, higher SES does not seem to protect African-American and Hispanic children against obesity. In these groups, childhood obesity does not seem to be associated significantly with parental income and education. Health consequences of childhood obesity include a higher prevalence of type 2 diabetes and an increased risk for adverse levels of lipids, lipoproteins, and blood pressure. The effects of recently reported unprecedented levels of childhood overweight on subsequent risk for obesity in middle age are not known until future longitudinal data can be collected. It seems likely, however, that future health consequences of current early and severe childhood obesity will be staggering. Funding for adult follow-up of longitudinal studies of high-risk African American, Hispanic, and Native-American children is needed urgently to provide information on the long-term effects of childhood obesity. Halting the obesity epidemic is a formidable task, but the success in recent decades of drastically reducing childhood undernutrition offers hope and should spur similar action and leadership efforts. Promotion of efforts to reduce excess caloric intake with efforts to increase energy expenditure should receive paramount attention in the design of health programs. Given the relatively few published obesity-prevention and treatment studies that are designed to address specific cultural issues, it is important to promote the development of culturally appropriate intervention strategies that are shown to be effective among youth of diverse backgrounds. Although the dietary and activity goals will be similar, parental, family, and community messages and techniques grounded in cultural traditions and norms will be different for each ethnic group. This approach is crucial in the United States, a country with an increasingly diverse population.

Black or African American↗
PubMed2001

The neuroendocrinology of childhood obesity.

The regulation of energy balance is enormously complex, with numerous genetic, hormonal, neural and behavioral, and societal influences. Although the current epidemic of obesity clearly has its underpinnings in the changes in culture during the past half-century (see other articles in this issue), the role of the neuroendocrine system in the genesis of obesity, as described in this article, is physiologically and therapeutically unavoidable. An understanding of this system has suggested organic causes (and therapies) for some rare and not-so-rare forms of obesity. With so many inputs, it is not far-fetched to assume that dysfunction of other parts of this feedback system will be found to explain other forms of obesity in the future. What does this mean for obese children entering the pediatrician's office? Fortunately or unfortunately, diet and exercise are the mainstays of obesity therapy for children and adults. Most diet-exercise programs result in an acute 11-kg weight loss in adults; the question is whether it can be sustained without significant long-term behavioral modification. For instance, the European Sibutramine Trial of Obesity Reduction and Maintenance trial showed that 42% of treated subjects drop out; of those remaining, 77% of subjects lost more than 5% of initial body weight, but only 43% of those maintained more than 80% of this over 2 years. Could there be an organic component in those who do not respond? Of course, obesity pharmacotherapies sometimes have beneficial acute effects, but these drugs work for only as long as they are consumed; discontinuation tends to result in a "rebound" weight gain, suggesting that the cause of the obesity is still present. Furthermore, in 2001, there are no obesity drugs approved for children. A useful guiding principle is that children deserve at the minimum an initial medical evaluation, including birth weight, medical history, family history, dietary evaluation, and exercise assessment. Perhaps the most important feature that can distinguish "organic" from "behavioral" weight gain in childhood is the age of the "adiposity rebound." The Centers for Disease Control and Prevention now supplies BMI charts for boys and girls at www.cdc.gov/growthcharts. Plotting of the BMI versus age allows pediatricians to determine the age at which the BMI starts to increase (mean, 5.5 years). The earlier the adiposity rebound, the more likely the child will be obese as an adult, and the more likely that an organic cause can be determined. In such patients, thyroid levels and fasting insulin and leptin levels should be measured. An initial attempt at diet and exercise is essential; patients who do not respond with BMI stabilization should be investigated for a more ominous cause of their obesity. As the nosology of obesity improves, pediatricians will be able to increase the diagnostic efficiency and therapeutic success of this unfortunate, debilitating, and expensive epidemic.

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