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PubMed2001

Cerebrospinal fluid and plasma concentrations of leptin, NPY, and alpha-MSH in obese women and their relationship to negative energy balance.

Leptin and its principal mediators, NPY and alpha-MSH are postulated to play a pivotal role in energy balance. To determine the possibility of the disturbance in neuropeptides in human obesity and their consequent changes in response to negative energy balance, we evaluated plasma and cerebrospinal fluid (CSF) leptin, NPY, and alpha-MSH levels in obese women before and after weight loss in comparison with normal control women. Subjects included 16 obese women [mean body mass index (BMI), 35.6 kg/m(2)] before and after weight loss induced by a 2-wk very low caloric diet (800 kcal/d) and 14 normal weight women (mean BMI, 20.4 kg/m(2)). The CSF to plasma leptin ratio in normal weight subjects was 2.3-fold higher than that in obese subjects. After weight loss in obese subjects, plasma leptin levels decreased by 40% and CSF levels decreased by 51%. There was a positive linear correlation between CSF and plasma leptin levels at baseline in obese subjects (r = 0.74, P < 0.05) and a positive logarithmic correlation in normal weight subjects (r = 0.89, P < 0.05) and in obese subjects after weight loss (r = 0.64, P < 0.05). The BMI was negatively correlated with the CSF to plasma leptin ratio (r = -0.86, P < 0.05) in all subjects. Neither the baseline plasma levels nor the baseline CSF levels of NPY were different between normal weight subjects and obese subjects. After weight loss, the CSF NPY level decreased significantly compared with baseline values in obese subjects. The alpha-MSH levels in plasma and CSF did not differ significantly from controls in obese subjects at baseline or after weight loss. Baseline CSF leptin level correlated with neither the baseline CSF NPY level nor the baseline CSF alpha-MSH level. In conclusion, this study demonstrated that the efficiency of brain leptin delivery is reduced in human obesity and central nervous system leptin uptake involves a combination of a saturable and an unsaturable mechanism. CSF NPY and alpha-MSH did not differ from controls in human obesity, and the CSF NPY level decreased significantly whereas alpha-MSH did not differ after weight loss in obese subjects compared with baseline. There was no significant correlation between CSF leptin and CSF NPY or alpha-MSH. This could be the result of leptin resistance present in human obesity and/or the more complex mechanisms involved in modulating appetite and regulating energy balance in human obesity.

Adult↗
PubMedDate not supplied

Insulin resistance and hyperinsulinemia in prepubertal obese children.

BACKGROUND: Tissue resistance to insulin has been demonstrated in obese individuals. Pancreatic beta-cells respond to the reduced tissue sensitivity with increased insulin secretion so that glucose homeostasis is maintained. OBJECTIVE: The purpose of this prospective study was to investigate the presence of hyperinsulinemia and insulin resistance in obese children and adolescents. SUBJECTS AND METHODS: Fasting glucose (FG) and insulin (FI) levels and fasting glucose to insulin ratio (FGIR) were measured in 26 obese prepubertal children and 20 obese adolescents, as compared to 20 non-obese prepupertal children and 20 adolescents with normal body weight. Furthermore, obese children and adolescents underwent an oral glucose tolerance test with measurements of glucose and insulin 2 hours post glucose load. RESULTS: In 14/26 (54%) obese prepubertal children and in 16/20 (80%) obese adolescents FI was >24 microU/ml. FGIR was <6 in 23/26 (88%) prepubertal obese children and in all obese adolescents. All non-obese prepubertal children and adolescents had normal FI. However, FGIR was <6 in 6/20 (30%) non-obese prepubertal children and in 15/20 (75%) non-obese adolescents. CONCLUSION: Hyperinsulinemia and insulin resistance are already present in prepubertal obese children. As hyperinsulinemia is a potentially reversible condition and the complications related to it may be prevented, early measurements should be undertaken so that obese children lose body weight before the onset of puberty which may enhance the problem of insulin insensitivity.

Age Factors↗
PubMed2006

Plasminogen activator inhibitor-1 (PAI-1) gene polymorphism (-675 4G/5G) associated with obesity and vascular risk in children.

UNLABELLED: Atherothrombotic complications in insulin resistance are partly attributed to impaired fibrinolysis caused by increased PAI-1 plasma levels, and 4G/5G promotor polymorphism of the PAI-1 gene may modulate PAI-1 transcription. OBJECTIVE: To investigate PAI-1-675 4G/5G allele gene polymorphism and its relationship with obesity in children. CHILDREN AND METHOD: The study participants were 133 apparently healthy non-obese children, 24 probable exogenously obese without family history (Group I), 66 probable familial obese (Group II), and 44 obese children who were referred to the pediatric endocrinology department with any complication of obesity (Group III). Group I and Group II obese children were gathered from a school-based epidemiological study. RESULTS: Incidence of obesity was 19% in a school with high socio-economic status, whereas it was 4% in a school with low socio-economic status. Frequencies of 4G/4G gene polymorphisms were 24.81%, 37.50%, 64.80% and 61.11% in the control group, and groups I, II, and III, respectively. In groups II and III, 4G/4G gene polymorphism, and in non-obese control children 5G/5G gene polymorphism, was common. In obese children in the presence of family history for obesity and metabolic syndrome (odds ratio [OR]: 4.48, 95% confidence interval [CI]: 1.26-15.82), carriage of the 4G allele either in heterozygous or homozygous state increased the risk of vascular disease (OR: 6.10, 95% CI 1.64-22.90). In patients with acanthosis nigricans, high HOMA-IR values, hypertriglyceridemia and elevated atherogenic index, 4G/4G genotype frequency was remarkably higher compared to patients with other features of metabolic syndrome. CONCLUSION: The increasing prevalence of childhood obesity in high socio-economic status is associated with health risks. In obese children with family history of obesity and cardiovascular disease or type 2 diabetes mellitus and in obese children who had any feature of metabolic syndrome, frequency of 4G/4G genotype was more than the 4G/5G and 5G/5G genotypes in the PAI-1 gene. These patients can be at increased risk for developing vascular disease. Acanthosis nigricans, high HOMA-IR value, hypertriglyceridemia and high atherogenic index can also reflect the high risk of vascular disease in metabolic syndrome.

Adult↗
PubMed1999

Influence of the home environment on the development of obesity in children.

CONTEXT: Obesity is the most common health problem facing children. The most recent data from the National Health and Nutrition Examination Survey III suggest that 22% of children and adolescents are overweight and that 11% are obese. OBJECTIVE: To investigate prospectively the association between the home environment and socioeconomic factors and the development of obesity in children. DESIGN: Prospective cohort study. SETTING: The National Longitudinal Survey of Youth. Population. A total of 2913 normal weight children between the ages of 0 and 8 years were followed over a 6-year period. We examined the roles of race, marital status, maternal education, family income, and parental occupation, as well as standardized measures of the home environment (The Home Observation for Measurement of the Environment [HOME]-Short Form) on the development of childhood obesity. PRIMARY OUTCOME MEASURE: Incidence of obesity. Obesity was defined as a body mass index >95th percentile for age and gender at the 6-year follow-up. RESULTS: Maternal obesity was the most significant predictor of childhood obesity (OR: 3.62 [2. 65-4.96]). The HOME-Short Form cognitive scores and household income were also significant predictors of childhood obesity (OR, low HOME-cognitive: 2.64 [1.48-4.70], medium HOME-cognitive: 2.32 [1. 39-3.88]; low income: 2.91 [1.66-5.08], medium income: 2.04 [1.21-3. 44]). Children who lived with single mothers were also significantly more likely to become obese by the 6-year follow-up, as were black children, children with nonworking parents, children with nonprofessional parents, and children whose mothers did not complete high school. Neither the child's gender nor the HOME-emotional scores contributed to the development of obesity. After controlling for the child's initial weight-for-height z-score, maternal body mass index, race, marital status, occupation, education, and HOME emotional scores, only the HOME cognitive score and family income remained significant predictors of childhood obesity. CONCLUSION: Children with obese mothers, low family incomes, and lower cognitive stimulation have significantly elevated risks of developing obesity, independent of other demographic and socioeconomic factors. In contrast, increased rates of obesity in black children, children with lower family education, and nonprofessional parents may be mediated through the confounding effects of low income and lower levels of cognitive stimulation.

Chi-Square Distribution↗
PubMed2002

Economic burden of obesity in youths aged 6 to 17 years: 1979-1999.

OBJECTIVE: To examine the trend of obesity-associated diseases in youths and related economic costs. METHODS: Using a multiyear data file of the National Hospital Discharge Survey, 1979-1999, we analyzed the changes in obesity-associated diseases and economic costs in youths (6-17 years of age) over time. Diabetes, obesity, sleep apnea, and gallbladder disease were examined to explore the trend of the disease burden. Other obesity-associated diseases for which obesity was listed as a secondary diagnosis were also analyzed. Obesity-associated hospital costs were estimated from the discharges with obesity listed as a principal or secondary diagnosis. RESULTS: From 1979-1981 to 1997-1999, the percentage of discharges with obesity-associated diseases increased. The discharges of diabetes nearly doubled (from 1.43% to 2.36%), obesity and gallbladder diseases tripled (0.36% to 1.07% and 0.18% to 0.59%, respectively), and sleep apnea increased fivefold (0.14% to 0.75%). Ninety-six percent of discharges with a diagnosis of obesity listed obesity as a secondary diagnosis. Asthma and some mental disorders were the most common principal diagnoses when obesity was listed as a secondary diagnosis. Obesity-associated annual hospital costs (based on 2001 constant US dollar value) increased more than threefold; from $35 million (0.43% of total hospital costs) during 1979-1981 to $127 million (1.70% of total hospital costs) during 1997-1999. CONCLUSIONS: Among all hospital discharges, the proportion of discharges with obesity-associated diseases has increased dramatically in the past 20 years. This increase has led to a significant growth in economic costs. These findings may reflect the impact of increasing prevalence and severity of obesity. Diet and physical activity interventions should be developed for weight loss and prevention of weight gain in youths.

Adolescent↗
PubMed2000

Mechanisms of dysregulation of 11 beta-hydroxysteroid dehydrogenase type 1 in obese Zucker rats.

Obesity has been associated with alterations in glucocorticoid metabolism in both man and rodents, but the underlying mechanisms remain undefined. We have previously reported tissue-specific alterations in 11 beta-hydroxysteroid dehydrogenase type 1 (11 beta-HSD1) in obese Zucker rats predicting that reactivation of corticosterone is decreased in liver but increased in omental fat. The mechanisms of dysregulation of 11 beta-HSD1 in obesity are not known, and in this study we have investigated the potential role of glucocorticoids and insulin. In one experiment lean and obese Zucker rats were adrenalectomised, and in a second experiment they were sensitised to insulin by treatment with either metformin or rosiglitazone. Adrenalectomy (ADX) of obese animals attenuated weight gain, normalised hepatic 11 beta-HSD1 kinetics by an effect on V(max) (V(max)in sham-operated animals, 6.6+/-1.1 nmol/min per mg in lean vs 3.4+/-0.6 in obese, P<0.01; in ADX animals 5.9+/-1.1 in lean vs 6.9+/-1.8 in obese, NS), and reversed the difference in omental fat 11 beta-HSD1 activity (18.9+/-4.2% in lean ADX vs 8.2+/-2.3 in obese ADX, P=0.03). Both metformin and rosiglitazone improved insulin sensitivity in obese, but not lean animals, and had no effect on 11 beta-HSD1 activity in either liver or fat. However, both treatments normalised adrenal hypertrophy in obese animals (48+/-29 mg in obese vehicle vs 37+/-1.2 in metformin and 38+/-1.8 in rosiglitazone treated, both P<0.01), and rosiglitazone tended to attenuate hypercorticosteronaemia in obese rats. Neither treatment attenuated weight gain; in fact, weight gain was enhanced by rosiglitazone in obese rats. In summary, altered 11 beta-HSD1 activity in obese Zucker rats is reversible following adrenalectomy, but the mechanism is unclear since adrenalectomy also normalises many other metabolic abnormalities. The current study suggests that hyperinsulinaemia is not responsible for tissue-specific dysregulation of 11 beta-HSD1. However, insulin sensitisation did reverse adrenal hypertrophy, suggesting that hyperinsulinaemia may be a key factor contributing to activation of the hypothalamic- pituitary-adrenal (HPA) axis in obesity independently of tissue-specific changes in 11 beta-HSD1.

11-beta-Hydroxysteroid Dehydrogenases↗
PubMed1993

The pathogenesis of hypertension in obese subjects.

Obese subjects are at an increased risk of becoming hypertensive and vice versa. Essential hypertension and obesity are commonly accompanied by insulin resistance (defined as impaired insulin-mediated glucose disposal) and hyperinsulinaemia. In the offspring of patients with essential hypertension, insulin resistance and hyperinsulinaemia, as well as related increases in serum low density lipoproteins and triglycerides, often occur prior to the development of essential hypertension, overweight or central redistribution of body fat. Moreover, once obesity, and in particular central obesity, is present, insulin resistance is more marked in hypertensive than in normotensive obese subjects. Hyperinsulinaemia and/or insulin resistance in turn promote body fat deposition and impaired glucose tolerance. This cycle helps to explain why a familial predisposition to essential hypertension poses an increased risk of developing not only hypertension but also dyslipidaemia, obesity and non-insulin-dependent (type 2) diabetes. It is still unclear whether insulin resistance and/or hyperinsulinaemia also promote hypertension per se. Regardless of insulin's exact pathogenic role, obesity and/or a high dietary intake of carbohydrates, salt, etc. can induce several potential pressor mechanisms: 1) higher plasma noradrenaline (norepinephrine) and adrenaline (epinephrine) levels, suggesting a higher sympathetic tone in obese than in nonobese subjects, and in hypertensive obese than in normotensive obese subjects; 2) similarly, a tendency to hyperaldosteronism, with largely normal plasma renin activity, in obese hypertensive patients; 3) enhanced sensitivity of blood pressure to salt; 4) increased total blood volume (although it is normal relative to body surface area), leading to increased cardiac output and eventually eccentric left ventricular hypertrophy; and 5) increased cytosolic free Ca++ levels and reduced intracellular Mg++ levels in the blood cells of obese hypertensive patients and patients with non-insulin-dependent diabetes, although this finding cannot necessarily be extrapolated to cationic levels in vascular muscle cells. Total peripheral vascular resistance is usually low in normotensive obese subjects and rises with the development of hypertension; compared with lean patients with essential hypertension, obese hypertensive patients tend to have a slightly lower level of total peripheral vasoconstriction and a slightly higher cardiac output. Considering the intimate association between essential hypertension and obesity, as well as the prevalence and prognostic relevance of this combination, the spectrum of accompanying metabolic and cardiovascular abnormalities deserves careful consideration in the evaluation of therapeutic care for such patients.

Humans↗
PubMed1999

Plasma leptin and insulin levels in weight-reduced obese women with normal body mass index: relationships with body composition and insulin.

Obesity is a complex disease with multiple features that has confounded efforts to unravel its pathophysiology. As a means of distinguishing primary from secondary characteristics, we compared levels of fasting plasma leptin and insulin in a cohort of weight-reduced obese women who have attained and maintained a normal BMI for more than 1 year with the levels in cohorts of never-obese and currently obese women. Weight-reduced obese women showed decreased plasma concentrations of leptin and insulin compared with obese women, but these levels remained significantly higher than those of never-obese women. Plasma leptin levels were highly correlated with plasma insulin levels (r = 0.60, P < 0.001). To further explore relationships with body composition, total body fat was determined by dual-energy X-ray absorptiometry and body fat distribution by computed tomography in subsets of these groups. Weight-reduced obese women had a significantly greater percent body fat and subcutaneous abdominal fat mass than did the never-obese women, and these were highly correlated with plasma leptin (r = 0.90, P < 0.001, and r = 0.52, P < 0.001, respectively). In these weight-reduced obese women, visceral fat mass was similar to that of the never-obese. The insulin sensitivity index and first-phase insulin response were also comparable. These results demonstrate that higher leptin levels in weight-reduced obese women are related to the higher total fat and particularly the subcutaneous fat masses. Normalization of visceral fat mass in the weight-reduced obese was accompanied by normalization of insulin sensitivity index and first-phase insulin response. This study suggests that increases in plasma leptin and insulin in obesity are secondary features of the obese state.

Absorptiometry, Photon↗
PubMed2001

Hypertension in obesity.

AIM: To review various topics regarding the relationship between obesity and hypertension. DATA SUMMARY: Obesity is a widespread and increasingly prevalent condition associated with a large number of comorbid diseases, one of the most important of which is obesity-induced hypertension (HTN). The association between obesity and HTN has been well documented in most racial, ethnic and socio-economic groups, although the relationship between body mass index (BMI) and blood pressure values depends on age, gender, type of obesity and race differences. Obesity-induced HTN has some unique characteristics that differ from those observed in lean hypertensive patients. The hemodynamic profile of obese subjects is characterised by high cardiac output, high plasma and total blood volume, and inappropriately normal to total peripheral resistance. Clinically, hypertensive obese subjects are more likely to develop left ventricular hypertrophy and kidney damage than their lean counterparts. Various common factors are involved in establishing sodium retention and vascular resistance and may be critically influenced by the neurobiological/genetic mechanisms leading to obesity, in which insulin, leptin and the adrenergic system play major roles. Obesity is one of the main causes of therapeutic failure, and a number of studies have demonstrated that obese subjects need more antihypertensive drugs than sex and age-matched lean hypertensives. Long-term dietary treatment, consisting of a moderate restriction of energy and salt intake, is the most effective and safe treatment for obesity-associated HTN. The use of treatments other than calorie restriction should be considered with caution. Drugs that increase energy expenditure or reduce appetite may variably increase blood pressure (BP) and are unsuitable for hypertensive subjects. There do not seem to be any clear differences in the efficacy of the various antihypertensive drug classes. The clustering of cardiovascular risk factors other than HTN needs to be taken into account when choosing antihypertensive treatment for obese subjects. CONCLUSIONS: Obesity is a highly prevalent condition that causes or exacerbates many health problems including HTN. Combined interventions at different levels can help in losing weight and therefore reduce the cardiovascular risk, morbidity and mortality associated with obesity.

Age Factors↗
PubMed2005

[Obesity and cardiac failure].

Obesity alone is the cause of 11% of cases of cardiac failure in men and 14% of cases in women in the United States. The frequency of obesity continues to rise in our country, 41% of our compatriots being obese or overweight. It is expected that obesity will become an important cause of cardiac failure in the coming years. The Framingham study showed that, after correction for other risk factors, for every point increase in body mass index, the increase in risk of developing cardiac failure was 5% in men and 7% in women. There are three physiopathological mechanisms to explain the adverse effects of obesity on left ventricular function: an increase in ventricular preload secondary to increased plasma volume induced by the high fatty mass; an increase in left ventricular afterload due to the common association of hypertension generated by activation of the sympathetic nervous system by hyperinsulinism; and systolic and diastolic dysfunction due to changes in the myocardial genome and coronary artery disease induced by risk factors of atherosclerosis aggravated by obesity. The adipocyte also secretes a number of hormones which act directly or indirectly on the myocardium: angiotensin II, leptin, resistin, adrenomedulin, cytokines. These haemodynamic and hormonal changes profoundly modify the genetic expression of the myocardium in obesity, favourising hypertrophy of the myocyte and the development of interstitial fibrosis. Whether it be eccentric in the absence of hypertension or concentric when hypertension is associated with obesity, left ventricular hypertrophy, although normalising left ventricular wall stress, has adverse consequences causing abnormal relaxation and decreased left ventricular compliance. Therefore, in obese patients, two forms of cardiac failure may be observed. The more common is due to diastolic dysfunction, obesity being one of the principal causes of cardiac failure with preserved systolic function. Cardiac failure due to systolic dysfunction is less common and may be observed in cases with inappropriate left ventricular hypertrophy which does not normalise abnormal left ventricular wall stress leading to cardiomyopathy, and in cases with associated coronary artery disease. Whatever the underlying mechanism, the diagnosis of cardiac failure is made more difficult by obesity. From the prognostic point of view, in the global population of patients with cardiac failure, obesity improves survival because it counteracts the adverse effect of cachexia; however, obesity increases the risk of sudden death. In fact, obesity is associated with dynamic change in QT interval. In cases of cardiac failure secondary to obesity-related cardiomyopathy, loss of weight leads to an improved functional status and a reduction of left ventricular remodelling and an increase of the ejection fraction.

Cardiomyopathy, Dilated↗
PubMed1982

Plasma catecholamines and autonomic responsiveness in obesity.

The autonomic responsiveness of lean women to standing, passsive vertical tilting, noradrenaline infusion and the valsalva manoeuvre has been compared with that of obese women and a group of formerly obese women (post-obese). Upon standing, the lean and obese groups had comparable cardiovascular responses with similar rises in plasma noradrenaline. With passive 85 degrees head-up tilting at an ambient temperature of 26 degrees C the obese and post-obese subjects had a greater rise in plasma noradrenaline than the lean group who were less able to withstand the test. Noradrenaline infusions (at 26 degrees C) in the lean and post-obese subjects led to similar increases in plasma noradrenaline, systolic and diastolic pressures and plasma free fatty acids but the post-obese showed a greater bradycardia. The response to the valsalva manoeuvre was normal in lean and obese patients and was unaltered after a reduced energy intake in the obese. On energy restriction for two weeks 10 obese subjects showed a fall in pulse rate, in systolic and diastolic pressures and in plasma noradrenaline while the subjects remained supine. On standing there was less of a rise in plasma noradrenaline than when energy intake was high. The response in noradrenaline was restored to that seen on high energy intakes by giving L-dopa. Seasonal changes in venous noradrenaline concentrations were apparent in obese and post-obese patients but not in lean subjects. These differences may relate to altered responses to environmental temperature or to an altered food intake in the two obese groups. There appears to be no generalised in the autonomic system in obese women either before or after weight loss but the process of slimming does lead to a reduction in plasma noradrenaline levels.

Autonomic Nervous System↗
PubMed1994

Prevalence of gastrointestinal symptoms in obese and normal weight binge eaters.

OBJECTIVES: Disturbances in gastrointestinal function may result from disordered eating and may lead to increases in gastrointestinal (GI) symptoms. We compared GI symptoms in obese and non-obese binge eaters and non-binge eaters. METHODS: One hundred nineteen obese and 77 normal-weight females completed a questionnaire on bowel symptoms and binge eating behaviors for the previous 3 months. Based on binge behaviors and body mass index (> 30 kg/m2), individuals were grouped as obese binge eaters (n = 73), obese non-binge eaters (n = 43), non-obese binge eaters (n = 14), and normal-weight controls (n = 61). RESULTS: Obese binge eaters reported more upper GI symptoms than normal controls or obese non-binge eaters (p < 0.001). Compared with normal controls, nausea, vomiting, and bloating was 2-4 times more prevalent in both binge eating groups. Indigestion was more prevalent in both obese groups. Obese binge eaters reported more lower GI symptoms than normal-weight controls (p < 0.05). Binge eating in both weight groups was associated with more frequent abdominal pain and dyschezia. Obesity was associated with more frequent constipation, diarrhea, straining, and flatus, whether or not subjects reported binge eating. Chi-square showed a significant association between obesity, binge eating, and symptoms of irritable bowel syndrome, using the Manning criteria. CONCLUSIONS: Specific GI symptoms were associated with binge eating and obesity. Overall, symptoms were more prevalent and more severe in obese binge eaters. The high prevalence of GI symptoms in obese patients who indulge in binge eating should be considered in their evaluation and treatment.

Analysis of Variance↗
PubMed1996

Fat intake and adiposity in 8 to 11-year-old obese children.

OBJECTIVE: To investigate the relationships between diet composition, body composition, and macronutrient oxidation at rest in obese and non-obese children. DESIGN: Cross-sectional study on fat intake, adiposity and postabsorptive macronutrients oxidation rates. SUBJECTS: 82 prepubertal (age: 9.1 +/- 1.1 y) children, 30 obese (FM = 32.6 +/- 6.1%) and 52 non-obese (FM = 15.6 +/- 5.1%). MEASUREMENTS: Subcutaneous skinfold thickness for body composition, diet history for energy and nutrient intake, indirect calorimetry for resting metabolic rate (RMR) and RQ measurement. RESULTS: Energy intake (EI) was comparable in obese and non-obese children. Adjusted for RMR by ANCOVA, using RMR as the covariate, EI was significantly lower in obese than in non-obese children indicating either a blunted physical activity or a systematic underestimation of EI. Protein and carbohydrate intakes expressed as a percentage of total energy intake (%EI) were not significantly different in the two groups. Lipid intake (%EI) was slightly but significantly higher in the obese than in the non-obese group either unadjusted or adjusted for RMR by ANCOVA. The postabsorptive RQ was significantly lower in obese than in non-obese children. In the total group, %FM was weakly but significantly correlated to lipid intake (%EI). CONCLUSION: Obese prepubertal children have a higher relative fat intake than non-obese children and their FM is associated with this factor. The lower postabsorptive RQ of obese children may indicate a compensatory mechanism to achieve fat equilibrium by enhanced fat oxidation.

Adipose Tissue↗
PubMed1996

The prevalence of hypertension in gynaecoid and android obese women.

Until now the different epidemiological studies performed have yielded widely different results in terms of the prevalence of hypertension in obese patients. This is mainly due to methodological errors in blood pressure (BP) measurements, including such false positives as white-coat or cuff hypertension, and more recently, to the different distribution in the study population of obese subjects at risk of hypertension (android obesity type). In 803 obese outpatient women (body mass index range: 28-45) randomly selected and subdivided into younger and older groups, and into android and gynaecoid, the casual BP was measured in the morning with a large size cuff. In addition, in 82 obese outpatients casual BP was measured simultaneously with the large and a standard size cuff. Another group of 94 patients was submitted to 24-h ambulatory blood pressure monitoring (ABPM). The aim was to observed if the use of inappropriate cuffs, or the incidence of white-coat hypertension and the prevalence of obese subjects at risk of hypertension, may contribute considerably to overestimating the prevalence of hypertension in obesity. The hypertension prevalence rate was 37.6% for the entire study group. The prevalence rate was 26.2% in women with gynaecoid type of obesity and 47.1% in android obese subjects. We could conclude that the use of inappropriate cuffs, office or white-coat hypertension and the prevalence of obese subjects at risk of hypertension, may contribute considerably to overestimating the prevalence of hypertension in obesity. The number of hypertensive subjects in younger obese subjects with gynaecoid fat distribution is similar to non-obese subjects who are age-adjusted, but our data confirm that the prevalence of hypertension in android type of obesity is significantly higher than in non-obese subjects.

Adult↗
PubMedDate not supplied

Childhood obesity in Taiwan.

As other developed countries of the world, obesity has become a major health problem of children and adolescents in Taiwan. According to an island-wide survey, the prevalence of obesity varied from 4.3% to 17.4% in children aged three to nineteen years. Obesity is defined as an excess of body fat. Since the standard references of weight-for-height and body mass index for Taiwanese are not available, a weight-for-length index has been introduced. We have found that its easy computation and interpretation with high reliability make it a desirable measure of relative weight either in clinical practice or in research. The family background of the obese children has been investigated by many workers. In our own series, the obese children were about five times as likely to have an obese parent as control. There was also a significant difference in the chance of having an obese sibling between the obese and control groups. Several health sequelae of childhood obesity have been studied in Taiwan. Obese children appear to have high prevalence of hypertension, hyperlipidemia, and abnormal glucose metabolism. Of several cutaneous manifestations of obesity, colored striae were sometimes overlooked. In our experience, 40% of the moderate to severe obese cases have such striking marks prominently located on the thighs, arms and abdomen. A few pediatric weight-losing programs have been carried out in Taiwan. In our Pediatric Anti-Obesity Club, four fundamental components: diet, exercise, behavior modification and parent involvement were included in the treatment program. In family-based parent-directed program, 11% of the participants showed decreases in degree of obesity after one year follow-up, compared to 3% of a control group. In another individualized outpatient counseling clinic, the success rate was 59% after one year. Although the long-term effectiveness cannot determined, it seems rational that a realistic and culturally sensitive weight reduction program should be developed for countries, such as Taiwan, with increasing prevalence of childhood obesity.

Adolescent↗
PubMed1995

Eating and emotional disorders in adolescent obese girls with insulin-dependent diabetes mellitus.

OBJECTIVE: To study eating and emotional disorders in adolescent insulin-dependent diabetic (IDDM) girls. METHODS: 98 adolescent girls, aged 13-19 years, were studied: 15 obese and 37 non-obese IDDM girls, 22 obese non-diabetic and 24 non-obese girls, DSM-III-R eating disorders (anorexia nervosa, bulimia nervosa, eating disorders NOS) and eating habits (snacking, sweet compulsions) were evaluated by a semi-structured diagnostic interview (Kiddie-SADS-E and Eating Habits Interview). Emotional disorders were assessed using self-questionnaires (State-Trait Anxiety Inventory for Children, Beck Depression Inventory, Coopersmith Self-Esteem Inventory). Psychological characteristics were correlated with BMI and, for IDDM girls, with HbA1C. RESULTS: IDDM and non-diabetic obese girls showed high rates of eating disorders NOS (sub-clinical bulimia: 60 and 41%, respectively) and they had more extra-snacks than non-obese girls, suggesting that obesity was the main risk factor for additional eating disorders. However, non-obese IDDM girls had more eating disorders NOS (sub-clinical bulimia: 27%) than did the normal girls (4%). Three IDDM girls had typical bulimia nervosa, while none of the non-diabetic did. The risk of depression was increased by both IDDM and obesity (16 and 18% dysthymia, respectively; 8% in normal girls); both factors cumulated in obese IDDM girls (47% dysthymia). Obesity was linked to marked changes in self-esteem scores and mild effects on anxiety. IDDM had little effect on anxiety and none on self-esteem; it even seemed to preserve the self-esteem of obese girls. Patients with bulimia nervosa had poorer metabolic control than other girls with IDDM. There was no correlation between HbA1C and eating or emotional disorders. CONCLUSIONS: Adolescent IDDM girls are at increased risk of eating and emotional disorders. Obesity appears to be an important factor for psychiatric complications; more obese IDDM girls suffered from eating disorders NOS sub-clinical bulimia), dysthymia, anxiety disorders, depression and low self-esteem (Family Satisfaction SEI sub-score) than did non-obese IDDM girls.

Adolescent↗
PubMed1990

Dynamic of the GRF-induced GH response in genetically obese Zucker rats: influence of central and peripheral factors.

To determine the time onset of the growth hormone (GH) alteration in the genetically obese rat, we studied the in vivo and in vitro rat growth hormone releasing factor (rGRF(1-29)NH2)-induced GH secretion in 6- and 8-week-old lean and obese male Zucker rats. Under sodium pentobarbital anesthesia, rGRF(1-29)NH2 (GRF) was injected intravenously at two doses: 0.8 and 4.0 micrograms/kg b.w. Basal serum GH concentrations were similar in lean and obese age-matched animals. The GH response to both GRF doses tested was unchanged in 6-week-old obese rats as compared to their lean litter mates. In contrast, a significant decrease of the GH secretion in response to 4.0 micrograms/kg b.w. GRF was observed in the 8-week-old obese rats. The effect of GRF (1.56, 6.25 and 12.5 pM) was further studied in vitro, in a perifusion system of freshly dispersed anterior pituitary cells of lean and obese Zucker rats. Basal GH release was similar in the 6-week-old animal group. In contrast, it was significantly decreased in 8-week-old obese rats as compared to their lean litter mates. Stimulated GH response to 1.56 and 6.25 pM GRF was significantly greater in the 6-week-old obese group than in the age-matched control group. In contrast, the GH response to all GRF concentrations tested was significantly decreased in the 8-week-old obese rats as compared to their respective lean siblings. In 8-week-old obese rats, a decrease of GH pituitary content and an increase of hypothalamic somatostatin (SRIF) concentration were observed. Insulin and free fatty acid serum were significantly increased in 8-week-old obese rats. In contrast, lower insulin-like growth factor I serum levels were observed in the obese animals as compared to their lean litter mates. Finally, to further clarify the role of the periphery in the inhibition of GH secretion observed in the 8-week-old fatty rats, we exposed cultured pituitary cells of 8-week-old lean animals to 17% serum of their obese litter mates. A significant decrease of GRF-stimulated GH secretion of lean rat pituitary cells exposed to the obese serum was noted (P less than 0.05). This study demonstrates that, in the obese Zucker rat, an alteration of the GH response to GRF is evident by the 8th week of life. This defective GH secretion could be related to peripheral and central abnormalities.

Age Factors↗
PubMed2004

Attenuation of hyperinsulinemia by NN414, a SUR1/Kir6.2 selective K-adenosine triphosphate channel opener, improves glucose tolerance and lipid profile in obese Zucker rats.

Chronic attenuation of hyperinsulinemia by diazoxide (DZ), a K-adenosine triphosphate (ATP) channel opener and an inhibitor of glucose-mediated insulin secretion, improved glucose tolerance and lipid profile and decreased the rate of weight gain in obese Zucker rats. To determine whether suppression of hyperinsulinemia alters daily food consumption, rate of weight gain, glucose tolerance, and lipid profile, we compared the effects of NN414, a potent and SUR1/Kir6.2 selective K(atp)() channel opener, with DZ in obese and lean Zucker rats. DZ (150 mg/kg/d), low-dose (LDNN414: 10 mg/kg/d), high-dose (HDNN414: 30 mg/kg/d), and vehicle (C) were administered to 7-week-old obese and lean female Zucker rats for a period of 6 weeks. Each animal underwent an intraperitoneal glucose tolerance test (IPGTT) at the end of study period. While NN414 treatment did not affect food intake and rate of weight gain in any of the strains, DZ treatment reduced food intake (P <.001) and rate of weight gain (P <.001) in obese rats. The fasting plasma insulin levels and area under the curve (AUC) insulin response to IPGTT were significantly attenuated in LDNN414 (P <.05), HDNN414 (P <.01), and DZ (P <.01) obese and lean rats compared with their controls. This was accompanied by a significant reduction in AUC glucose only in LDNN414 (P <.05), HDNN414 (P <.01), and DZ (P <.01) obese rats compared with controls. While hemoglobin A(1c) (HbA(1c)) was not affected in LDNN414 obese rats, it was higher in HDNN414 obese animals (P <.001), LD-, HDNN414 (P <.001), and DZ (P <.005) lean rats compared with their respective controls. DZ obese rats showed lower HbA(1c) levels than C obese rats (P <.02). The plasma free fatty acid (FFA) levels were only decreased in HDNN414 (P <.05) and DZ (P <.002) obese rats, whereas plasma triglyceride (TG) levels were decreased in LDNN414 (P <.05), HDNN414 (P <.001), and DZ (P <.001) obese rats compared with controls. Finally, plasma leptin level was only decreased in DZ obese rats compared with controls (P <.001). The new SUR1/Kir6.2 selective K(atp)() channel opener, NN414, reduced hyperinsulinemia in a dose-dependent manner without a significant effect on food consumption and rate of weight gain. NN414-induced beta-cell rest in obese rats was associated with a significant improvement in glucose responsiveness, suggesting an increase in insulin sensitivity after its withdrawal. There was an overall deterioration in glycemic control at the high dose as measured by HbA(1c). There was a dose-dependent improvement in lipid profiles of obese Zucker rats. These results suggest that pharmacologic attenuation of hyperinsulinemic state by low-dose NN414 may be therapeutically beneficial in insulin-resistant states without any deterioration in overall glycemic control.

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