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PubMed2005

[Early arterial atherosclerosis and level of plasma homocysteine in simply obese children].

OBJECTIVE: To understand whether hyperhomocysteinemia and early arterial atherosclerosis exist in simply obese children. METHODS: Totally 68 simply obese children (age 6-14 years, mean 10.8 +/- 2.3 years) were enrolled in this study, 50 were male and 18 were female. Body mass index (BMI) of the obese children was equal to or more than 22. The height of the children was (145 +/- 22) cm. Meanwhile, 26 normal children (age 6 - 14 years, mean 10.9 +/- 2.0 years) were selected as control group, 17 of these children were male and 9 were female. Their height was (148.5 +/- 5.8) cm. There were no significant differences in height and age between the obese and the control children. The carotid intimal-medial thickness (IMT), brachial artery flow-mediated vasodilation were examined by Doppler Flow/Dimension System and the liver was examined by B-mode ultrasound imager. Plasma homocysteine was determined by the automated chemiluminescent enzyme immunoassays. Serum lipid concentration was determined by biochemical analytic method. Blood pressure of the right upper limbs was measured. A detailed medical and family history was systematically recorded. RESULTS: BMI was (27.8 +/- 4.5) in the obese children and (16.2 +/- 2.5) in the controls. There was significant difference between two groups (P < 0.01). The obese children had significantly increased values than the controls for the carotid intimal-medial thickness (P < 0.01). Right carotid IMT, right inner-carotid IMT, left carotid IMT and left inner-carotid IMT were respectively (0.54 +/- 0.13) mm, (0.69 +/- 0.14) mm, (0.52 +/- 0.12) mm and (0.67 +/- 0.14) mm in obese children and were respectively (0.45 +/- 0.04) mm, (0.46 +/- 0.04) mm, (0.45 +/- 0.05) mm and (0.46 +/- 0.03) mm in control groups. Conversely, the flow-mediated brachial artery dilation of the obese children was significantly lower than that of the controls [(11.0 +/- 4.3)% vs. (17.5 +/- 4.9)%, P < 0.01]. The obese children had higher level of plasma homocysteine than the controls [(7.9 +/- 2.7) micromol/L vs. (5.6 +/- 2.1) micromol/L, P < 0.01]. Total cholesterol (TC) in the obese children dramatically increased, so did triglyceride concentration (TG), LDL-cholesterol (LDL-ch) and apolipoprotein-B (apo-B). Of the obese children, had fatty liver or the tendency to fatty liver. Six cases of the 68 obese children (8%) had hypertension. Of the 68 obese children, 57 (84%) had the history of consuming excessive food or taking less exercise. Forty-four percent of the obese children (30/68) came from the obese families in which at least one of the parents or grandparents was obese. Twenty-nine percent (20/68) and 22% (15/68) of the obese children respectively came from the families in which at least one of the parents or grandparents suffered from hypertension or coronary heart disease. CONCLUSION: Early arterial atherosclerotic changes existed in simply obese children. Hyperhomocysteinemia may be an important factor of the obesity-induced early arterial atherosclerosis during childhood.

Adolescent↗
PubMed1995

Central obesity and hypertension: pathophysiologic role of renal haemodynamics and function.

OBJECTIVE: To investigate the role of alterations in renal haemodynamics and function and in plasma renin activity on obesity-induced hypertension. DESIGN: Renal haemodynamics and function, salt-regulating hormones and structural cardiac parameters were evaluated in 20 lean normotensives and in 64 obese subjects with central or peripheral fat distribution, 43 of them were normotensives and 21 of them were hypertensives. Obesity and central fat distribution were defined according to sex-specific 85th percentile respectively of Body Mass Index (BMI) and Waist to Hip Ratio (WHR). MEASUREMENTS: Serum immunoreactive insulin (IRI), plasma renin activity (PRA), plasma aldosterone (PA), microalbuminuria (UAE) and 24h urinary excretion of sodium (NaU) were evaluated by current methods. Renal haemodynamics was evaluated by radionuclide study according to Schlegel's and Gate's methods. By radionuclide study, effective renal plasma flow (ERPF), effective renal blood flow (ERBF), glomerular filtration rate (GFR), filtration fraction (FF) and renal vascular resistances (RVR) were measured. Left ventricular mass (LVM) and indexed for body height (LVM/H), cardiac output (CO) and total peripheral resistances (TPR) by ecocardiography were also calculated. RESULTS: CO, LVM and LVM/H were significantly (P < 0.05) higher in all the obese groups than lean controls. In addition, LVM and LVM/H were significantly (P < 0.05) higher in obese hypertensives than obese normotensives either with central fat distribution. TPR values were significantly (P < 0.05) higher in central obese hypertensives than peripheral obese hypertensives and than central obese normotensives. Moreover, IRI levels were significantly (P < 0.05) higher in central normotensive and hypertensive obese subjects than lean subjects. ERBF and ERPF were significantly (P < 0.05) lower and PRA levels were significantly higher only in central obese than lean subjects. On the contrary RVR were significantly (P < 0.05) higher in both obese hypertensive groups and in central obese normotensives than lean subjects. Comparisons between peripheral and central obese groups indicated that PRA, RVR and UAE were significantly (P < 0.05) higher and ERBF and ERPF values were significantly (P < 0.05) lower in both central obese groups than comparable subjects with peripheral obesity. Multiple regression analysis indicated that RVR increased significantly (P < 0.05) with WHR and PRA but not with CO and IRI. CONCLUSIONS: Our results indicate that obesity with body fat distribution of central type, more than obesity of peripheral type, is associated to abnormalities in renal haemodynamics and function. These data are consistent with the indication that change in renal haemodynamics take place at an early stage in the obesity-induced hypertension.

Adult↗
PubMed1993

Familial aggregation of morbid obesity.

Recent studies have shown major gene effects for obesity in randomly ascertained families. To investigate the familial aggregation of a specific subset of obesity, which is particularly prone to medical complications, families with morbid obesity were studied. This condition occurs in 1%-2% of the population and is defined as 45.5 kg (100 pounds) or more over ideal weight. First-degree relatives of 221 morbidly obese probands (1560 adults) were identified, and height and weight (current and greatest) were obtained from each family member. Morbid obesity occurred in the family members of the probands 8 times more often than in the general population. Of the morbidly obese probands, 48% had one or more first-degree relatives who were also morbidly obese compared to a 6% population estimate. By the ages of 20-24, 12% of the morbidly obese probands were already 45.5 kg or more overweight, and 45% were 22.7 kg (50 pounds) or more overweight. There was little difference in the prevalence of familial morbid obesity by the gender of the probands: 47% of the male probands and 48% of the female probands had another morbidly obese relative, while 67% and 53% of the early onset (before age 25) male and female probands, respectively, had one or more first-degree relatives who were also morbidly obese. In addition to the extreme degree of familial aggregation, the prevalence of morbid obesity in parent-offspring sets was calculated within the morbidly obese families. Morbidly obese families who have one or two morbidly obese parents have a 2.6 times increased risk (p<0.002) of having one or more morbidly obese adult offspring, compared to families who have neither parent morbidly obese. Evidence for trimodality of the body mass index distribution was found for each gender (p = 0.0006 for male relatives and p = 0.075 for female relatives). The strong familial aggregation of morbid obesity indicates the need for further understanding of the genetic determinants of this extreme clinical disorder and how environmental factors affect the genetic expression of the trait.

Adult↗
PubMed2006

Central obesity as a risk factor for prostatic hyperplasia.

OBJECTIVE: Obesity-related metabolic diseases may influence prostatic hyperplasia. This study examined the impact of obesity on prostate volume in men without overt obesity-related metabolic diseases. RESEARCH METHODS AND PROCEDURES: We recruited 146 men over the age of 40 years who did not have overt obesity-related diseases, such as diabetes, impaired fasting glucose, hypertension, or dyslipidemia. Transrectal ultrasonography was performed on all subjects. The subjects were divided into three groups according to their BMI: normal (18.5 to 22.9 kg/m2), overweight (23 to 24.9 kg/m2), and obese (> or = 25 kg/m2), and two groups according to their waist circumference: normal waist (< or = 90 cm) and central obesity (> 90 cm). The classification of the subgroups was based on the Asia-Pacific criteria of obesity. We compared the prostate volume among subgroups and assessed factors related to prostatic hyperplasia. RESULTS: Mean prostate volume was 18.8 +/- 5.0, 21.8 +/- 7.2, and 21.8 +/- 5.6 mL in the normal, overweight, and obese groups, respectively, and was 20.0 +/- 5.9 and 23.7 +/- 5.3 mL in the normal waist and central obesity group, respectively. Prostate volume was significantly greater in the obese group than in the normal group (P = 0.03) and in the central obesity group compared with the normal waist group (P = 0.002). Prostate volume was positively correlated with BMI and waist circumference after adjustment for age. After adjusting for confounding factors, central obesity was an independent factor affecting prostatic hyperplasia, which was defined as a prostate volume > 20 mL (odds ratio = 3.37, p = 0.037). Relative to men with both low BMI (18.5 to 22.9 kg/m2) and normal waist circumference, those with high BMI (> or = 25 kg/m2) and central obesity were at significantly increased risk of prostatic hyperplasia (odds ratio = 4.88, p = 0.008). However, those with high BMI (> or = 25 kg/m2) and normal waist circumference were not at significantly increased risk. DISCUSSION: Prostate volume was greater in the obese and central obesity groups than in the normal group after patients with overt obesity-related metabolic diseases were excluded. Although both BMI and waist circumference were positively correlated with prostate volume, central obesity was the only independent factor affecting prostate hyperplasia. We suggest that central obesity is an important risk factor for prostatic hyperplasia.

Abdominal Fat↗
PubMed2006

Habitual physical activity and sedentary behaviour in a clinical sample of obese children.

OBJECTIVE: To objectively measure habitual physical activity and sedentary behaviour in a clinical sample of obese children and to compare with age- and sex-matched non-obese controls. DESIGN: Pairwise comparison of obese children matched for age and gender with non-obese controls. SUBJECTS: A total of 116 obese children (body mass index (BMI)> or =98th centile) and 53 non-obese control children (BMI<85th centile). Controls were matched with 53 of the obese children (mean age 8.6, s.d. 2.0 years; 25 M and 28 F). MEASUREMENT: Habitual physical activity and sedentary behaviour were measured over a 7-day period using CSA accelerometers. Total physical activity (mean accelerometry count per minute (c.p.m.)), percentage of monitored time in sedentary behaviour, light and moderate to vigorous intensity physical activity (MVPA) were compared. RESULTS: Obese children (n=116) spent on average 80.4% of their monitored time in sedentary behaviour and 2.5% of their monitored time in MVPA. Total activity (mean c.p.m.) was significantly higher in the non-obese group (n=53) than the obese group (n=53), 729 vs 648 c.p.m.; 95% confidence interval (CI) 7, 155. Time spent in sedentary behaviour averaged 80.9% (s.d. 6.6) in the obese group and 79.3% (s.d. 6.2) in the non-obese group, with no significant between-group difference (95% CI -3.9, 0.6). Light intensity activity was similar in the obese and non-obese groups (15.9 vs 17.3%; 95% CI -0.3, 3.0). Participation in MVPA was significantly higher in the non-obese vs obese group (3.9 vs 2.4%; 95% CI 0.6, 2.0). CONCLUSION: This study supports the hypothesis that a clinical sample of obese children is less physically active than non-obese children, although the difference in total activity and MVPA between the groups was small.

Acceleration↗
PubMed1991

[Diurnal changes in postheparin lipolytic activity (PHLA) and the role of PHLA in triglyceride catabolism in young and middle-aged obese individuals].

The diurnal changes in postheparin lipolytic activity (PHLA) were studied as on aspect of its physiological changes in eight healthy volunteers in a fasting state. Serum lipids and PHLA in obese males were measured to determine the etiology of obesity-associated hypertriglyceridemia with respect to triglyceride (TG) catabolism. In the healthy nonobese volunteers, the lipoprotein lipase (LPL) activity did not show any diurnal changes, but decreased with time during fasting. The hepatic triglyceride lipase (HTGL) activity underwent diurnal changes, and was high in the morning and low at night. Perceiving the metabolic difference between young obese individuals (obese since childhood) and middle-aged obese individuals (obese since adulthood), PHLA and serum lipids were simultaneously determined and examined from the aspect of TG catabolism in a young male group aged 17-27 and an older male group aged 35-62. The lower-age group consisted of 15 normal-weight men and 25 obese men with 11 years (mean) of a history of obesity. The higher-age group consisted of 15 normal-weight men and 25 obese men with 12 years of a history of obesity. No differences were found in total cholesterol and LDL-cholesterol between the normal-weight and obese individuals of both groups. However, HDL-cholesterol was significantly decreased, only in the obese individuals of the higher age group, compared to the normal-weight individuals of this group. Serum TG and insulin were significantly higher in the obese individuals than normal-weight individuals of both groups. In the obese individuals in both groups, a positive correlation was demonstrated between serum TG and insulin. This suggested the increased production of TG in association with hypertriglyceridemia. In addition, TG positively correlated with LPL and HTGL activities in young obese individuals, while a negative correlation was demonstrated only between TG and LPL activity in older obese individuals. These results indicated an age-related difference in TG catabolism in obese individuals with obesity-associated hypertriglyceridemia.

Adolescent↗
PubMed2002

Reduction in resting metabolic rate and ratio of plasma leptin to urinary nitric oxide: influence on obesity-related hypertension.

BACKGROUND: Multiple factors are involved in the pathogenesis of hypertension in the obese individual OBJECTIVE: To evaluate the role of a decrease in sympathetically mediated thermogenesis and the effect of the correlation between the plasma leptin and daily urinary nitric oxide levels on obesity-related hypertension. METHODS: We evaluated three groups: 25 obese hypertensive patients (age 45.7 +/- 1.37 years, body mass index 34.2 +/- 1.35 kg/m2, systolic/diastolic blood pressure 155 +/- 2.9/105 +/- 1.3, mean arterial pressure 122 +/- 1.50 mmHg); 21 obese normotensive patients (age 39.6 +/- 1.72, BMI 31.3 +/- 0.76, SBP/DBP 124 +/- 2.1/85.4 +/- 1.8, MAP 98.2 +/- 1.80); and 17 lean normotensive subjects (age 38.1 +/- 2.16, BMI 22.1 +/- 0.28, SBP/DBP 117 +/- 1.7/76.8 +/- 1.5, MAP 90.1 +/- 1.50). We determined basal resting metabolic rates, plasma insulin (radio-immunoassay), norepinephrine (high performance liquid chromatography) in all subjects. Thereafter, 14 obese hypertensives underwent a weight reduction diet. At weeks 6 (n = 14) and 14 (n = 10) of the diet the above determinations were repeated. Plasma leptin (enzyme-linked immunosorbent assay) and UNOx (spectrophotometry) were assayed in 17 obese hypertensives and 17 obese normotensives, and in 19 obese hypertensives versus 11 obese normotensives, respectively. RESULTS: Obese hypertensive patients had significantly higher basal RMR and plasma NE levels insulin levels were lower in the lean group, with no difference between the hypertensive and normotensive obese groups. At weeks 6 and 14, BMI was significantly lower, as were insulin and NE levels. RMR decreased to values of normotensive subjects. MAP normalized but remained significantly higher than in obese normotensives. Leptin blood levels and the leptin/UNOx ratio were significantly higher in the obese hypertensive compared to the obese normotensive patients. Both these parameters were strongly correlated to BMI, MAP, RMR, and plasma NE and insulin. Obese hypertensive patients excreted less urinary NO metabolites. A strong correlation was found between MAP and the leptin/UNOx ratio. CONCLUSIONS: A reduction in sympathetically mediated thermogenesis, as reflected by RMR, results in normalization of obesity-related hypertension. In contrast, insulin does not seem to play a major role in the pathogenesis of hypertension associated with obesity. Increased leptin levels in conjunction with decreased NO production in the presence of enhanced sympathetic activity may contribute to blood pressure elevation in the obese.

Adult↗
PubMed1985

Obesity and hormonal factors in sleep and sleep apnea.

The presence of obesity, defined as weight 20 per cent or more above ideal body weight or increased body fat content, significantly increases risk of pulmonary, cardiovascular, metabolic, and gastrointestinal problems. Obesity is a major cause of shortened life expectancy. While obesity is not essential for the development of the obstructive sleep apnea syndrome, a significant percentage of patients with obstructive sleep apnea are obese. When evaluating these patients who have obstructive sleep apnea, it is important to search diligently for medical problems that are commonly found among the obese. While there is an increased incidence of obese patients among those who have obstructive sleep apnea, the exact reason for this is uncertain. The study of endorphins and enkephalins may expand our understanding of obesity, ventilatory regulation, and obstructive sleep apnea. This may, in fact, enable us to understand better the interrelationship between obesity and obstructive sleep apnea. The role that thyroid hormone, testosterone, and progesterone play in obstructive sleep apnea has also been reviewed. Patients who have obstructive sleep apnea should not be treated with testosterone. All patients given testosterone should be observed quite closely for the possible signs and symptoms of obstructive sleep apnea. Progesterone seems to be of some help in patients who have obesity hypoventilation syndrome. Its effectiveness in patients with obstructive sleep apnea is less clear. The obesity hypoventilation syndrome as described by Burwell is relatively uncommon. Many of the manifestations of the obesity hypoventilation syndrome, however, are found in patients with obstructive sleep apnea. The recognition that the symptoms stem from underlying obstructive sleep apnea offers great potential for therapy. Weight reduction is valuable therapy for patients with obesity and pulmonary dysfunction, obesity and obstructive sleep apnea, and obesity hypoventilation syndrome. Weight reduction and weight maintenance, while difficult, are essential in patients with obesity, obesity and obstructive sleep apnea, and the hypoventilation syndrome. Obesity should be viewed as a medical problem deserving medical attention and long-term medical follow-up.

Adult↗
PubMed1979

Is genetically transmitted obesity due to an adipose tissue defect?

1. The aim of this investigation was to ascertain of a variety of obese rodents whether the primary cause of fat cell enlargement lay in the fat cell itself, or in its environment. Rodents studied were the mutant mice 'diabetic' (db/db), 'adipose' (dbad/dbad), and 'yellow obese' (Ay/+), New Zealand obese mice, CBA mice made obese with gold thioglucose, and obese BIO 4.24 hamsters. 2. Gonadal fat of obese or lean genotype was transplanted under the kidney capsule of an obese or lean host. Grafts were left in place for at least one month, then examined histologically to measure fat cell diameters, from which fat cell masses were calculated. 3. Immunological rejection of grafts was avoided either by using mice syngeneic except for the obesity producing mutation (db/db, dbad/dbad or Ay/+) or by transplanting into F1 hybrids (NZO X BALB/c) made by mating the strains acting as donors of obese or lean fat. Transplantation of fat between lean BIO 4.22 hamsters and obese BIO 4.24 hamsters was possible because these had common histocompatibility antigens. 4. In all the forms of murine obesity studied, 'lean' fat cells enlarged in an obese recipient to the size typical of cells in 'obese' fat whilst 'obese' fat cells shrunk in a lean recipient to, at least, the size typical of 'lean' fat. Lean hamster fat cells also enlarged in an 'obese' environment and 'obese' hamster cells shrunk in a 'lean' environment. 5. Environment therefore contributes to the determination of fat cell size in all the rodents studied, and in several rodents (db/db, dbad/dbad, Ay/+, and gold thioglucose obese mice) our results showed that environmental factors are of paramount importance in determining cell size, and factors associated with the fat cell itself make a negligible contribution.

Adipose Tissue↗
PubMed1994

The male obese Wistar diabetic fatty rat is a new model of extreme insulin resistance.

The male obese Wistar Diabetic Fatty (WDF) rat is a genetic model of obesity and non-insulin dependent diabetes (NIDDM). The obese Zucker rat shares the same gene for obesity on a different genetic background but is not diabetic. This study evaluated the degree of insulin resistance in both obese strains by examining the binding and post binding effects of muscle insulin receptors in obese rats exhibiting hyperinsulinemia and/or hyperglycemia. Insulin receptor binding and affinity and tyrosine kinase activity were measured in skeletal muscle from male WDF fa/fa (obese) and Fa/? (lean) and Zucker fa/fa (obese) and Fa/Fa (homozygous lean) rats. Rats were fed a high sucrose (68% of total Kcal) or Purina stock diet for 14 weeks. At 27 weeks of age, adipose depots were removed for adipose cellularity analysis and the biceps femoris muscle was removed for measurement of insulin binding and insulin-stimulated receptor kinase activity. Plasma glucose (13.9 vs. 8.4 mM) and insulin levels (14,754 vs. 7440 pmol/L) were significantly higher in WDF obese than in Zucker obese rats. Insulin receptor number and affinity and TK activity were unaffected by diet. Insulin receptor number was significantly reduced in obese WDF rats ( 2.778 +/- 0.617 pmol/mg protein), compared to obese Zucker rats (4.441 +/- 0.913 pmol/mg potein). Both obese strains exhibited down regulation of the insulin receptor compared to their lean controls. Maximal tyrosine kinase (TK) activity was significantly reduced in obese WDF rats (505 +/- 82 fmol/min/mg protein) compared to obese Zucker rats (1907 +/- 610 fmol/min/mg protein). Only obese WDF rats displayed a decrease in TK activity per receptor. These observations establish the obese WDF rat as an excellent model for exploring mechanisms of extreme insulin resistance, particularly post-receptor tyrosine kinase-associated defects, in non-insulin dependent diabetes.

Adiposity↗
PubMed1995

Dietary fat is shunted away from oxidation, toward storage in obese Zucker rats.

Previous measurements of lipoprotein lipase (LPL) activity in adipose tissue (ATLPL) of lean and obese Zucker rats have consistently documented increased activity in obese rats relative to lean. Since LPL is considered to be rate limiting for the delivery of triglyceride fatty acids (TGFA) to muscle and adipose tissue, these data have been used to suggest that the metabolic partitioning of TGFA favors storage over oxidation in obese rats. To document the partitioning of TGFA directly, the fate of 14C labeled oleic acid (42nmols) was fed to lean, obese, and obese Zucker rats fed a hypocaloric diet designed to chronically reduce weight 25% below that of obese controls (reduced-obese). The amount of 14C recovered in CO2 over 6 hours following ingestion was significantly less in obese rats compared to lean (0.45 +/- 0.06 vs. 0.88 +/- 0.09nmols, p = .0004) and less still in the reduced obese group (0.34 +/- 0.06nmols p = .00003). Six hours after ingestion, the quantity of label found in adipose tissue was significantly greater in the obese rats compared to lean (14.51 +/- 1.92 vs. 1.38 +/- 0.29nmols p < .00001), but was intermediate in the reduced-obese group (9.23 +/- 0.98nmols p = .0003). At 2.2 hours there was significantly more label in skeletal muscle of lean rats compared to either obese or reduced-obese (2.33 +/- 0.24; 1.35 +/- 0.04nmols p = .01; 1.41 +/- 0.27nm p = .02). However, at 6 hours these differences between groups were no longer present. These finding Indicate that dietary fat is shunted away from oxidation toward storage in obese Zucker rats. Additionally it appears that there may be a relative block in the oxidation of TGFA that is taken up by skeletal muscle in obese rats. Finally the relative normalization of this partitioning defect in reduced-obese rats is at variance with what was suggested by previous measurements of tissue specific levels of LPL, and suggests an enhanced recirculation of fatty acids from adipose tissue to muscle in reduced-obese rats. This could occur through increased delivery of non-esterified fatty acids (NEFA) to muscle as a result of an increase in net lipolysis.

Adipose Tissue↗
PubMed1995

Fasting plasma insulin level is an important risk factor for the development of complications in Japanese obese children--results from a cross-sectional and a longitudinal study.

It is not known what types of factors may contribute to the development of complications in obese children. In the current investigation, we have performed a cross-sectional and a longitudinal study in Japanese obese children to clarify the relationship of the extent of obesity, fat distribution, insulin resistance, and aging to the development of obesity-related complications. In the cross-sectional study of 329 obese boys and 142 obese girls aged 7 to 15 years, the fasting plasma immunoreactive insulin (IRI) level was significantly higher than that of 46 non-obese boys and 48 non-obese girls (boys, 13.4 +/- 6.7 v 4.9 +/- 1.9 microU/mL, P < .001; girls, 14.0 +/- 5.9 v 4.8 +/- 1.8, P < .001). Linear regression analysis demonstrated that fasting plasma IRI correlated positively with fasting plasma glucose (FPG), triglycerides (TG), uric acid (UA), and systolic blood pressure (SBP) in obese boys, and with TG, SBP, and diastolic blood pressure (DBP) in obese girls, and negatively with serum high-density lipoprotein cholesterol (HDL-C) in both obese boys and girls. Multiple regression analysis demonstrated that fasting plasma IRI was independently and positively correlated with FPG, TG, and SBP in obese boys. Fasting plasma IRI in obese girls was positively correlated with TG, SBP, and DBP, and negatively with HDL-C. FPG decreased significantly in non-obese children at the onset of puberty, but it remained unchanged in obese children. Fasting plasma IRI and the IRI to glucose ratio increased with age in obese children, whereas they did not show any significant changes in non-obese children.(ABSTRACT TRUNCATED AT 250 WORDS)

Child↗
PubMed2004

Influence of obesity on in-hospital and early mortality and morbidity after myocardial revascularization.

OBJECTIVE: Obese patients are thought to have an increased risk for complications in coronary artery bypass surgery. Several risk stratification systems do not identify obesity as a variable for risk adjustment. The aim of this study is to evaluate the in-hospital and early (one year) mortality and morbidity in obese and non-obese patients after a CABG in the UMC St Radboud. METHODS: The data of 1130 patients undergoing a myocardial revascularization from January 2000 to August 2002 were analyzed. Obesity was measured by the body mass index (BMI). A BMI>or=30 kg/m2 was defined as obese. We compared 206 obese patients with 924 non-obese patients. Uni- and multivariate analysis were used to analyze the results. The 1-year survival was analyzed using Kaplan-Meier methods. RESULTS: There were no significant differences between obese and non-obese patients according to postoperative myocardial infarction, re-operation for bleeding, in-hospital mortality, renal complications, neurological complications, pulmonary complications, gastrointestinal complications, re-intubation, re-admission on intensive care, ventilation time, days on intensive care, days in hospital and late mortality. Only the incidence of postoperative wound infections was increased in obese patients, 8.3% in the obese versus 4.4% in the non-obese (P=0.02). Multivariate analysis identified obesity only as risk factor for postoperative for wound infections (P=0.04, odds ratio: 1.97). CONCLUSIONS: Obese patients do not have an increased risk of in-hospital and early (1 year) mortality after CABG. However, obese patients have an increased risk of postoperative wound infections compared to non-obese patients.

Aged↗
PubMed1997

Pediatric obesity. An overview of etiology and treatment.

Pediatric obesity is a chronic and growing problem for which new ideas about the biologic basis of obesity offer hope for effective solutions. Prevalence of pediatric and adult obesity is increasing despite a bewildering array of treatment programs and severe psychosocial and economic costs. The definition of obesity as an increase in fat mass, not just an increase in body weight, has profound influence on the understanding and treatment of obesity. In principle, body weight is determined by a balance between energy expenditure and energy intake, but this observation does not by itself explain obesity. There is surprisingly little evidence that the obese overeat and only some evidence that the obese are more sedentary. Understanding of the biologic basis of obesity has grown rapidly in the last few years, especially with the identification of a novel endocrine pathway involving the adipose tissue secreted hormone leptin and the leptin receptor that is expressed in the hypothalamus. Plasma leptin levels are strongly correlated with body fat mass and are regulated by feeding and fasting, insulin, glucocorticoids, and other factors, consistent with the hypothesis that leptin is involved in body weight regulation and may even be a satiety factor (Fig. 2, Table 1). Leptin injections have been shown to reduce body weight of primates, although human clinical trials will not be reported until summer 1997. So many peptides influencing feeding have been described that one or more may have therapeutic potential (Fig. 2, Table 1). Although the complexity of pathways regulating body weight homeostasis slowed the pace of understanding underlying mechanisms, these complexities now offer many possibilities for novel therapeutic interventions (Fig. 2). Obesity is a major risk factor for insulin resistance and diabetes, hypertension, cancer, gallbladder disease, and atherosclerosis. In particular, adults who were obese as children have increased mortality independent of adult weight. Thus, prevention programs for children and adolescents will have long-term benefits. Treatment programs focus on modification of energy intake and expenditure through decreased calorie intake and exercise programs. Behavior-modification programs have been developed to increase effectiveness of these intake and exercise programs. These programs can produce short-term weight loss. Long-term losses are more modest but achieved more successfully in children than in adults. Several drug therapies for obesity treatment recently have been approved for adults that produce sustained 5% to 10% weight losses but experience with their use in children is limited. Identification of the biochemical pathways causing obesity by genetic approaches could provide the theoretic foundation for novel, safe, and effective obesity treatments. The cloning of leptin in 1994 has already led to testing the efficacy of leptin in clinical trials that are now underway. Although novel treatments of obesity are being developed as a result of the new biology of obesity, prevention of obesity remains an important goal.

Adolescent↗
PubMed1985

Childhood obesity.

Several conclusions can be drawn on the basis of the research reviewed: Obese children are more likely to become obese adults than are their thinner peers. Parent weight may interact with child weight status in the etiology of adult obesity. Obese children with obese parents are more likely to become obese adults than are obese children with thin parents. The prediction of adult obesity from childhood obesity improves with the age of the child. As the obese child gets older, he or she is more likely to become an obese adult. The inclusion of parents in the treatment process is important for the success of childhood weight control. It may be best to see the parent and child separately in treatment meetings rather than together. Children with thin parents may do better in weight control than children of obese parents. Adherence to exercise is likely to be a problem with obese children, and the choice or design of an exercise program should take these adherence problems into account. Nutritional adequacy of the child's diet should be evaluated both in terms of what the child is eating as well as in terms of the prescribed diet. Likewise, growth of the obese child during dieting should be monitored and should be related to expected height, which can be based on parent height. In summary, childhood obesity is a problem that places a child at great risk for becoming an obese adult. However, a growing body of research has emerged that has identified important risk factors for the development of obesity in children. Likewise, treatment methods have been developed that produce significant and long-lasting effects on childhood weight status. Continued development of treatment methods would be of great potential importance in the prevention and treatment of this prevalent problem.

Adolescent↗
PubMed1997

Plasma atrial natriuretic peptide and natriuretic peptide receptor gene expression in adipose tissue of normotensive and hypertensive obese patients.

OBJECTIVE: Human and rat adipose tissue contain very high levels of natriuretic peptides clearance receptor messenger (m)RNA, and fasting inhibits its gene expression in adipose tissue. In this study we evaluated plasma atrial natriuretic peptide (ANP) and gene expression of biologically active type A natriuretic peptide receptor (NPr-A) and clearance natriuretic peptide receptor (NPr-C) in adipose tissue of obese hypertensive and obese normotensive patients. DESIGN AND METHODS: We studied 27 untreated obese hypertensives, 26 obese normotensives (body mass index > or = 30 kg/m2), 24 non-obese essential hypertensives and 23 lean healthy subjects (body mass index < or = 25 kg/m2). Blood samples were withdrawn for ANP, plasma renin activity and aldosterone radioimmunoassays. Subcutaneous peri-umbilical adipose tissue samples were obtained, by needle aspiration, in 13 obese hypertensives and in 12 obese normotensives and used for RNA extraction. Then, complementary synthesis and semiquantitative polymerase chain reaction (PCR) with primers complementary to sequences of different exons of the genes encoding for NPr-A, NPr-C and beta-actin, were performed. 32P-labeled PCR products were separated by electrophoresis, blotted onto nylon membranes, and the exposed autoradiographic films were analysed by densitometry. NPr signals were normalized by the beta-actin expression level. RESULTS: Plasma ANP was lower in obese hypertensives than in obese normotensives (37.5+/-7 versus 43.2+/-6 pg/ml, P< 0.05), but was higher in non-obese hypertensives than in non-obese normotensives. In contrast, plasma renin activity and aldosterone were higher in the obese hypertensives. Although NPr-A and NPr-C expression were not statistically different between the two obese groups, the NPr-A: NPr-C mRNA ratios were significantly lower in obese hypertensives (P < 0.03). CONCLUSIONS: Our data suggest that in obese hypertensives compared to obese normotensives, the lower NPr-A: NPr-C ratio might determine decreased biological activity and/or an increased clearance of natriuretic peptide in adipose tissue, suggesting that the natriuretic peptide and its receptor system may be important in obesity-related hypertension where ANP levels are lower.

Actins↗
PubMed1999

Neural mechanisms in human obesity-related hypertension.

OBJECTIVE: Two hypotheses concerning mechanisms of weight gain and of blood pressure elevation in obesity were tested. The first hypothesis is that in human obesity sympathetic nervous system underactivity is present, as a metabolic basis for the obesity. The second hypothesis, attributable to Landsberg, is that sympathetic nervous activation occurs with chronic overeating, elevating blood pressure. These are not mutually exclusive hypotheses, since obesity is a heterogeneous disorder. DESIGN AND METHODS: Whole body and regional sympathetic nervous system activity, in the kidneys and heart, was measured at rest using noradrenaline isotope dilution methodology in a total of 86 research voluteers in four different subject groups, in lean and in obese people who either did, or did not, have high blood pressure. RESULTS: In the lean hypertensive patients, noradrenaline spillover for the whole body, and from the heart and kidneys was substantially higher than in the healthy lean volunteers. In normotensive obesity, the whole body noradrenaline spillover rate was normal, mean renal noradrenaline spillover was elevated (twice normal), and cardiac noradrenaline spillover reduced by approximately 50%. In obesity-related hypertension, there was elevation of renal noradrenaline spillover, comparable to that present in normotensive obese individuals but not accompanied by suppression of cardiac noradrenaline spillover, which was more than double that of normotensive obese individuals (P<0.05), and 25% higher than in healthy volunteers. There was a parallel elevation of heart rate in hypertensive obese individuals. CONCLUSIONS: The sympathetic underactivity hypothesis of obesity causation now looks untenable, as based on measures of noradrenaline spillover, sympathetic nervous system activity was normal for the whole body and increased for the kidneys; the low sympathetic activity in the heart would have only a trifling impact on total energy balance. The increase in renal sympathetic activity in obesity may possibly be a necessary cause for the development of hypertension in obese individuals, although clearly not a sufficient cause, being present in both normotensive and hypertensive obese individuals. The discriminating feature of obesity-related hypertension was an absence of the suppression of the cardiac sympathetic outflow seen in normotensive obese individuals. Sympathetic nervous changes in obesity-related hypertension conformed rather closely to those expected from the Landsberg hypothesis.

Adolescent↗
PubMed2005

Maternal outcomes in pregnancies complicated by obesity.

OBJECTIVE: To investigate the relationship between prepregnancy obesity and maternal outcomes. METHODS: A 15-year, population-based cohort study using the Nova Scotia Atlee Perinatal Database compared maternal outcomes in obese and nonobese women. Prepregnancy weight of 55-75 kg was considered nonobese, and weight greater than 90 kg was considered obese. Obese women were categorized into moderate obesity (90-120 kg) and severe obesity (> 120 kg) groups. Univariate and multivariable logistic regression analysis was performed, and odds ratios (ORs), adjusted ORs, and 95% confidence intervals (CIs) were calculated. P < .05 was considered statistically significant. RESULTS: In 142,404 singleton pregnancies, 10,134 (7.2%) women were identified as obese (moderate obesity 92.3%, severe obesity 7.7%). The proportion of women in the obese categories increased from 3.2% in 1988 to 10.2% in 2002. Moderately obese women had an increased risk of pregnancy-induced hypertension (PIH) (adjusted OR 2.38, 95% CI 2.24-2.52), antepartum venous thromboembolism (adjusted OR 2.17, 95% CI 1.30-3.63), labor induction (adjusted OR 1.94, 95% CI 1.86-2.04), cesarean delivery (adjusted OR 1.60, 95% CI 1.53-1.67), and wound infection (adjusted OR 1.67, 95% CI 1.38-2.00). Severely obese women had an increased risk of PIH (adjusted OR 3.00, 95% CI 2.49-3.62), antepartum venous thromboembolism (adjusted OR 4.13, 95% CI 1.26-13.54), induction of labor (adjusted OR 2.77, 95% CI 2.39-3.21), cesarean delivery (adjusted OR 2.46, 95% CI 2.15-2.81), anesthesia complications (adjusted OR 2.01, 95% CI 1.33-3.06), and wound infection (adjusted OR 4.79, 95% CI 3.30-6.95). This implies that, relative to nonobese women, there was 1 excess case of PIH per 10 moderately obese women and 1 per 7 severely obese women. For antepartum venous thromboembolism, there was 1 excess case per 857 moderately obese women and 1 per 321 severely obese women. CONCLUSION: Prepregnancy maternal obesity increases the risk of PIH, antepartum venous thromboembolism, labor induction, cesarean delivery, and wound infection.

Adult↗