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PubMed2004

Serum concentrations of nitric oxide, tumor necrosis factor (TNF)-alpha and TNF soluble receptors in women with overweight and obesity.

The aims of the present study was to examine how overweight and obesity affect serum concentrations nitric oxide (NO) metabolites and to determine whether there is association between serum concentrations tumor necrosis factor (TNF)-alpha and TNF soluble receptors (sTNF-R) in subjects with overweight and obesity. The study groups involved 154 women: 102 obese (81 obese with body mass index [BMI] 30 to 40 kg/m2 and 21 obese with BMI > 40 kg/m2), 24 overweight patients, and 28 lean controls. Serum concentrations of NO metabolites and of TNF-alpha and its soluble receptors (sTNF-R1, sTNFR-2) were measured by enzyme-linked immunosorbent assay (ELISA) kits. Serum concentration of insulin was measured by radioimmunoassay (RIA). Plasma glucose, cholesterol, high-density lipoprotein (HDL)-cholesterol, and triglicerydes were determined by enzymatic procedure. Body composition was determined by impedance analysis using Bodystat (Douglas, British Isles). Serum concentrations of NO in the overweight group (35.1 +/- 12.1 micromol/L) and the obese groups with BMI 30 to 40 kg/m2 (32.8 +/- 9.3 micromol/L) and with BMI greater than 40 kg/m2 (33.3 +/- 8.5 micromol/L) were significantly higher when compared to controls (28.2 +/- 8.1 micromol/L): P < .05; P < .01, and P < .01, respectively. There was no difference in levels of NO between the overweight group and both obese groups. Serum concentration of TNF-alpha was also significantly higher in the group with overweight (6.5 +/- 3.1 pg/mL), in the obese group with BMI 30 to 40 kg/m2 (6.8 +/- 3.1 pg/mL), and in the obese group with BMI greater than 40 kg/m2 (7.4 +/- 2.6 pg/mL) when compared to controls (2.9 +/- 2.2 pg/mL): P < .00005; P < .00005, and P < .0000001, respectively. However, serum concentrations of sTNF-R1 and -R2 did not differ significantly between the overweight group, both obese groups, and controls. In conclusion, we observed increased serum concentrations of TNF-alpha and NO in overweight and obese women. It seems that there is an association between serum concentrations of TNF-alpha and NO; however, this relationship depends on the degree of obesity.

Adult↗
PubMed2005

Physiological difference between obese (fa/fa) Zucker rats and lean Zucker rats concerning adiponectin.

Obese (fa/fa) Zucker rat is a spontaneous genetic obesity model and, by comparison with lean Zucker rat, exhibits hyperphagia, hyperinsulinemia, and hyperlipidemia. The aim of this study was to examine the physiological difference concerning adiponectin between obese (fa/fa) Zucker rats and control lean Zucker rats. We therefore measured plasma adiponectin level and analyzed adiponectin and adiponectin receptor 1 mRNA expression in retroperitoneal white adipose tissue (RT WAT), brown adipose tissue (BAT), liver, and soleus muscle. We also examined the tissue mRNA expression of peroxisome proliferator-activated receptor alpha (PPAR alpha), PPAR delta, and PPAR gamma, which regulate adiponectin expression sensitivity to a PPAR gamma agonist shown by brown adipocytes from obese (fa/fa) Zucker rats and lean Zucker rats, by measuring adiponectin release from these cells. Plasma adiponectin levels of obese (fa/fa) Zucker rats were significantly higher than those of lean Zucker rats. Adiponectin mRNA expression levels in RT WAT were lower in obese (fa/fa) Zucker rats than in lean Zucker rats, but those in BAT were higher. Adiponectin receptor 1 expression levels in RT WAT, BAT, and liver of obese (fa/fa) Zucker rats were lower than in lean Zucker rats. The expression level of PPAR alpha, PPAR delta, and PPAR gamma in BAT was lower in obese (fa/fa) Zucker rats than in lean Zucker rats. Moreover, the PPAR gamma agonist increased adiponectin release only from the brown adipocytes isolated from lean Zucker rats. It is the conclusive difference between obese (fa/fa) Zucker rats and lean Zucker rats that plasma adiponectin levels of obese (fa/fa) Zucker rats are significantly higher than those of lean Zucker rats. Moreover, we clarified that mRNA expression level of adiponectin receptor 1 in RT WAT, BAT, and liver of obese (fa/fa) Zucker rats is low despite high plasma adiponectin level, and low expression of PPARs in BAT leads to less sensibility of adiponectin release from brown adipocytes to a PPAR gamma agonist in obese (fa/fa) Zucker rats.

Adipocytes↗
PubMed2006

Beneficial effects of physical exercise on hypertension and cardiovascular adverse remodeling of diet-induced obese rats.

BACKGROUND AND AIMS: Obesity is present among all age groups and in all socioeconomic groups. This study on obese rats aims to quantify the beneficial effects of physical exercise on blood pressure (BP), the heart, the elasticity and resistance of arteries. METHODS AND RESULTS: Obese male Wistar rats, (obesity due to a high fat diet with 30% fat), and non-obese rats, were assigned to four groups (n=5): sedentary obese; exercise-practice obese; sedentary control; and exercise-practice control (motor treadmill for 13 weeks). Their organs were studied through light microscopy and stereology. The diet-induced obesity caused mild hypertension with adverse cardiovascular changes. Physical exercise diminished the alterations associated with BP elevation and obesity. The pressure-lowering effect observed in obese rats submitted to physical exercise improved the myocardial vascularization and the aortic and the carotid wall structure by reducing the thickness and normalizing both the elastic lamellae and the smooth muscle cells. The adaptive response of the gluteus superficialis muscle to physical exercise also improved the peripheral resistance arteries of obese rats. CONCLUSION: Current research supports the notion of physical exercise as a potential non-pharmacological antihypertensive treatment for diet-induced obesity hypertension.

Animals↗
PubMed2005

Factors promoting and ameliorating the development of obesity.

Obesity develops when energy intake exceeds expenditure. A constant neural, metabolic and hormonal "conversation" between the brain and periphery underlies the defense of a given level of adiposity. For the majority of humans, obesity becomes a permanent condition once it develops, possibly because of irreversible changes in the distributed network of specialized "metabolic sensing" neurons which regulate energy intake, expenditure and storage. Plasma leptin and insulin are catabolic hormones whose levels reflect the amount of adiposity and act as signal to metabolic sensing neurons. Obesity-prone individuals have an inborn reduction in their catabolic responses to glucose, leptin and insulin. These raised metabolic and hormonal sensing thresholds precede the development of obesity and predispose individuals to become and remain obese on energy dense diets. High fat diets exacerbate this problem by independently inhibiting central insulin and leptin signaling. In addition, intake of highly palatable diets overrides the homeostatic controls of ingestion because it is regulated by neural systems mediating reward and motivation. The genetic predisposition to become obese is accentuated in offspring of mothers who are obese or nutritionally deprived during gestation and/or lactation or by overfeeding during the early postnatal period. On the other hand, chronic stress and illness can both reduce adiposity, as does gastric bypass surgery. However, for chronic obesity treatment, both exercise and pharmacotherapy help but both must be continued chronically to provide sustained lowering of body weight in obese subjects. Given the permanent upward resetting of body weight set-point that occurs when genetically predisposed individuals become obese, identification of factors that prevent the development of obesity is likely to be the most successful means of ameliorating the current obesity epidemic.

Energy Metabolism↗
PubMed2005

Obesity in renal transplantation: analysis of 2691 patients.

OBJECTIVE: Obesity is a cardiovascular risk factor in renal transplantation (RT). The objective of this study was to analyze the prevalence of post-RT obesity and risk factors associated with its development. PATIENTS AND METHODS: The study included all patients with a functioning renal transplant on December 31, 2003, who were residents of Catalonia, aged older than 14 years and who underwent transplantation between 1990 and 2003 (n = 2793); 102 patients (3.7%) were excluded due to lack of data for 1 or more study variables. Mean age was 53 +/- 14 years (range, 15-83) (61% men). Mean transplant duration was 63.0 +/- 44.5 months (range, 0-168). The chi-square test was used to compare proportions, analysis of variance (ANOVA) to compare mean values, and logistic regression to study risk factors for post-RT obesity. All data were taken from the Renal Registry of Catalonia (RMRC). RESULTS: Among RT patients, 38% were overweight (body mass index [BMI], 25-29.9 kg/m(2)) and 16% were obese (BMI >30). Prevalence of obesity was higher in women (21% vs 13%; P < .0001). Age was associated with obesity in RT patients aged 45-64 (20%) and 65-74 (18%) with respect to the group aged 15-44 years (9%) or >74 years (13%) (P < .0001). A total of 26% of patients who were normal weight before RT (BMI, 20-24.9) became overweight post-RT and 6% developed obesity (P < .0001). Among patients who were overweight pre-RT, 68% persisted with post-RT excess weight and 16% progressed to obesity (P < .0001). In the multivariate study, significant risk factors for developing post-RT obesity included the following: female (relative risk [RR], 2.46; P < .0001), age (45-64 years; RR, 2.36; P < .0001; and 65-74 years; RR, 2.23; P = .002), high blood pressure (RR, 1.44; P = .03), duration of transplant (RR, 1.06; P < .0001), cardiomyopathy (RR, 1.51; P = .007), and, particularly, the presence of excess weight (RR, 2.69; P < .0001) and pre-RT obesity (RR, 59.02; P < .0001). CONCLUSIONS: There is a high prevalence of post-RT excess weight and obesity. Adequate control of cardiovascular risk in renal transplant recipients should also include strict measures to prevent and treat obesity.

Adolescent↗
PubMed2004

Laparoscopic radical nephrectomy in obese patients: outcomes and technical considerations.

OBJECTIVES: To review our technique and experience with laparoscopic radical nephrectomy (LRN) in the obese patient population. Obesity has been considered a potential risk factor for poor outcomes in a variety of surgical procedures and has been considered a relative contraindication to laparoscopy. Since 1996, with increased experience and technical modifications, obesity has not been considered a contraindication for laparoscopy at our institution. METHODS: Retrospective data were obtained for all patients who underwent LRN from January 1997 to December 2000. A body mass index (Quetelet's index) greater than 30 was used to define obese patients. Technical modifications included slightly greater insufflation pressures and a lateral shift in trocar sites. The obese laparoscopic group was compared with the nonobese laparoscopic group. RESULTS: Of 101 patients who underwent LRN, 69 were not obese and 32 were obese. No statistically significant differences were observed in any of the analyzed operative data between the nonobese laparoscopic group and obese laparoscopic group, including a mean operative time of 220 and 242 minutes, respectively. Other factors assessed were the time to ambulation, length of hospital stay, conversion rate to an open procedure, and complication rate, which also demonstrated no statistically significant difference. Only one conversion to an open procedure was required in both the obese and the nonobese laparoscopic groups. CONCLUSIONS: With minor technical modifications, LRN can be safely performed in obese patients. Proper trocar site selection and greater insufflation pressures were critical for success. The differences in the intraoperative and postoperative course of LRN in obese and nonobese patients were not statistically significant. Obesity should not be considered a contraindication to laparoscopic nephrectomy.

Aged↗
PubMed2002

The risks of moderate and extreme obesity for coronary artery bypass grafting outcomes: a study from the Society of Thoracic Surgeons' database.

BACKGROUND: Obesity is epidemic in the United States and afflicts 97 million adults. Prior single center studies have been contradictory as to obese patients having higher risks with coronary artery bypass operations. Our objective was to assess the independent effect of both moderate (body mass index [BMI], 35 to 39.9) and extreme (BMI > or = 40) obesity on bypass operation outcomes using the Society of Thoracic Surgeons National Cardiac Database. METHODS: The study population consisted of 559,004 patients from the Society of Thoracic Surgeons database who underwent first-time, isolated coronary artery bypass grafting between January 1997 and December 2000. We compared 42,060 moderately obese patients (BMI, 35 to 39.9) and 18,735 extremely obese patients (BMI > or = 40) with 498,209 normal or mildly obese patients (BMI, 18.5 to 34.9). Multivariable logistic regression was used to determine whether BMI subgroups were independent predictors of operative risk after adjusting for other preoperative factors. RESULTS: Compared with normal or mildly obese patients (BMI, 18.5 to 34.9), moderate and severely obese patients were younger and more likely to be diabetic and hypertensive. After adjusting for these and other known preoperative risk factors, moderate obesity slightly elevated patients' operative risk (adjusted odds ratio, 1.21; confidence interval, 1.13 to 1.29). In contrast, extremely obese patients had marked higher risk for operative mortality (adjusted odds ratio, 1.58; confidence interval, 1.45 to 1.73). Major perioperative complications, particularly deep sternal wound infection, renal failure, and prolonged postoperative hospital stay also increased for extremely obese patients. CONCLUSIONS: Extreme obesity (body mass index > or = 40) is a significant independent predictor for adverse outcomes and prolonged hospitalization after coronary artery bypass operation.

Body Mass Index↗
PubMed1998

Serum leptin in obese women with polycystic ovary syndrome is correlated with body weight and fat distribution but not with androgen and insulin levels.

Leptin is a hormone produced in the adipose tissue and its concentrations in peripheral blood are significantly correlated with the amount of body fat. Whether other factors, including the pattern of body fat distribution and several hormones (such as insulin, sex steroids, and glucocorticoids), may be involved in the regulation of circulating blood leptin levels is controversial. Women with the polycystic ovary syndrome (PCOS) are hyperandrogenic and most of them are characterized by hyperinsulinemia, insulin resistance, and obesity, particularly the visceral phenotype. To assess the potential contribution of anthropometric factors, androgens, and insulin in determining leptin levels, we examined their relationship with body-mass index (BMI), visceral (VAT) and subcutaneous (SAT) adipose tissue areas, basal androgen levels, and fasting and glucose-stimulated (AUC) insulin in different groups of obese women with PCOS (n = 23) and of age-matched obese (n = 16) and non-obese (n = 10) otherwise healthy controls. The VAT/SAT ratio was measured as a parameter of body fat distribution. Serum leptin levels were significantly higher in obese PCOS women than in obese and normal-weight healthy controls and, within the controls, in the obese than in the non-obese group. In all women considered together, and in each group separately, leptin concentrations were highly significantly correlated with BMI. In addition, after adjusting for BMI, both VAT and the VAT/SAT ratio were positively and significantly correlated with leptin. Partial correlations with the VAT/SAT ratio remained significant in both the obese PCOS group and in controls considered separately, whereas the correlation with the SAT value was significant only in the control group. After adjusting for BMI, no correlation between leptin, androgens and fasting or stimulated (like AUC) insulin was found. These findings indicate that leptin levels in obese women with PCOS are higher than those observed in obese and non-obese controls. Moreover, they suggest that, other than BMI, the pattern of body fat distribution may be an independent factor related to circulating leptin levels, which, on the contrary, do not appear to be related to either androgen or insulin concentrations.

Adipose Tissue↗
PubMed1984

Energy expenditure in obesity.

Energy expenditure of obese subjects living in a respiration chamber is higher than that of lean controls; this is due to a greater basal metabolic rate in the obese. Groups of obese subjects with a family history of obesity and/or a childhood onset of obesity have a reduced thermogenic response after glucose or meal ingestion. However, this defect in diet-induced thermogenesis is not a uniform finding, since only a third of an unselected group of obese women exhibit a reduced response. Moreover, obese subjects with reduced thermogenesis have a higher overall energy expenditure than lean people, even in situations in which a thermogenic response is produced. After inducing loss of weight with a hypocaloric diet, the thermogenic defect does not disappear. Since basal metabolic rate decreases with weight loss, the postprandial energy expenditure of some 'post-obese' subjects can be lower than that of lean controls. It is concluded that a thermogenic defect can contribute to the development of obesity in some predisposed subjects. The mechanisms of the thermogenic defect in the obese are presently unknown; insulin resistance and/or a blunted response of the sympathetic nervous system have been reported, but this topic remains controversial. After weight loss, energy expenditure decreases by about 84 kJ/24 h (20 kcal/24 h) per kg of weight loss in all patients. The need to reset energy intake to a lower level than the previous maintenance food consumption represents a major difficulty in the treatment of obesity; failure to adjust energy intake to the new requirements contributes to the frequent relapse of body weight gain in the obese after completion of a period on a hypocaloric diet.

Adult↗
PubMed2001

Contrasting clinical properties and exercise responses in obese and lean hypertensive patients.

OBJECTIVES: We sought to test whether the differences in activity of the renin-angiotensin and sympathetic nervous systems at rest or during exercise can explain the differing cardiovascular properties and outcomes of lean and obese hypertensive patients. BACKGROUND: Although lean hypertensive patients have fewer metabolic abnormalities than obese hypertensive patients, paradoxically they appear to have a poorer cardiovascular prognosis. METHODS: To evaluate the heightened risks in lean hypertensive patients, this study compared metabolic, neuroendocrine and cardiovascular characteristics at rest and during a standardized treadmill protocol in obese (body mass index [BMI] = 32.5 +/- 0.3 kg/m2, n = 55) and lean (BMI = 24.3 +/- 0.2 kg/m2, n = 66) hypertensive patients. Normotensive obese (n = 21) and lean (n = 55) volunteers served as control subjects. RESULTS: Compared with the lean normotensive subjects, the lean and obese hypertensive patients had greater left ventricular mass index (LVMI) values, but on multivariate analysis, LVMI correlated with plasma renin activity (p < 0.001) and plasma norepinephrine (PNE) (p < 0.01) in the lean but not the obese hypertensive patients. Arterial compliance (stroke volume/pulse pressure ratio) was reduced in the lean hypertensive patients, in whom it correlated (p = 0.033) with PNE. The PNE rose less (22%) in the obese than in the lean (55%) hypertensive patients in response to standing (p < 0.05). Likewise, during treadmill exercise, there were lesser increases in renin (65% vs. 145%, p < 0.01) and epinephrine (200% vs. 500%, p < 0.05) in the obese hypertensive patients. These changes were also less in obese patients than in lean control subjects, indicating attenuated neurohormonal responses to stress in obesity. CONCLUSIONS: Compared with obese hypertensive patients, cardiovascular properties in lean hypertensive patients are more dependent on catecholamines and the renin system. The different neuroendocrine responses to dynamic stimuli in lean and obese patients also might help to explain the disparity in their cardiovascular outcomes.

Adult↗
PubMed2001

The importance of age and obesity on the relation between diabetes and left ventricular mass.

OBJECTIVES: The study investigated the relation of age with diabetes, obesity and hypertension on left ventricular mass (LVM). BACKGROUND: Epidemiological studies demonstrate a general rise of LVM with aging, but whether this phenomenon is independent or a function of coexisting diseases that accompany the aging process is unclear. Although obesity, hypertension and diabetes often coexist and increase in prevalence with age, studies of LVM in diabetics have been reported in mostly nonobese populations, and with little regard to the age-hypertension-obesity interactions and effects on LVM. METHODS: We prospectively measured LVM in 875 consecutive, mostly obese individuals (673 men, 202 women). Clinical data were obtained by chart review and clinical history. Echocardiographic measurements of LVM (American Society of Echocardiography criteria) were calculated using the Devereux formula and corrected for height2.7 (LVM/Ht). RESULTS: Mean age was 49.3+/-12.3 years, body mass index 33.3+/-8.0 kg/m2, and LVM/Ht2.7 41.7+/-13.4 g/m2.7. Of the total cohort, 673 patients were men, 519 obese, 228 hypertensive, and 52 diabetic. Of the 519 obese, 183 were hypertensive and 44 were diabetic (22 of those were hypertensive). Of the 228 hypertensives, 183 were obese and 26 were diabetic. On multivariate analysis, obesity (p = 0.0001), age (p = 0.0001), hypertension (p = 0.0003) and diabetes (p = 0.62) were all independently associated with LVM/Ht2.7. Obesity was the most potent independent predictor of LVM/Ht2.7, associated with an increase of 8.1 g/m2.7 in LVM/Ht2.7. In diabetics, obesity had a synergistic effect on LVM/Ht2.7 (p = 0.006), which was further amplified by age (p = 0.03). CONCLUSIONS: Age, obesity, hypertension and diabetes are all independent determinants of LVM. The magnitude of the effect of diabetes on LVM is mainly consequent to a significant interaction of diabetes with obesity and age.

Age Factors↗
PubMed1997

Personalities and alimentary behaviors in obese patients.

The actual tendency in the care of obese patients is the association of dietetic information with an eating behavior therapy. Studies attempting to attribute the origin of obesity to psychiatric pathologies are contradictory. We studied whether certain eating disorders are more specific to a personality type. We studied eating disorders with the Eating Disorder Inventory (EDI) test in 281 obese women compared to 252 age-matched non-obese women. Both obese patients and non-obese volunteers were divided into four groups depending upon their personality (PERSONA test). This test defines four types of personality, based on the level of emotion (expansive or reserved) and the degree of power (dominant or consenting). According to our study, eating disorders vary between the four personality groups and were significantly higher in the facilitating group (consenting and expansive) compared to the three other obese groups. Neither promoting (expansive and dominant) nor controlling obese patients (dominant and reserved) present eating disorders. The analyzing obese patients (reserved and consenting) are reticent when it comes to consulting (18%) since they distrust others. Analyzing obese patients present an interpersonal distrust and an interoceptive awareness. The group which presents most eating disorders is that of facilitating obese patients (consenting and expansive). These present eating disorders of the compulsive types favored by interoceptive awareness, body dissatisfaction, ineffectiveness, and maturity fears. The diversity, even the absence, of eating disorders brought to evidence by our tests based upon different personality types should allow better understanding of the psychological and behavioral causes of weight gain and the means for improving compliance in the following of an obese patient.

Adult↗
PubMed2002

Effect of obesity and starvation on thyroid hormone, growth hormone, and cortisol secretion.

Obesity and starvation have opposing affects on normal physiology and are associated with adaptive changes in hormone secretion. The effects of obesity and starvation on thyroid hormone, GH, and cortisol secretion are summarized in Table 1. Although hypothyroidism is associated with some weight gain, surveys of obese individuals show that less than 10% are hypothyroid. Discrepancies have been reported in some studies, but in untreated obesity, total and free T4, total and free T3, TSH levels, and the TSH response to TRH are normal. Some reports suggest an increase in total T3 and decrease in rT3 induced by overfeeding. Treatment of obesity with hypocaloric diets causes changes in thyroid function that resemble sick euthyroid syndrome. Changes consist of a decrease in total T4 and total and free T3 with a corresponding increase in rT3. untreated obesity is also associated with low GH levels; however, levels of IGF-1 are normal. GH-binding protein levels are increased and the GH response to GHRH is decreased. These changes are reversed by drastic weight reduction. Cortisol levels are abnormal in people with abdominal obesity who exhibit an increase in urinary free cortisol but exhibit normal or decreased serum cortisol and normal ACTH levels. These changes are explained by an increase in cortisol clearance. There is also an increased response to CRH. Treatment of obesity with very low calorie diets causes a decrease in serum cortisol explained by a decrease in cortisol-binding proteins. The increase in cortisol secretion seen in patients with abdominal obesity may contribute to the metabolic syndrome (insulin resistance, glucose intolerance, dyslipidemia, and hypertension). States of chronic starvation such as seen in anorexia nervosa are also associated with changes in thyroid hormone, GH, and cortisol secretion. There is a decrease in total and free T4 and T3, and an increase in rT3 similar to findings in sick euthyroid syndrome. The TSH response to TRH is diminished and, in severe cases, thyroid-binding protein levels are decreased. In regards to GH, there is an increase in GH secretion with a decrease in IGF-1 levels. GH responses to GHRH are increased. The [table: see text] changes in cortisol secretion in patients with anorexia nervosa resemble depression. They present with increased urinary free cortisol and serum cortisol levels but without changes in ACTH levels. In contrast to the findings observed in obesity, the ACTH response to CRH is suppressed, suggesting an increased secretion of CRH. The endocrine changes observed in obesity and starvation may complicate the diagnosis of primary endocrine diseases. The increase in cortisol secretion in obesity needs to be distinguished from Cushing's syndrome, the decrease in thyroid hormone levels in anorexia nervosa needs to be distinguished from secondary hypothyroidism, and the increase in cortisol secretion observed in anorexia nervosa requires a differential diagnosis with primary depressive disorder.

Adrenal Glands↗
PubMed2003

Non-obese (body mass index < 25 kg/m2) Asian Indians with normal waist circumference have high cardiovascular risk.

OBJECTIVE: Although the prevalence of obesity is not high in Asian Indians, increased prevalence rates of metabolic perturbations and cardiovascular risk factors have been reported. In this study, we evaluated body mass index (BMI), anthropometric measurements, and body fat profiles of obese and non-obese subjects and correlated those values with cardiovascular risk factors. METHODS: This cross-sectional study involved 639 subjects (170 men and 469 women) from low socioeconomic stratum residing in urban slums of New Delhi. Non-obese subjects were categorized into quartiles of percentage of body fat (%BF) and waist circumference (WC). Using logistic regression analysis, the odds ratios (ORs) and 95% confidence intervals (CIs) for the occurrence of cardiovascular risk factors (diabetes mellitus [DM], hypertension, hypercholesterolemia, hypertriglyceridemia, low levels of high-density lipoprotein cholesterol, and high levels of low-density lipoprotein cholesterol) were computed with first quartile in the non-obese group as the reference category for the following five categories: %BF and WC quartiles in the non-obese group and obese group (BMI > or = 25 kg/m(2)). RESULTS: In the non-obese group, approximately 66% of men and 88% of women had at least one risk factor. In non-obese women, significantly high ORs and 95% CIs were found for hypertension (3.2, 1.4-7.2), DM (2.8, 1.2-6.3), and hypertriglyceridemia (3.9, 1.9-8.3) in the upper quartiles of %BF, and significantly high OR (95% CIs) was observed for hypertriglyceridemia (3.9, 1.4-10.8) in non-obese men. Among non-obese men, significantly high OR (95% CIs) was found for hypertriglyceridemia (3.2, 1.0-10.3); among non-obese women, significantly high ORs (95% CIs) were observed for hypertension (2.5, 1.1-5.8) and hypertriglyceridemia (2.5, 1.2-5.2) in the normal range of WC (70-80 cm). CONCLUSION: The study showed that Asian Indians have excess cardiovascular risk at BMI and WC values considered "normal." These data suggested that definitions of "normal" ranges of BMI and WC need to be revised for Asian Indians.

Adult↗
PubMed2003

The effect of obesity on mid-term survival following coronary artery bypass surgery.

OBJECTIVE: Several studies have shown no significantly increased risk of in-hospital mortality for obese patients after coronary artery bypass grafting (CABG). However, the effect of obesity on mid-term survival has not been adequately studied. We set out to examine whether mid-term survival following CABG is affected by obesity. METHODS: We performed a retrospective study of 4713 consecutive patients undergoing isolated CABG between April 1997 and September 2001. Body mass index (BMI) was used as the measure of obesity, with 3429 patients categorised as non-obese (BMI<30 kg/m(2)), and 1284 patients as obese (BMI> or = 30 kg/m(2)). Patient records were linked to the National Strategic Tracing Service, which records all deaths in the community, to establish current vital status. Deaths occurring over time were described using Kaplan-Meier techniques. To control for differences in patient characteristics, we used Cox proportional hazards analysis to calculate adjusted hazard ratios (HR) and 95% confidence intervals (CI). RESULTS: Three hundred and thirty (7.0%) deaths occurred during the study period, with a mean follow-up of 2.4+/-1.4 years. The crude HR of mid-term mortality for obese patients was 1.09 (95% CI 0.86-1.39; P=0.457). After adjustment for core pre-operative factors, the adjusted HR of mid-term mortality for obese patients was 1.28 (95% CI 1.01-1.64; P=0.048). The adjusted freedom from death in the obese patients at 30 days, 1, 2, 3, and 4 years was 97.9, 95.9, 94.2, 92.4 and 90.5%, respectively, compared with 98.4, 96.8, 95.5, 94.0 and 92.5% for the non-obese patients. CONCLUSIONS: Although in-hospital mortality after CABG does not seem to be adversely affected by obesity there appears to be a significant increase in mortality in obese patients during a 4-year follow-up period.

Aged↗
PubMed1999

Variables independently associated with self-reported obesity in the European Union.

OBJECTIVE: The rapid increase in obesity rates over recent years suggest that cultural and societal influences are affecting the adjustment in the energy balance equation in addition to other physiopathological or genetic determinants. Therefore, a pan-EU study was carried out to explore the influence of sociodemographic factors as well as some attitudes (smoking and exercise) on the prevalence of obesity in the adult population of all 15 member states of the EU. DESIGN: Overall, a sample of 15,239 individuals aged 15 years and upwards in the EU completed the questionnaire. Subject selection was quota-controlled to make the sample nationally representative following a multistage stratified cluster sampling. Self-reported height and weight were used to calculate body mass index (BMI). RESULTS: From the EU average results, it can be seen that only about half of the EU population (48%) is within the normal weight range, while the obesity (BMI > or = 30 kg m(-2)) prevalence was about 10% in the EU and the overweight prevalence was 36.6% and 25.6% among men and women, respectively. UK subjects had the highest prevalence of obesity (12%), while Italians, French and Swedes had the lowest levels of obesity (about 7%). Concerning age and social class interactions, logistic regression analysis showed that high social class and younger individuals in all groups had a lower odds ratio for obesity prevalence. People with a higher level of education are less likely to be obese, while the interaction between educational levels and obesity was different for men and women. A low participation in various leisure-time physical activities, the lack of interest (precontemplation) in being involved in exercise/physical activity and the increasing number of hours sitting down at work appear to be predictors of obesity. Single individuals were less prone to become obese than couples or widowed/divorced people. Finally, smoking status was statistically linked to the prevalence of obesity, since non-smokers or ex-smokers for more than 1 year presented a higher tendency for a BMI > 30. CONCLUSIONS: This survey confirms that a priority area for health intervention aimed at preventing the development of obesity should be to increase levels of physical activity, although the approach will depend on the population, especially with respect to educational and socioeconomic aspects.

Adolescent↗
PubMed2002

The impact of obesity in renal transplantation: an analysis of paired cadaver kidneys.

BACKGROUND: Previous studies indicate that obesity is a risk factor in renal transplantation. However, these analyses did not control for variable donor factors that may strongly influence outcome. To control for donor variables such as age, cause of death, procurement techniques, preservation methods, cold ischaemia time and implantation technique, we analysed patient and graft survival in recipients of paired kidneys, derived from the same procurement procedure, preserved in the same manner, subjected to similar cold ischaemia time and implanted by the same surgical team. Between June 1992 and August 1999, 28 procurement procedures provided kidneys which were transplanted into one obese and one non-obese recipient. Body mass index (BMI) was calculated as kg/m2. Recipients were classified as obese (BMI > 30) or non-obese (BMI < 30). Immunotherapy for all recipients consisted of a triple therapy regimen of cyclosporine or prograf, azathioprine or cellcept, and prednisone. Patients with delayed graft function (DGF), defined as the need for dialysis within 72 h of the transplant procedure, were treated with anti-thymocyte globulin (ATG) or thymoglobulin (TMG) induction for 5-7 d. The rate of DGF (7.1 versus 10.7%) and acute rejection (39.3 versus 35.7%) were similar in the obese and non-obese recipient groups. Patient survival was similar at 1, 3 and 5 yr in both groups. In addition, graft survival was similar at 1 yr. However, a trend toward decreased medium-term graft survival, which reached significance at 5 yr, was observed in the obese group. Furthermore, mean serum creatinine at 1 yr was higher in the obese group (2.0) compared with the non-obese group (1, 4) (p=0.12). This analysis of paired cadaver kidneys indicated that obesity is not a risk factor for DGF, acute rejection, and 1-yr graft survival. However, a decreased medium- and long-term graft survival trend, which reached statistical significance at 5 yr, was observed in obese recipients.

Adult↗
PubMed2001

Exercise capacity in lean versus obese women.

The aim of this study was to assess the nature and magnitude of the differences in submaximal and maximal exercise capacity parameters between lean and obese women. A total of 225 healthy obese women 18-65 years (BMI> or=30 kg/m(2)) and 81 non-athletic lean women (BMI< or=26 kg/m(2)) were selected. Anthropometric measurements (weight and height), body composition assessment (bioelectrical impedance method) and a maximal exercise capacity test on a bicycle ergometer were performed. Oxygen uptake (VO(2)), carbon dioxide production (VCO(2)), expired ventilation (VE), respiratory quotient (RQ), breathing efficiency (VE/VO(2)), mechanical efficiency (ME) and anaerobic threshold (AT) were calculated. At a submaximal intensity load of 70 W, VO(2) (l/min) was larger in the obese women and was already 78% of their peak VO(2), whereas in the non-obese it was only 69% (P=0.0001). VE (l/min) was larger, VE/VO(2) did not differ and ME was lower in obese compared to the lean women. AT occurred at the same percentage of peak VO(2) in both lean and obese women. At peak effort, achieved load, terminal VO(2) (l min(-1) kg(-1)), VE, heart rate, RQ respiratory exchange ratio and perceived exertion were lower in obese subjects compared to the non-obese. Obese subjects mentioned significantly more musculoskeletal pain as a reason to end the test, whereas in lean subjects it was leg fatigue. Lean women recovered better as after 2 min they were already at 35% of the peak VO(2), whereas in the obese women it was 47% (P=0.0001). Our results confirm that exercise capacity is decreased in obesity, both at submaximal and peak intensity, and during recovery. Moreover, at peak effort musculoskeletal pain was an important reason to end the test and not true leg fatigue. These findings are important when designing exercise programs for obese subjects.

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