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PubMed1992

Increased free testosterone but normal 5 alpha-reduced testosterone metabolites in obese premenopausal women.

OBJECTIVE: The aim of the study was to investigate whether the absence of increased 5 alpha-reductase activity explained the absence of hirsutism in premenopausal obese women with increased free testosterone (FT) levels. DESIGN: As in hyperandrogenicity there generally exists evidence for increased 5 alpha-reductase activity, we measured, as parameters of 5 alpha-reductase activity, plasma levels of 5 alpha-androstane-3 alpha,17 beta-diol glucuronide (ADG) and androsterone glucuronide (ADTG) as well as their precursor levels in obese women without hirsutism, obese hirsute women, non-obese hirsute women, and non-obese, non-hirsute women. PATIENTS: Eighty-two premenopausal women (20-45 years old) were studied, in four age matched groups: 39 controls, 18 obese without hirsutism, 11 non-obese hirsute and 14 obese hirsute women. MEASUREMENTS: Blood samples were taken between days 5 and 7 of the menstrual cycle. Steroid hormone levels were measured by radioimmunoassay. Free testosterone levels were measured by equilibrium dialysis. RESULTS: Compared to controls, mean free testosterone levels were increased (P less than 0.01) in obese, obese hirsute and hirsute patients, whereas mean DHEAS levels were increased in hirsute and obese hirsute (P less than 0.01), but not in obese, women. Mean androstanediol glucuronide levels were markedly increased in hirsute and obese hirsute patients (P less than 0.01), but not in obese women. Plasma androsterone glucuronide levels were increased in hirsute (P less than 0.01), in the normal range in obese hirsute, and decreased in obese women (P less than 0.01). CONCLUSIONS: These results show that, despite the presence of higher free testosterone levels, neither 5 alpha-reductase activity (as suggested by normal androstanediol glucuronide levels) nor adrenal androgen precursor levels (DHEAS) are increased in obese women without hirsutism.

3-Oxo-5-alpha-Steroid 4-Dehydrogenase↗
PubMed1996

Transplantation of lean fetal hypothalamus restores hypothalamic function in Zucker obese rats.

Rats with lesions to the ventromedial hypothalamus (VMH) manifest obesity, hyperphagia, and hyperinsulinemia, and fetal VMH transplantation into the third cerebroventricle of VMH-lesioned rats reduces the development of obesity caused by the lesion. The aim of this study was to determine whether the hyperphagia, hyperlipidemia, and hyperinsulinemia of obsese Zucker rats could be corrected by the transplantation of lean fetal Zucker hypothalamic tissue into the third cerebral ventricle of Zucker obese rats. After the fetal hypothalamic transplant (obese-HY), the rate of weight gain was significantly diminished compared with the unoperated Zucker obese rats and the obese rats that received the transplantation of a similar amount of frontal cortical tissue from the same fetus (obese-FC). Food intake was significantly lower, and plasma triacylglycerol and insulin concentrations were also significantly reduced in the obese-HY rats compared with the obese and obese-FC rats. The weight of the adrenal glands, the plasma adrenocorticotropic hormone concentration, the liver weight, and the liver lipid content in obese-HY were significantly less than those observed in the obese and obese-FC animals. There were no significant differences between the obese and the obese-FC animals or between unoperated Zucker lean rats and lean rats transplanted with lean fetal hypothalamus in all the parameters we determined in this study. Neovascularization and normal cellular morphology of the transplanted fetal hypothalamic tissue suggest that the transplanted neural and glial cells were viable and physiologically functional. In conclusion, this study offers evidence suggesting that the hypothalamic-pituitary-adrenal function is defective in Zucker obese rats, resulting in excessive weight gain, hyperphagia, hyperlipidemia, and hyperinsulinemia. The hypothalamic dysfunction in the Zucker obese rats is corrected by the transplantation of lean fetal hypothalamus.

Adrenal Glands↗
PubMed1993

Developmental and sex-related changes of the growth hormone axis in lean and obese Zucker rats.

The development and sex-related changes in the hypothalamic-pituitary GH axis were examined in lean and obese Zucker male and female rats from 6 to 12 weeks of age. Pituitary GH content was not different in any phenotype/sex group at 6 weeks. GH content increased with age in male rats, but at 10 and 12 weeks content was decreased in obese male rats relative to lean rats. GH content did not increase in female rats and there was no difference in content between lean and obese female rats. Hypothalamic GHRH content was not different between the groups. Hypothalamic SS content was decreased in obese male rats compared to lean male rats (95%) and in obese female rats compared to lean female rats (78%). Individual 6-hour plasma GH profiles from rats 6-7 weeks of age showed the characteristic sexually dimorphic GH secretory patterns. However, spontaneous GH secretion was dramatically reduced in obese animals when compared to sex-matched lean rats. GH peak amplitude (25% of lean) and mean GH concentration (19% of lean) were decreased in obese male rats without a significant alteration in GH peak frequency or baseline level. In obese female rats, the number of GH peaks, peak amplitude, baseline GH, and mean GH concentration were all decreased compared to lean. The reduction in peak amplitude (14% of lean) and in mean GH concentration (20% of lean) was similar to the reduction in obese male rats. Serum IGF-I concentrations were not different among the groups at 6 weeks. IGF-I levels in male rats increased with age but were not different between lean and obese rats. IGF-I concentrations in female rats were unchanged with time and were not different between lean and obese rats. Serum insulin was increased in obese male and female rats at 6 through 12 weeks. We conclude (1) GH secretion is depressed at 6-7 weeks in obese male and female rats with the magnitude of reduction similar to previous observations in male rats 12 weeks or older; (2) pituitary GH content is depressed only in obese male rats and occurs after the defect in GH secretion; (3) hypothalamic GHRH content is unchanged and hypothalamic SS is slightly to moderately decreased in obese rats; (4) serum IGF-I is not different between lean and obese rats; (5) obese male and female rats were hyperinsulinemic.(ABSTRACT TRUNCATED AT 400 WORDS)

Aging↗
PubMed1996

The effects of dexfenfluramine on weight loss and cardiovascular risk factors in female patients with upper and lower body obesity.

BACKGROUND: Obesity has been identified as a risk factor for atherosclerosis, and fat distribution has proved to be a critical variable. Weight loss improves health, but failure rates in dietary treatment are high. The effects of dexfenfluramine, which is useful in many patients, were studied on cardiovascular risk factors in obese female patients with upper and lower body obesity. METHODS: In a placebo-controlled, double-blind trial, which was part of a multicentre study, 52 obese female patients (body mass index 35.1 +/- 7.8 kg/m2, age 43.3 +/- 6.4 years) were given either 15 mg dexfenfluramine twice daily, or placebo in addition to a calorie-restricted diet (1500 kcal/day) for 12 months. Forty-two patients (20 with upper body obesity, 12 dexfenfluramine and 10 placebo; 22 with lower body obesity, 16 dexfenfluramine and six placebo) completed the 14-month study. RESULTS: Patients with upper body obesity lost 14.2 +/- 2.20 kg with dexfenfluramine, and 4.92 +/- 2.99 kg with placebo (P < or = 0.05). In contrast, patients with lower body obesity lost 11.1 +/- 2.89 kg with dexfenfluramine and 2.6 +/- 2.32 kg with placebo (P < 0.05). With dexfenfluramine, patients with upper body obesity lost more weight than patients with lower body obesity (P < 0.05). After 1 year of dexfenfluramine treatment, reduction of systolic blood pressure in patients with upper body obesity (157 +/- 10 versus 133 +/- 8 mmHg, P < 0.05) was significantly (P < 0.05) greater than in patients with lower body obesity (136 +/- 14 versus 127 +/- 12 mmHg). During dexfenfluramine treatment cardiovascular risk factors improved. In upper body obesity blood glucose (5.18 +/- 0.28 versus 4.40 +/- 0.34 mmol/l, P < 0.05), serum insulin (23.4 +/- 8.9 versus 13.2 +/- 4.2 microU/ml, P < 0.05) and triglycerides (1.96 +/- 0.45 versus 1.23 +/- 0.54 mmol/l, P < 0.05) decreased, and high-density lipoprotein cholesterol increased (1.0 +/- 0.14 versus 1.21 +/- 0.14 mmol/l P < 0.05). In lower-body obesity, cardiovascular risk factors were in the normal range and did not change significantly during the study. CONCLUSIONS: Dexfenfluramine lowers body weight in obese patients with upper and lower body obesity and reduces the cardiovascular risk factors clustering in upper body obesity.

Adult↗
PubMed1998

Effect of acute pharmacological reduction of plasma free fatty acids on growth hormone (GH) releasing hormone-induced GH secretion in obese adults with and without hypopituitarism.

In obesity, there is a markedly decreased GH secretion. The diagnosis of GH deficiency (GHD) in adults is based on peak GH responses to stimulation tests. In the severely obese, peak GH levels after pharmacological stimulation are often in the range that is observed in hypopituitary patients. To distinguish obese subjects from GHD patients, it will be necessary to demonstrate that reduced GH responsiveness to a given test is reversible in the former, but not in the latter, group. Recent studies have shown that reduction of plasma free fatty acids (FFA) with acipimox in obese patients restores their somatotrope responsiveness. There are no data evaluating GH responsiveness to acipimox plus GHRH in obese adults with hypopituitarism. The aim of the present study was to evaluate the effect of acute pharmacological reduction of plasma FFA on GHRH-mediated GH secretion in obese normal subjects and obese adults with hypopituitarism. Eight obese patients with a body mass index of 34.2+/-1.2; eight obese adults with hypopituitarism, with a body mass index of 35.5+/-1.9; and six control subjects were studied. All the patients showed an impaired response to an insulin-tolerance test (0.15 U/kg, i.v.), with a peak GH secretion of less than 3 microg/L. Two tests were carried out. On one day, they were given GHRH (100 microg, i.v., 0 min), preceded by placebo; and blood samples were taken every 15 min for 60 min. On the second day, they were given GHRH (100 microg, i.v., 0 min), preceded by acipimox (250 mg, orally, at -270 min and -60 min); and blood samples were taken every 15 min for 60 min. The administration of acipimox induced a FFA reduction during the entire test. Normal control subjects had a mean peak (microg/L) of 23.8+/-4.8 after GHRH-induced GH secretion; previous acipimox administration increased GHRH-induced GH secretion, with a mean peak of 54.7+/-14.5. In obese patients, GHRH-induced GH secretion was markedly reduced, with a mean peak (microg/L) of 3.9+/-1; previous administration of acipimox markedly increased GHRH-mediated GH secretion, with a mean peak of 16.0+/-3.2 (P < 0.05). In obese adults with hypopituitarism, GHRH-induced GH secretion was markedly reduced, with a mean peak (microg/L) of 2+/-0.7; previous acipimox administration did not significantly modify GHRH-mediated GH secretion, with a mean peak of 3.3+/-1.1 (P < 0.05). The GH response of obese patients and obese adults with hypopituitarism was similar after GHRH alone. In contrast, the GH response after GHRH plus acipimox, was markedly decreased in obese adults with hypopituitarism (mean peak, 3.3+/-1.1), compared with obese patients (mean peak, 16.0+/-3.2) (P < 0.05) and control subjects (mean peak, 54.7+/-14.5) (P < 0.01). In conclusion, GH secretion, after GHRH-plus-acipimox administration, is reduced in obese adults with hypopituitarism patients, when compared with obese normal patients. Testing with GHRH plus acipimox is safe and is free from side effects and could be used for the diagnosis of GHD in adults.

Adult↗
PubMed2004

Contribution of pathogens in human obesity.

Obesity is increasing rapidly in the United States as well as in other countries. The World Health Organization considers obesity a worldwide epidemic that poses a major public health threat. In humans, obesity causes or exacerbates a number of other diseases and co-morbidities. Etiology of obesity includes genetic, metabolic, social, behavioral and cultural factors. Although obesity has multiple causes, an often overlooked possibility is that of obesity due to an infection. Over the past two decades, seven pathogens are reported to cause obesity in animals. Canine distemper virus was the first reported obesity-promoting virus. Rous-associated virus-7, an avian retrovirus, causes stunted growth, obesity and hyperlipidemia in chickens. Borna disease virus was noted to cause obesity in rats. Scrapie agents were reported to induce obesity in mice. These pathogens appear to produce obesity by damaging the central nervous system. Next, three adenoviruses were reported to promote obesity, but their mechanisms are not clear. Animals experimentally infected with SMAM-1, an avian adeno-virus, or two human adenoviruses, adenovirus type 36 (Ad-36) and Ad-37, developed adiposity. Notably, SMAM-1 and Ad-36 were associated with obesity in humans. Although more research is needed to further define the mechanisms and the role of pathogens in the etiology of obesity, they should be included in the long list of potential etiological factors for obesity. Determination of the role of pathogens in human obesity is critical for its successful treatment and prevention.

Animals↗
PubMed2000

Accuracy of teen and parental reports of obesity and body mass index.

OBJECTIVES: Adolescent obesity is becoming an increasing public health problem. This study determines: 1) differences in teen and parental report of obesity, 2) amount of misclassification using body mass index (BMI) from self-reported versus measured height and weight as an indicator of obesity, and 3) whether misclassification varies by gender and socioeconomic status. DESIGN: Weighted data from 15 483 baseline (T1) youth and parental interviews from the National Longitudinal Study of Adolescent Health were used. Seventy-four percent of teens were reinterviewed 1 year later (T2). Parents reported socioeconomic status indicators and whether their teen was obese. Teens reported height, weight, and weight perception. BMI was calculated from both self-reported height and weight at T1 and T2 and from measured height and weight at T2. Those with a BMI > or =95% corrected for age and gender were considered obese. RESULTS: At T1, nearly one half of teens (47%) reporting they were very overweight were not obese by BMI. For teens obese by BMI, 19.6% were reported to be obese by both parent and teen, 6.4% by teen only, 29. 9% by parent only, and 44.2% by neither teen nor parent. For those with persistent obesity, teen and/or parental report failed to identify more than one third (34%) as obese; 23.4% were identified by both teen and parent report, 5.4% by teen report only, and 37.2% by parent only. At T2, the correlation between BMI calculated from self-reported versus measured height and weight for the overall population was very strong (r = .92). Specificity of obesity status based on self-reported BMI, compared with obesity status based on measured BMI was .996; sensitivity, .722; positive predictive value, .860; and negative predictive value, .978. Overall, 3.8% of teens were misclassified using self-report measures. Girls were no more likely than boys to be misclassified as obese using BMI from self-reported height and weight. CONCLUSIONS: Parental report is a better indicator of obesity than teen report of weight status, but parental and teen reports are both poor predictors of adolescent obesity. Using BMI based on self-reported height and weight correctly classified 96% as to obesity status. Thus, studies can use self-reported height and weight to understand teen obesity and its correlates/sequelae.

Adolescent↗
PubMed1987

Role of lipid oxidation in pathogenesis of insulin resistance of obesity and type II diabetes.

Increased lipid oxidation is generally observed in subjects with obesity and diabetes and has been suggested to be responsible for the insulin resistance associated with these conditions. We measured, by continuous indirect calorimetry, lipid and glucose oxidation and nonoxidative glucose disposal in 82 obese subjects during a 100-g oral glucose tolerance test (OGTT) and in 26 during a euglycemic insulin (40 mU.min-1.m-2) clamp. The obese subjects were subdivided into those with normal glucose tolerance (group A), those with impaired glucose tolerance (group B), and those with overt diabetes (group C). Forty-five healthy nonobese subjects were subdivided into a young and an older control group, which were age-matched to the nondiabetic obese (groups A and B) and diabetic obese (group C) subjects, respectively. In the postabsorptive state, as well as in response to insulin stimulation (both OGTT and insulin clamp), lipid oxidation was significantly increased in all three obese groups in comparison with either young or older controls. Basal glucose oxidation was significantly decreased in obese nondiabetic and obese glucose--intolerant subjects (groups A and B) compared with age-matched controls. During the OGTT and during the insulin clamp, insulin-stimulated glucose oxidation was decreased in all three obese groups. In contrast, nonoxidative glucose disposal was markedly inhibited in nondiabetic and diabetic obese patients during the euglycemic insulin clamp but not during the OGTT. After glucose ingestion, nonoxidative glucose uptake was normal in nondiabetic obese and glucose-intolerant obese subjects and decreased in diabetic obese subjects. Statistical analysis revealed that lipid and glucose oxidation were strongly and inversely related in the basal state, during euglycemic insulin clamp, and during OGTT. The negative correlation between lipid oxidation and nonoxidative glucose uptake, although significant, was much weaker. Fasting and post-OGTT hyperglycemia were the strongest (negative) correlates of nonoxidative glucose disposal in both single and multiple regression models. We conclude that 1) reduced glucose oxidation and reduced nonoxidative glucose disposal partake of the insulin resistance of nondiabetic obese and diabetic obese individuals; 2) hyperglycemia provides a compensatory mechanism for the defect in nonoxidative glucose disposal in nondiabetic obese subjects; however, this compensation is characteristically lost when overt diabetes ensues; and 3) increased lipid oxidation may contribute, in part, to the defects in glucose oxidation and nonoxidative glucose uptake in obesity.

Adult↗
PubMed2001

Serum leptin changes during weight loss in obese diabetic subjects with and without microalbuminuria.

To evaluate the changes of serum leptin levels after weight reduction in diabetic subjects with and without microalbuminuria, we studied 10 obese healthy subjects, 12 obese diabetics with persistent microalbuminuria and 10 obese diabetic subjects without microalbuminuria. Obese diabetic patients with microalbuminuria showed serum leptin levels significantly higher than normoalbuminuric diabetics, while no difference was found between obese diabetics without microalbuminuria and healthy controls. All obese subjects followed a 12-month intensive weight reduction program during which the mean change in body mass index was similar between obese diabetic and obese healthy subjects (obese diabetics without microalbuminuria: 35.2+/-4.3 vs 29.9+/-4.1, p<0.05; obese diabetics with microalbuminuria: 35.7+/-3.9 vs 30.3+/-4.0, p<0.05; obese healthy subjects: 35.5+/-4.0 vs 30.1+/-3.9, p<0.05). The mean changes in serum leptin levels tended to be similar in two groups of subjects studied (obese diabetics without microalbuminuria: 37.6+/-4.1 vs 19.7+/-4.9, p<0.001; obese healthy subjects: 37.1+/-4.3 vs 20.1+/-5.1, p<0.001); obese microalbuminuric subjects showed higher leptin levels (42.4+/-4.0 vs 30.3+/-4.2, p<0.001) than normoalbuminuric diabetic and obese healthy subjects. In conclusion, during weight loss, independently from the quality of metabolic control, serum leptin concentrations declined in both groups of obese diabetics. The changes of leptin in diabetics seem to be similar to those observed in healthy obese subjects.

Adolescent↗
PubMed2004

[Dynamic analysis on the prevalence of obesity and overweight school-age children and adolescents in recent 15 years in China].

OBJECTIVE: In order to develop strategies on prevention and cure for obesity, a study regarding dynamic analyses on the prevalence of obesity and overweight of Chinese children and adolescents was carried out. METHODS: Data of more than 980 thousands students of Han nationality, aged 7 through 18 years old were collected from National Surveys on Chinese Students' Constitution and Health which were carried out in 1985, 1991, 1995 and 2000. Samples were divided into four groups as "metropolis", "medium and small sized cities", "prosperous village" and "below-averaged village". Study targets were screened using the new criterion-the "Reference Norm for Screening Overweight and Obesity in Chinese Children and Adolescents" which was set up by the Working Group on Obesity in China. The prevalence of overweight and obesity in various groups in different years were compared and analyzed. RESULTS: The prevalence rates of obesity in 1985 including from the metropolis area, were only 0.2% and 0.1% for boys and girls, and the prevalence of overweight was between 1% and 2% indicating that was no trend of obesity epidemic then. However, a rapid increase of overweight prevalence has been noticed since the early 1990s, and the increments were more seen in the urban than in the rural areas and more in boys than in girls. In the most developed cities including Beijing, the prevalence rates of obesity appeared to be 4.7%, 3.8% and 3.2%, among three groups with higher risk: the 7 - 9, 10 - 12 year-old boys and 7 - 9 year-old girls, respectively. Both high prevalence rates of malnutrition and overweight were also found in that period. Around 1995, a large scale of increments of overweight were found both in the urban and rural groups. In the most developed metropolis, the prevalence of overweight was two to three folds more than that of 10 years ago. The prevalence of obesity were 6% - 8% for boys and 4% - 6% for girls, respectively. Since 2000, most of the Chinese metropolis have started the so called 'overall increment period' of obesity. The prevalence rates of obesity plus overweight had reached 25.4%, 25.5%, 17.0% and 14.3% for boys aged 7 - 9 years and 10 - 12 years, and girls aged 7 - 9 years and 10 - 12 years, respectively. Among them, the prevalence rates of obesity were 12.9% and 9.1% for boys aged 7 - 9 and 10 - 12 years, which had already reached the average level seen in the medium-developed countries in the world. Although the increments of overweight were high, the prevalence of obesity was still low in most of the other groups: 4.8% for boys and 2.6% for girls in the "medium sized" group, 1.5% for boys and 1.7% for girls in the "prosperous village" group, and 0.9% for boys and 1.2% for girls in the "below-averaged village" group, respectively. CONCLUSIONS: The prevalence of obesity in Chinese children and adolescents was considered to be still relatively low. However, the rapid increasing of both obesity and overweight, in both urban and rural areas would arouse special attention. Comprehensive strategies of intervention should include periodical monitoring, education on pattern of nutrition, oxygen-consuming physical exercises and healthy dietary behavior. Two areas on obesity prevention to protect the child from becoming overweight in early ages, and to control the tendency of obesity from overweight, should be emphasized in order to improve the health status and life quality of the Chinese children and adolescents.

Adolescent↗
PubMed1984

The development of obesity in animals: the role of genetic susceptibility.

There are a number of animals in which obesity is genetically determined. In some the inheritance is polygenic while in others it is by a single-gene mutation. In the most widely studied single-gene mutants--the obese (ob/ob) mouse, the diabetic-obese (db/db) mouse and the Zucker (fa/fa) rat-obesity is very substantial and is initiated before the animals are weaned. Although hyperphagia is a feature of all the major obese mutants, it is not a prerequisite for the development of obesity. The initiation of the disorder during the suckling period takes place on a normal energy intake, and excess rates of energy deposition will still continue after weaning if the obese mutants are pair-fed to the ad libitum energy intake of lean siblings. The ability to become obese without hyperphagia indicates that one or more components of energy expenditure must be reduced in the obese mutants. Studies on the ob/ob mouse have demonstrated that a reduction in thermogenesis in BAT is the main way by which this is achieved. The reduction in energy expenditure in BAT is due primarily to a low activity of the sympathetic innervation to the tissue. Once hyperphagia is established, apparently as a secondary feature of the obese syndrome, the development of obesity is accelerated, the obese mutants having an impairment in the dietary stimulation of BAT thermogenesis. Studies on different types of obese animal suggest that an inability to respond to dietary stimuli is a general feature of obesity. The final syndrome presented by genetically obese animals is of considerable metabolic and endocrinological complexity. However, it is now possible to begin to integrate some of the endocrinological abnormalities within the energy balance framework, centred on BAT, that has been developed over the past few years. This is particularly evident in the case of adrenal function in the Zucker rat; adrenalectomy of this mutant has important effects on energy balance and in the normalization of the thermogenic activity of BAT. The sensitivity of BAT to insulin is also emerging as a possible factor of importance in the modulation of thermogenesis in obese animals.(ABSTRACT TRUNCATED AT 400 WORDS)

Adipose Tissue, Brown↗
PubMed2002

Correlates of overweight and obesity in 644 patients with bipolar disorder.

OBJECTIVE: Overweight and obesity are common clinical problems encountered in the treatment of bipolar disorder. We therefore assessed the prevalence and clinical correlates of overweight, obesity, and extreme obesity in 644 bipolar patients. METHOD: 644 outpatients with DSM-IV bipolar disorder in the Stanley Foundation Bipolar Treatment Outcomes Network were evaluated with structured diagnostic interviews and clinician- and self-administered questionnaires to determine bipolar disorder diagnoses, demographic and historical illness characteristics, comorbid Axis I diagnoses, medical histories, health habits, and body mass indices (BMMs). RESULTS: Fifty-eight percent of the patients with bipolar disorder were overweight, 21% were obese, and 5% were extremely obese. American patients had significantly higher mean (p < .0001) BMIs and significantly higher rates of obesity (p < .001) and extreme obesity (p < .001) than European patients. Significant associations (p < or = .001) were found between overweight, obesity. and extreme obesity and gender, age, income level, comorbid binge-eating disorder, hypertension, arthritis, diabetes mellitus, exercise habits, and coffee consumption. Current BMI and weight were each correlated with the number of weight gain-associated psychotropics to which patients had been exposed. Multinomial logistic regression (adjusted for site and eating disorder diagnosis and corrected for multiple comparisons) showed that (1) overweight was significantly associated with male gender and hypertension (p < .001), (2) obesity was significantly associated with hypertension (p < .001), and (3) extreme obesity was significantly associated with hypertension and arthritis (p < .001). CONCLUSION: Overweight, obesity, and extreme obesity were common in this group of bipolar patients, although it was unclear that their prevalence rates were truly elevated, because overweight and obesity are increasingly common public health problems among the general population. Correlates of overweight and obesity in bipolar disorder include patient and treatment variables such as gender, geographical location, comorbid binge-eating disorder, age, income level, degree of exposure to weight gain-associated psychotropics, medical disorders associated with obesity, and health habits.

Adult↗
PubMed1997

The impact of pre-transplant obesity on renal transplant outcomes.

The impact of obesity on graft survival after renal transplantation continues to be controversial. We have reviewed our experiences with living donor and cadaver transplantation in the current decade, focusing specifically on the impact of obesity on transplant outcome. Preoperative body mass index (BMI, kg/m2) was calculated for all adult renal transplant recipients between January 1990 and December 1995 and was used to classify patients as non-obese, moderately obese or morbidly obese. The effect of the degree of obesity on early and late outcomes after renal transplantation was examined. Three hundred and thirty-three recipients had pre-transplant BMI < 30 (normal or mild obesity), 68 BMI 30-40 (moderate obesity), and 7 BMI over 40 (morbid obesity). There was no correlation between obesity and other demographic factors. Wound infections and delayed graft function occurred more commonly in moderately and morbidly obese than in other cadaver donor recipients. Obese patients gained more weight after surgery and were given lower doses per kilogram of cyclosporine. There was, however, no significant correlation between obesity and graft survival for either cadaver or living donor transplants. Although obese patients have an increased risk of delayed graft function with cadaver donor transplantation, obesity has no discernible impact on either immunologic or overall graft survival with cadaver or living donor transplantation. The impact of moderate obesity on transplant outcome is modest and should not prevent these patients from receiving a transplant.

Adult↗
PubMed1994

Characteristics of the obesity syndrome in Zucker-Brown Norway (ZBN) hybrid rats.

The existence of a restriction fragment length polymorphism (RFLP) closely linked to the fatty locus between the Zucker (Z) and Brown Norway (BN) rat strains allows evaluation of early effects of the fatty (fa) gene using offspring of back-crosses (N2) between F1 females and Zucker obese males. We examined several metabolic characteristics of N2 animals to determine if these hybrid animals exhibited similar characteristics of the obese syndrome to those of Zucker rats. Females from crosses of obese male Zucker (fa/fa) and lean female BN (+/+) rats were back-crossed to their sires, resulting in twelve N2 litters. At 9 weeks of age, liver, spleen, interscapular brown fat (IBAT), and gonadal, retroperitoneal (RP), and inguinal fat depots were removed and weighed. Samples of the RP depot were analyzed for cell size and number. Obese N2 rats were hyperphagic, with body weights in the range of those of obese Zucker rats. Obese N2 rats were also hyperinsulinemic [mean +/- SEM, microU/ml: females, 7.9 +/- 0.6 vs. 82.1 +/- 8.4 (lean vs. obese); males, 10.5 +/- 1.6 vs. 128.5 +/- 13.4 (lean vs. obese)] and mildly hyperglycemic [mean +/- SEM, mg/dl: females, 104.1 +/- 2.0 vs. 139.0 +/- 14.7 (lean vs. obese); males, 100.9 +/- 2.6 vs. 132.0 +/- 2.8 (lean vs. obese) p < or = 0.05]. White fat depots in obese rats were 3 to 7 times heavier than those in lean rats; adipocyte numbers in RP depots were 50% greater in obese than in lean rats; and cell size was more than 3 times larger. IBAT, liver, and spleen were also heavier in obese vs. lean rats, while tail lengths were shorter. Percent lean carcass mass and % carcass protein were about 30% greater in lean vs. obese rats, while % carcass fat in obese rats was 5 times greater than that of lean rats. Thus, phenotypic expression of the fa gene in ZBN hybrid animals, with approximately 25% of their genetic background coming from the BN strain, appears to be similar to that in Zucker rats. Given the similarity of phenotypic expression of the fa gene between the Zucker strain and ZBN hybrids, it is plausible to consider using ZBN hybrids for studies of early manifestations of fa gene action prior to onset of detectable obesity.

Adipocytes↗
PubMed1988

The cataract Shionogi mouse, a sister strain of the non-obese diabetic mouse: similar class II but different class I gene products.

We have studied with a series of monoclonal antibodies and restriction fragment analysis the K, D, and class II region of the major histocompatibility complex of the non-obese diabetic mouse in comparison with its sister strains, the non-obese non-diabetic and cataract Shionogi mouse. (1) K region: Monoclonal antibody 31-3-4S (anti-Kd) reacted with splenocytes from non-obese diabetic mice while other anti-K (Kb, Kk, Kq) monoclonals did not react. Splenocytes from non-obese non-diabetic mice reacted with both anti-Kb and Kk monoclonals while splenocytes from cataract Shionogi mice reacted with anti-Kd and Kk monoclonals. Both sister strains, therefore, differ from the non-obese diabetic and other known mice strains by monoclonal analysis of H-2K. (2) D region: Splenocytes from both non-obese diabetic and non-obese non-diabetic mice reacted with monoclonal antibody 28-14-8S (anti-Db) while splenocytes from cataract Shionogi mice did not react with any anti-D monoclonal antibody tested. (3a) Class II region (non-obese diabetic and non-obese non-diabetic mice): Three of 11 monoclonal antibodies to class II molecules reacted with splenocytes of the non-obese diabetic mouse. The 3 reacting monoclonals have I-Ak primary specificities though additional anti-I-Ak monoclonal antibodies were negative. Among these monoclonals, 39B and 40A reacted with the non-obese diabetic mouse but not with the non-obese non-diabetic mouse, while 10-2-16 reacted with non-obese diabetic, non-obese non-diabetic and cataract Shionogi mice. Monoclonal MKD6 (anti-I-Ad) reacted with non-obese non-diabetic but not non-obese diabetic mice.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2006

Obesity is a risk factor for failure of "fast track" extubation following coronary artery bypass surgery.

PURPOSE: Obesity is a common comorbid condition among patients undergoing coronary bypass surgery. Previous studies have shown inconsistent results as to whether obese patients require prolonged ventilation after cardiac surgery. Fast track recovery strategies have become common to reduce the duration of ventilation and intensive care. The purpose of this study was to determine whether, in our practice, obesity affects post-operative ventilation time using a fast track recovery strategy. METHODS: A retrospective continuous quality improvement audit of 200 patient records was performed. Patients were divided into Obese and Non-obese groups using a definition for obesity of body mass index >or= 30.0. Failure of fast track extubation was defined as intubation > six hours. RESULTS: Eighty-four (42.4%) of the patients audited met criteria for obesity. Although most patients successfully underwent fast track recovery, time to extubation was prolonged, and failure of fast track extubation was more common, in obese patients (63% Non-obese vs 46% Obese extubated in < two hours, 98% Non-obese and 85% Obese patients extubated in < six hours, P < 0.001). Increased body mass index, duration of operative time and postoperative serum creatinine were risk factors for failed fast track extubation among the obese patients. Postoperative blood loss through chest drains was reduced in obese patients. CONCLUSIONS: While most obese patients can undergo a fast track recovery strategy following cardiac surgery, in our institution the incidence of failure of early extubation is significantly higher than in non-obese patients. Our experience may assist in resource planning for postcardiac surgery patients.

Body Mass Index↗
PubMed2007

Impact of obesity on outcome and changes in quality of life after coronary artery bypass grafting.

BACKGROUND: An increasing proportion of patients undergoing coronary artery bypass grafting (CABG) are obese and are thought to carry a higher mortality and morbidity in association with surgery, but data on whether health-related quality of life (QOL) improves similarly after CABG in obese and non-obese patients are limited. We assessed in detail the effect of obesity on changes in health-related QOL (RAND-36 Health Survey) during the first year following CABG. METHODS: Comprehensive data on 508 CABG patients were prospectively collected. One hundred patients (19.7%) were categorized as obese (body mass index >or= 30 kg/m(2)). The RAND-36 Health Survey was used as an indicator of quality of life. Assessments were made preoperatively and repeated 12 months later. RESULTS: The obese group fared significantly worse than the non-obese group with regard to the likelihood of superficial wound infection (19.0% versus 7.1%, P < 0.001), impaired renal function (31.7% versus 14.4%, P = 0.01), and required on average 2 days longer in hospital (P < 0.05). The incidence of mediastinitis was not significantly higher among the obese patients (2.0% versus 1.2%, P = 0.55), and they less frequently needed postoperative red cell transfusions (29.0% versus 44.9%, P = 0.004). The obese improved significantly (P < 0.001) in 7, and the non-obese (P < 0.001) in all 8 RAND-36 dimensions. Physical Component Summary and Mental Component Summary scores on the RAND-36 improved significantly (P < 0.001) in obese as well as in non-obese patients. CONCLUSIONS: Although obese patients differ from non-obese patients in that they had inferior QOL before and in the year following CABG, they gain a similar improvement in QOL 1 year after surgery compared with non-obese patients. Excluding superficial wound infection, transient impaired renal function, and slightly longer hospital stay, obesity does not significantly increase the risk of other adverse outcomes during the first year following CABG.

Adult↗
PubMed1993

Abnormal polyunsaturated lipid metabolism in the obese Zucker rat, with partial metabolic correction by gamma-linolenic acid administration.

Below-normal proportions of phospholipid (PL) arachidonic acid (20:4 omega 6) have been reported in serum from obese humans and in liver from obese Zucker rats. This implies an abnormality of 20:4 omega 6 formation from linoleic acid (18:2 omega 6), possibly in the delta 6 desaturase step, or alternatively an abnormality in the catabolism or distribution of arachidonate. We previously speculated that a reduced proportion of 20:4 omega 6 in hepatic PL could contribute to the etiology of genetic obesity. Providing 18:3 omega 6 would bypass delta 6 desaturase and possibly normalize hepatic PL 20:4 omega 6. Therefore weanling Zucker rats were given free access to a defined diet (11% of energy as soy oil) and gavaged daily with 100 microL of either black currant oil concentrate ([BCO] 8% 18:2 omega 6 and 70% 18:3 omega 6) or soy oil ([Soy] 55% 18:2 omega 6 and < 0.1% 18:3 omega 6). Groups of eight lean and eight obese animals were randomized to receive Soy or BCO in a 2 x 2 design; 10 obese and 10 lean rats were fed a stock diet (nongavaged reference). All groups of lean rats had identical weight gain; food intake for Soy lean and BCO lean did not differ. The obese reference animals and Soy obese animals did not differ in weight gain. However, BCO obese animals ate less food (P < .06), gained less weight (P < .0001), and had lower percent body fat (P < .05) compared with the Soy obese animals. The fatty acid constituents from serum, liver, and adipose tissue showed marked differences between lean and obese animals. Hepatic PL 20:4 omega 6 was lower in Soy obese than in lean (P < .002), but was normalized by BCO gavage (diet effect, P < .007). The paucity of hepatic PL 20:4 omega 6 was not due to reduced desaturase activity, as the proportions of other desaturase products (20:3 omega 6, 20:3 omega 9, 20:5 omega 3) were significantly elevated in Soy obese rat liver and serum. Serum and hepatic cholesteryl ester 20:4 omega 6 levels were elevated in obese versus lean rats (P < .02 and P < .0001), indicating abnormal arachidonate distribution in the obese Zucker rat. Because BCO selectively reduced weight gain and percent body fat in obese Zucker rats, our results imply a role for abnormal omega 6 fatty acid metabolism in the etiology of Zucker obesity.(ABSTRACT TRUNCATED AT 400 WORDS)

Adipose Tissue↗